As blood flow slows, oxygen tension declines with a coincident increase in hematocrit ( 15). Multiple postmortem studies have demonstrated the propensity for venous thrombi to form in the sinuses adjacent to venous valves ( 12- 14). While valves help to promote blood flow through the venous circulation, they are also potential locations for venous stasis and hypoxia. Venous thrombosis tends to occur in areas with decreased or mechanically altered blood flow such as the pockets adjacent to valves in the deep veins of the leg ( 11). The clinical conditions most closely associated with DVT are fundamentally related to the elements of Virchow’s Triad these include surgery or trauma, malignancy, prolonged immobility, pregnancy, congestive heart failure, varicose veins, obesity, advancing age, and a history of DVT ( 10). However, the concurrent presence of venous stasis and vascular injury or hypercoagulability greatly increases the risk for clot formation ( 9). Venous stasis is the most consequential of the three factors, but stasis alone appears to be insufficient to cause thrombus formation ( 8). Virchow’s Triad, first described in 1856, implicates three contributing factors in the formation of thrombosis: venous stasis, vascular injury, and hypercoagulability. With more therapeutic options, clinicians are now better able to incorporate disease- and patient-specific considerations into the medical management of DVT. Several recent clinical trials have addressed this question and demonstrated a similar safety and efficacy profile between the two drug classes. The advent of direct oral anticoagulants (DOACs) has generated a need to compare these newer agents with the more conventional vitamin K-antagonists (VKAs) for the treatment of DVT. The 30-day mortality rate exceeds 3% in patients with DVT who are not anticoagulated, and this mortality risk increases 10-fold in patients who develop PE ( 7). Anticoagulation is the mainstay of therapy for DVT, with the goal of preventing progression to PE and recurrence of thrombosis. Much of the morbidity of DVT results from the development of post-thrombotic syndrome, which occurs in up to 50% of patients within 2 years of DVT and encompasses a number of symptoms including leg pain, swelling, and in severe cases, venous ulcers ( 5, 6). Pulmonary embolism (PE), a dreaded complication of DVT, occurs in up to one-third of cases and is the primary contributor to mortality ( 4). The incidence of VTE is estimated to be 1 per 1,000 people annually ( 1, 2), with DVT accounting for approximately two-thirds of these events ( 3).

Accepted for publication Aug 23, 2017.ĭeep vein thrombosis (DVT), a subset of venous thromboembolism (VTE), is a major preventable cause of morbidity and mortality worldwide. Keywords: Deep vein thrombosis (DVT) vitamin K-antagonists (VKAs) warfarin direct oral anticoagulants (DOACs) anticoagulants In this review, we summarize the pathogenesis, diagnosis, and medical management of DVT, with particular emphasis on anticoagulation therapy and the role of DOACs in the current treatment algorithm. More recently, a number of large-scale clinical trials have validated the use of direct oral anticoagulants (DOACs) in place of warfarin in select cases. With few exceptions, the standard therapy for DVT has been vitamin K-antagonists (VKAs) such as warfarin with heparin or fractionated heparin bridging. Anticoagulation therapy is essential for the treatment of DVT. Clinical, biochemical, and radiological tests are used to increase the sensitivity and specificity for diagnosing DVT.

Virchow’s Triad distills the multitude of risk factors for DVT into three basic elements favoring thrombus formation: venous stasis, vascular injury, and hypercoagulability. Normal blood physiology hinges on a delicate balance between pro- and anti-coagulant factors. Venous thromboembolism (VTE), which includes DVT and pulmonary embolism (PE), affects an estimated 1 per 1,000 people and contributes to 60,000–100,000 deaths annually. Abstract: Deep vein thrombosis (DVT) is a major preventable cause of morbidity and mortality worldwide.

Deep vein thrombosis definition