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Review
. 2017 Dec;7(Suppl 3):S276-S284.
doi: 10.21037/cdt.2017.09.01.

Deep vein thrombosis: pathogenesis, diagnosis, and medical management

Affiliations
Review

Deep vein thrombosis: pathogenesis, diagnosis, and medical management

Jonathan Stone et al. Cardiovasc Diagn Ther. 2017 Dec.

Abstract

Deep vein thrombosis (DVT) is a major preventable cause of morbidity and mortality worldwide. 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. Normal blood physiology hinges on a delicate balance between pro- and anti-coagulant factors. Virchow's Triad distills the multitude of risk factors for DVT into three basic elements favoring thrombus formation: venous stasis, vascular injury, and hypercoagulability. Clinical, biochemical, and radiological tests are used to increase the sensitivity and specificity for diagnosing DVT. Anticoagulation therapy is essential for the treatment of DVT. With few exceptions, the standard therapy for DVT has been vitamin K-antagonists (VKAs) such as warfarin with heparin or fractionated heparin bridging. 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. 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.

Keywords: Deep vein thrombosis (DVT); anticoagulants; direct oral anticoagulants (DOACs); vitamin K-antagonists (VKAs); warfarin.

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Conflict of interest statement

Conflicts of Interest: The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Venous color-flow Doppler. US Doppler imaging of the left femoral vein showing complete occlusion by a heterogeneous thrombus with dilatation of the vein at the site of thrombosis. No significant waveform is present. The adjacent artery is also shown for reference. US, ultrasound.
Figure 2
Figure 2
Contrast venography. Angiogram imaging of the left popliteal vein demonstrating a partially occlusive thrombus with irregular margins and diminished contrast flow. This thrombus was subsequently treated with catheter directed therapy.
Figure 3
Figure 3
CT venography. CT imaging demonstrating bilateral common iliac vein thrombi as hypodense occlusive masses with vein wall enhancement and dilatation. This thrombus extended far into the inferior vena cava. CT, computed tomography.
Figure 4
Figure 4
MR venography. MR imaging demonstrating a focal thrombus in the left common iliac vein that was seen extending superiorly to the inferior vena cava. No thrombus is seen on the contralateral side. MR, magnetic resonance.

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