alt=Artistic rendering of<unk>  Traditionally, the three factors of Virchow's triad—venous stasis, hypercoagulability, and changes in the endothelial blood vessel lining—contribute to VTE and were used to explain its formation. More recently, inflammation has been identified as playing a clear causal role. Other related causes include activation of immune system components, the state of microparticles in the blood, the concentration of oxygen, and possible platelet activation. Various risk factors contribute to VTE, including genetic and environmental factors, though many with multiple risk factors never develop it. Acquired risk factors include the strong risk factor of older age, which alters blood composition to favor clotting. Previous VTE, particularly unprovoked VTE, is a strong risk factor. A leftover clot from a prior<unk>  increases the risk of a subsequent<unk> . Major surgery and trauma increase risk because of tissue factor from outside the vascular system entering the blood. Minor injuries, lower limb amputation, hip fracture, and long bone fractures are also risks. In orthopedic surgery, venous stasis can be temporarily provoked by a cessation of blood flow as part of the procedure. Inactivity and immobilization contribute to venous stasis, as with orthopedic casts, paralysis, sitting, long-haul travel, bed rest, hospitalization, catatonia, and in survivors of acute stroke. Conditions that involve compromised blood flow in the veins are May–Thurner syndrome, where a vein of the pelvis is compressed, and venous thoracic outlet syndrome, which includes Paget–Schroetter syndrome, where compression occurs near the base of the neck. Infections, including sepsis, COVID-19, HIV, and active tuberculosis, increase risk. Chronic inflammatory diseases and some autoimmune diseases, such as inflammatory bowel disease, systemic sclerosis, Behçet's syndrome, primary antiphospholipid syndrome, and systemic lupus erythematosus (SLE) increase risk. SLE itself is frequently associated with secondary antiphospholipid syndrome. Cancer can grow in and around veins, causing venous stasis, and can also stimulate increased levels of tissue factor. Cancers of the blood, lung, pancreas, brain, stomach, and bowel are associated with high VTE risk. Solid tumors such as adenocarcinomas can contribute to both VTE and disseminated intravascular coagulation. In severe cases, this can lead to simultaneous clotting and bleeding. Chemotherapy treatment also increases risk. Obesity increases the potential of blood to clot, as does pregnancy. In the postpartum, placental tearing releases substances that favor clotting. Oral contraceptives and hormonal replacement therapy increase the risk through a variety of mechanisms, including altered blood coagulation protein levels and reduced fibrinolysis. The coagulation system, often described as a "cascade", includes a group of proteins that regulate clotting.<unk>  risk can be altered by abnormalities in the cascade. The regulators, antithrombin (ᾳTHR) and activated protein C (APC), are shown in green above the clotting factors they affect.|alt=Imagine showing the coagulation, which includes a group of proteins that regulate clots.<unk>  risk can be altered by abnormalities in the cascade. Dozens of genetic risk factors have been identified, and they account for approximately 50 to 60% of the variability in VTE rates. As such, family history of VTE is a risk factor for a first VTE. Factor V Leiden, which makes factor V resistant to inactivation by activated protein C, mildly increases VTE risk by about three times. Deficiencies of three proteins that normally prevent blood from clotting—protein C, protein S, and antithrombin—contribute to VTE. These deficiencies in antithrombin, protein C, and protein S are rare but strong, or moderately strong, risk factors. They increase risk by about 10 times. Having a non-O blood type roughly doubles VTE risk. Non-O blood type is common globally, making it an important risk factor. Individuals without O blood type have higher blood levels of von Willebrand factor and factor VIII than those with O blood type, increasing the likelihood of clotting. Those homozygous for the common fibrinogen gamma gene variant rs2066865 have about a 1.6 times higher risk of VTE. The genetic variant prothrombin G20210A, which increases prothrombin levels, increases risk by about 2.5 times. Additionally, approximately 5% of people have been identified with a background genetic risk comparable to the factor V Leiden and prothrombin G20210A mutations. Blood alterations including dysfibrinogenemia, low free protein S, activated protein C resistance, homocystinuria, hyperhomocysteinemia, high fibrinogen levels, high factor IX levels, and high factor XI levels are associated with increased risk. Other associated conditions include heparin-induced thrombocytopenia, catastrophic antiphospholipid syndrome, paroxysmal nocturnal hemoglobinuria, nephrotic syndrome, chronic kidney disease, polycythemia vera, essential thrombocythemia, intravenous drug use, and smoking. Some risk factors influence the location of<unk>  within the body. In isolated distal<unk> , the profile of risk factors appears distinct from proximal<unk> . Transient factors, such as surgery and immobilization, appear to dominate, whereas thrombophilias and age do not seem to increase risk. Common risk factors for having an upper extremity<unk>  include having an existing foreign body (such as a central venous catheter, a pacemaker, or a triple-lumen PICC line), cancer, and recent surgery.
Deep vein thrombosis
Hematoma
Varicose veins
Cellulitis
Superficial vein thrombosis
Lymphedema
Venous thrombosis
Baker's cyst