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While venous thrombosis of the legs is the most common form, venous thrombosis may occur in other veins. These may have particular specific risk factors: [5] Cerebral venous sinus thrombosis, cavernous sinus thrombosis and jugular vein thrombosis: thrombosis of the veins of the brain and head
The mainstay of VTE management is anticoagulation therapy, which prevents thrombus propagation and embolization. Such treatment reduces the risk of recurrence. [5] [4] [1] The choice and duration of anticoagulation depend on the individual patient's risk factors, bleeding risk, and preferences.
Studies of the pathophysiologic mechanisms for the increased risk of Venous thrombosis embolism or VTE after long-distance travel have not produced consistent results, but venous stasis appears to play a major role; other factors specific to air travel may increase coagulation activation, particularly in passengers with individual risk factors ...
Dozens of genetic risk factors have been identified, [14] and they account for approximately 50 to 60% of the variability in VTE rates. [4] As such, family history of VTE is a risk factor for a first VTE. [88] Factor V Leiden, which makes factor V resistant to inactivation by activated protein C, [88] mildly increases VTE risk by about three times.
Thrombosis prevention is initiated with assessing the risk for its development. Some people have a higher risk of developing thrombosis and its possible development into thromboembolism. [16] Some of these risk factors are related to inflammation.
When venous thromboembolism occurs when a patient is experiencing transient major risk factors such as prolonged immobility, surgery, or trauma, testing for thrombophilia is not appropriate because the outcome of the test would not change a patient's indicated treatment.
In detailing the pathophysiology surrounding pulmonary embolism, he alluded to many of the factors known to contribute to venous thrombosis. While these factors had already been previously established in the medical literature by others, [ 10 ] [ 11 ] for unclear reasons they ultimately became known as Virchow's triad.
A 2006 meta-analysis showed only a 1.3-fold increased risk for coronary disease. [6] Deficiencies in the anticoagulants Protein C and Protein S further increase the risk five- to tenfold. [2] Behind non-O blood type [7] and factor V Leiden, prothrombin G20210A is one of the most common genetic risk factors for venous thromboembolism. [4]
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