Venous thrombosis

Introduction

Venous thrombosis is a serious condition in which the formation of a thrombi (otherwise known as a thrombus) in the venous system. The thrombus acts as a plug in the vessel, blocking the flow, which has the potential to build up and increase in volume quite rapidly. Venous thrombosis most commonly develops in the deep veins of lower limbs, although it can also occur in other locations. Thrombosis developing in the deep system requires special attention. If left untreated, it can lead to dangerous complications, including pulmonary embolismand therefore an immediately life-threatening condition.

According to the latest epidemiological data, venous thrombosis affects up to two people per 1,000 inhabitants each year. The risk of its occurrence increases significantly with age. Among people over 75 years of age, the incidence can be as high as 5-8 cases per 1,000 people per year.

Factors that increase the risk
occurrence of venous thrombosis

Congenital factors

  • genetic mutations (e.g. factor V Leiden (F5), prothrombin G20210A, MTHFR C677T and A1298C, SERPINC1 gene, PROC gene, etc.).
  • deficiency of natural anticoagulants (protein C, protein S, antithrombin)
  • increased concentration of coagulation factors (VIII, IX, XI)
  • congenital fibrinolysis disorder (plasminogen deficiency, dysfibrinogenemia or increased plasminogen activator inhibitor type 1 levels)
  • blood type other than 0 (people with blood type A, B or AB have a higher risk of venous thrombosis compared to people with blood type 0)

Acquired factors

  • long immobilisation (flight over 4-6h, hospitalisation)
  • surgical and orthopaedic procedures
  • pregnancy and post-partum period
  • cancer
  • use of oral hormonal contraception or HTZ
  • obesity
  • venous insufficiency

Mechanism of venous thrombosis formation

The phenomenon of formation venous thrombosis is a rather complex pathophysiological process that develops on the basis of classical Virchow's triads (described by Rudolf Virchow w 1856 year). It includes the following factors: trauma to the venous vessel wall, excessive blood clotting and disturbances in blood flow. The onset of venous thrombosis is usually caused by damage to the vascular endothelium or a change in the blood flow conditions in the vein. Under normal conditions, the endothelium exhibits anticoagulant properties, but damage to the endothelium leads to the exposure of tissue factor (TF), which initiates the coagulation cascade.

Activation of the coagulation system by production of the complex TF-VIIa leads to an increase in the level of thrombin, a key enzyme in the clotting process. Thrombin converts fibrinogen into fibrin and activates platelets and further clotting factors, winding up the whole clotting cascade. The slowing down of blood flow in the vessel causes a local accumulation of clotting factors and reduces the effect of natural inhibitors of the process.

Activated platelets adhere to the damaged endothelium and release substances that enhance the thrombotic process. The thrombus that forms consists of a network of fibrin fibres, which, as it were, capture the morphotic elements of the blood.

Tomasz Grzela, MD, PhD, on venous insufficiency in young adults

Did you know?

Swelling, pain and redness of the limb are alarm signals that require immediate diagnosis. It is important that venous thrombosis is detected and treated as soon as possible after the first symptoms appear!

Tomasz Grzela, MD, PhD

Thrombus progression occurs when prothrombotic mechanisms operating in our body gain the upper hand. The thrombus may enlarge and occupy further segments of the venous vessel. Its enlargement is always associated with an increased risk of fragmentation of the thrombus. In the event of thrombus fragmentation, the following may occur pulmonary embolism. We are then talking about the so-called thromboembolism. A long-lasting thrombotic process can damage the venous valves irreversibly. This leads to the formation of what is known as a 'thrombosis'. post-thrombotic syndrome.

Recognition and diagnosis of venous thrombosis

Proper recognition venous thrombosis usually requires an understanding of the patient's medical history, a full clinical assessment together with imaging and laboratory investigations. Prompt and accurate diagnosis is crucial for effective treatment and prevention of serious complications.

  • clinical signs: pain in the limb, usually unilateral swelling, redness and warming of the skin, soreness of the limb on pressure, enhancement of superficial veins and bruising of the limb.
    It is important to note that the severity of symptoms may vary from patient to patient, and some cases of venous thrombosis may present with minimal symptoms. It is also important to note that these symptoms may be unilateral, which is characteristic of venous thrombosis.
  • diagnostic imaging: research Doppler ultrasound is the gold standard for diagnosis and CT angiography (less frequently angiography-MR) in cases of extensive femoropopliteal thrombosis and in cases of suspected thromboembolism and suspected oncological background of venous thrombosis.
  • laboratory tests (D-dimers - have a high sensitivity but low specificity for detecting venous thrombosis, blood count, coagulation parameters, diagnostics are indicated in selected cases thrombophilia, or hypercoagulability, which can be congenital or acquired).
    Normal D-dimer levels are very likely to rule out thrombosis, but elevated levels require further diagnosis.
Doppler ultrasound of the venous system is the gold standard for the diagnosis of venous thrombosis. It is important that the examination is also performed in the standing position with assessment of the deep system veins. © Department of Phlebology

Mostly
questions asked

  • D-dimers are not a sufficiently specific marker of venous thrombosis. They can be elevated in many other conditions: in pregnancy, after surgery and trauma, in cancer, in various types of infection and inflammation, in cases of haematomas and in the elderly.

  • The risk of venous thrombosis is estimated to be 4-5 times higher in pregnancy and as much as 20 times higher in the postpartum period compared to women who are not pregnant. The highest risk of thrombosis is in the third trimester of pregnancy and the period 3-6 weeks after delivery. There is a higher risk of venous thrombosis in the period after caesarean section. This may persist up to 12 weeks after delivery.

  • Yes, a susceptibility to venous thrombosis can be genetic and passed on to offspring. If there is a family history of venous thrombosis, it is worth informing your doctor. The most common mutations, leading to the so-called 'varicose vein thrombosis', are the following. congenital hypercoagulabilities, that:

    • Factor V Leiden mutation (G1691A mutation): 5-fold increased risk of thrombosis in heterozygotes, up to 50-fold in homozygotes
    • G20210A prothrombin gene mutation: 3-fold increased risk of thrombosis
    • Antithrombin III deficiency - is the most severe form of congenital thrombophilia; the risk of thrombosis increases 50-fold.
    • Protein C and S deficiency: cause an approximately 10-fold increased risk of venous thrombosis.
  • Yes, as much as possible. Particularly if it is first detected quite late and there is a post-thrombotic syndrome (PTS). Approximately 30-40% patients are likely to experience another episode of venous thrombosis within 10 years. For this reason, it is important to eliminate primary risk factors, use compression devices (compression therapy) as secondary prophylaxis and take anticoagulants regularly as prescribed by a phlebologist.

  • The standard treatment time for venous thrombosis is an average of 3-6 months. This is the case for thromboses with a known and transient risk factor, e.g. after a fracture with immobilisation or after surgery. It is important that anticoagulant treatment is accompanied by the wearing of compression therapy. For idiopathic thrombosis (without an identifiable cause), treatment is usually extended to 6-12 months. Prolongation of treatment time for venous thrombosis is necessary in cases of: recurrent deep vein thrombosis, presence of persistent risk factors, coexistence of congenital thrombophilia, thrombosis in an unusual location and in cases of severe post-thrombotic syndrome. Remember that the timing of anticoagulant treatment is always selected on an individual basis. Therapy must take into account all risk factors and benefits for the patient. Regular clinical assessment and adaptation of the treatment strategy to the changing disease situation is crucial.

    Explore our latest publications and research papers.

    The scientific activities of the team at the Department of Phlebology make a significant contribution to the development of modern phlebology. Our scientific research and publications confirm the effectiveness of innovative and proprietary treatment methods, setting new standards in the treatment of venous diseases.

    The doctors of the Phlebology Clinic have pioneered the causal treatment of venous disease worldwide. Our proprietary treatment methods, validated by scientific research and prestigious publications, have opened up new possibilities for all phlebology patients.

    The introduction of a proprietary haemodynamic and radiological classification used in the assessment of ovarian venous insufficiency has facilitated treatment planning for patients with pelvic venous insufficiency. This proprietary method allows for a precise assessment of blood flow abnormalities, enabling clinicians to select the optimal therapeutic strategy.

    The doctors of the Phlebology Clinic were pioneers in the use of the varicose vein bonding method in Poland. We were the first to introduce this innovative, minimally invasive technique into clinical practice in our country. We encourage you to read the results of a study comparing the effectiveness of adhesive and intravenous laser ablation in the treatment of venous insufficiency of the lower limbs.

    What are the symptoms of venous thrombosis?

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