Venous thromboembolism is a condition associated with disabling and sometimes life-threatening complications characterized by an obstruction of a vein by a thrombus.
Venous thromboembolism is a term used to define two related conditions – deep vein thrombosis and pulmonary embolism when a blood clot obstructs the vein and interferes with the blood flow. Although blood clotting (coagulation, thrombus formation) is a physiologic process by which the blood clot is formed out of the platelets to stop the bleeding from the injured vessel and prevent blood loss, certain conditions induce blood coagulation inside an unharmed blood vessel and result in thrombosis (obstruction of the vessel in which the blood clot occurs) or thromboembolism (obstruction of the other vessel by a thrombus that detached from another site).
Causes of thrombi formation
According to Virchow’s theory triad which includes
- hypercoagulability (alterations in the blood constitution, blood prone to coagulation),
- hemodynamic changes (stasis or turbulence of blood) and
- endothelial injury/dysfunction (vessel lining injury)
contributes to the development of thrombi in the veins with following thromboembolism or thrombosis. This triad activates the platelets and production of proinflammatory mediators, which in turn stimulate platelet aggregation and as the result thrombi arrangement.
Both inherited and acquired factors are related to the risk of thrombi formation. Despite the fact that the inherited disorders cannot be modified there is a large number of conditions which may be controlled in order to prevent the development of venous thrombosis and possibly life-threatening complications.
Inherited risk factors
Some genetic disorders are associated with hypercoagulation (increased blood coagulation) and, therefore, high risk of thrombosis. These prothrombotic states include:
- Antithrombin III deficiency;
- Factor V Leiden (activated protein C resistance) thrombophilia;
- Prothrombin gene (G20210A) defect;
- Protein C deficiency;
- Protein S deficiency;
- Disorders of plasminogen;
- Mutations of cystathionine β-synthase or methylenetetrahydrofolate reductase (MTHFR)
- High concentrations of Factors VIII or XI (or both);
The most common genetic mutations associated with venous thromboembolism are autosomal-dominant conditions – factor V Leiden and the prothrombin gene mutations.
Acquired risk factors
- Age over 40 years;
- Sedentary travels for long distance;
- Prior history of venous thromboembolism;
- Prior major surgical procedure (pelvic or abdominal), hip/knee replacement recently;
- Pregnancy and the postpartum period, recent Cesarean section, especially if performed emergently;
- Major trauma and especially hip fracture;
- Long-term immobilization or paralysis;
- Venous stasis;
- Varicose veins;
- Congestive heart failure;
- Myocardial infarction;
- Cigarette smoking;
- Oral contraceptive therapy;
- Hormone replacement therapy;
- Advanced malignancy and chemotherapy;
- Severe thrombocythemia (increased platelets levels in the blood);
- Paroxysmal nocturnal hemoglobinuria;
- Antiphospholipid antibody syndrome (including lupus anticoagulant);
- Congestive heart failure;
- Chronic obstructive pulmonary disease;
- Chronic kidney disease;
- Blood transfusion;
- Indwelling central venous catheter;
- Inflammatory bowel disease as well as other autoimmune disorders;
Thrombosis and pulmonary thromboembolism prevention
Some genetic features are associated with a person’s predisposition to thrombi formation and may be detected with the help of our genetic test. As pulmonary embolism is a life-threatening condition it is essential to detect individuals at high risk of developing thromboembolism and taking measures in order to prevent it – initiating anticoagulant therapy (warfarin, rivaroxaban, dabigatran, etc.) or implantation of vena cava filter and wearing medical compression stockings which significantly reduce the risk of thrombosis.