Deep vein thrombosis (DVT) occurs when a blood clot (thrombus) forms in one or more of the deep veins in your body, usually in your legs. Deep vein thrombosis can cause leg pain or swelling, but may occur without any symptoms.
Deep vein thrombosis can develop if you have certain medical conditions that affect how your blood clots. Deep vein thrombosis can also happen if you don't move for a long time, such as after surgery, following an accident, or when you are confined to a hospital or nursing home bed.Deep vein thrombosis, or deep venous thrombosis, (DVT) is the formation of a blood clot(thrombus) within a deep vein,[a] predominantly in the legs. Non-specific signs may include pain, swelling, redness, warmness, and engorged superficial veins. Pulmonary embolism, a potentially life-threatening complication, is caused by the detachment (embolization) of a clot that travels to the lungs. Together, DVT and pulmonary embolism constitute a single disease process known as venous thromboembolism. Post-thrombotic syndrome, another complication, significantly contributes to the health-care cost of DVT. Prevention options for at-risk individuals include early and frequent walking, calf exercises, anticoagulants, aspirin, graduated compression stockings, and intermittent pneumatic compression.
In 1856, German pathologist Rudolf Virchow postulated the interplay of three processes resulting in venous thrombosis, now known as Virchow's triad: a decreased blood flow rate (venous stasis), increased tendency to clot (hypercoagulability), and changes to the blood vessel wall. DVT formation typically begins inside the valves of the calf veins, where the blood is relatively oxygen deprived, which activates certain biochemical pathways. Several medical conditions increase the risk for DVT, including cancer, trauma, and antiphospholipid syndrome. Other risk factors include older age, surgery, immobilization (as with bed rest, orthopedic casts, and sitting on long flights), combined oral contraceptives, pregnancy, the postnatal period, and genetic factors. Those genetic factors include deficiencies with antithrombin,protein C, and protein S, the mutation of Factor V Leiden, and the property of having a non-Oblood type. The rate of new DVTs increases dramatically from childhood to old age; in adulthood, about 1 in 1000 adults develops it annually.
Individuals suspected of having DVT may be assessed using a clinical prediction rule such as the Wells score. A D-dimer test may also be used to assist with excluding the diagnosis (because of its high sensitivity) or to signal a need for further testing. Diagnosis is most commonly done with ultrasound of the suspected veins. Anticoagulation is the standard treatment; typical medications include a low-molecular-weight heparin and a vitamin K antagonist. Wearing graduated compression stockings appears to reduce the risk of post-thrombotic syndrome.
Common signs and symptoms of DVT include pain or tenderness, swelling, warmth, redness or discoloration, and distention of surface veins, although about half of those with the condition have no symptoms.[1] Signs and symptoms alone are not sufficiently sensitive or specific to make a diagnosis, but when considered in conjunction with known risk factors can help determine thelikelihood of DVT.[2] In most suspected cases, DVT is ruled out after evaluation,[3] and symptoms are more often due to other causes, such as cellulitis, Baker's cyst, musculoskeletal injury, orlymphedema.[4] Other differential diagnoses include hematoma, tumors, venous or arterialaneurysms, and connective tissue disorders.[5]
Phlegmasia cerulea dolens is a very large and dangerous type of DVT.[6] It is characterized by an acute and almost total venous occlusion of the entire extremity outflow, including the iliac andfemoral veins. The leg is usually painful, blue tinged in color, and swollen, which may result in venous gangrene.[7][8]
The three factors of Virchow's triad—venous stasis, hypercoagulability, and changes in theendothelial blood vessel lining (such as physical damage or endothelial activation)—contribute to DVT and are used to explain its formation.[9][10] Other related causes include activation of immune system components, the state of microparticles in the blood, the concentration of oxygen, and possible platelet activation.[11] Various risk factors contribute to DVT, though many at high risk never develop it.[12]
Acquired risk factors include the strong risk factor of older age,[10][12] which alters blood composition to favor clotting. Other important acquired risk factors include major surgery andtrauma, both of which may increase the risk because of tissue factor from outside the vascular system entering the blood.[9] In orthopedic surgery, venous stasis may be temporarily provoked by a cessation of blood flow as part of the procedure.[11] Cancer can grow in and around veins, causing venous stasis, and can also stimulate increased levels of tissue factor. Pregnancy causes blood to favor clotting, and in the postpartum, placental tearing releases substances that favor clotting. Oral contraceptives[b] and hormonal replacement therapy increase the risk through a variety of mechanisms, including altered blood coagulation protein levels and reduced fibrinolysis.[11]
The disease term venous thromboembolism (VTE) includes the development of either DVT orpulmonary embolism (PE).[15][16] Genetic factors that increase the risk of VTE include deficiencies of three proteins that normally prevent blood from clotting—protein C, protein S, and antithrombin—in addition to non-O blood type and mutations in the factor V and prothrombin genes. Deficiencies inantithrombin, protein C, and protein S are rare but strong, or moderately strong, risk factors.[9][11] These three thrombophilia[c] increase the risk of VTE by about 10 times.[17] Factor V Leiden, which makes factor V resistant to inactivation by activated protein C,[19] and the genetic variant prothrombin G20210A, which causes increased prothrombin levels, are predominantly expressed in Caucasians.[9][d] They moderately increase risk for VTE, by three to eight times for factor V Leiden and two to three times for prothrombin G20210A.[17][20] Having a non-O blood type approximately doubles VTE risk.[11] Non-O blood type is common in all races, making it an important risk factor.[21]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.[21]
Some risk factors influence the location of DVT within the body. In isolated distal DVT, the profile of risk factors appears distinct from proximal DVT. Transient factors, such as surgery and immobilization, appear to dominate whereas thrombophilias and age do not seem to increase risk.[22] In upper-extremity DVT, the most important risk factor is having a central venous catheter, and thoracic outlet syndromealso increases risk.
Deep vein thrombosis may sometimes occur without any noticeable symptoms.
If you develop signs or symptoms of deep vein thrombosis, contact your doctor for guidance.
If you develop signs or symptoms of a pulmonary embolism — a life-threatening complication of deep vein thrombosis — seek medical attention immediately.