Deep vein thrombosis overview
Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] ;Kashish Goel, M.D.; Assistant Editor(s)-In-Chief: Justine Cadet
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Overview
Deep vein thrombosis (also known as deep venous thrombosis or DVT and colloquially referred to as economy class syndrome) is the formation of a blood clot ("thrombus") in a deep vein. The risk is significantly increased if the thrombus embolizes to the lungs, causing pulmonary embolism. Occasionally, veins in the arm are also affected (known as Paget-Schrötter disease). Upper extremity DVT is less common but also may lead to PE, especially in the presence of a venous catheter.[1] Thrombophlebitis is swelling (inflammation) of a vein caused by a blood clot.
Classification
Deep vein thrombosis (DVT) is classified based on the site of occlusion or clot formation. Symptom presentation and complication is largely influenced by location of the embolus.
Pathophysiology
Venous thrombosis is composed of three mechanisms, collectively described as the Virchow's triad: 1. Alterations in blood flow (stasis): Venous stasis is a major risk factor for the development of thrombosis. It occurs in certain pathological conditions (as in heart failure) wherein it causes an increase in platelet to endothelium contact and decreases the dilution of clotting factors. This increases the risk of clot formation, and it forms microthrombi, which further grow and propagate. 2. Injury to the vascular endothelium (Endothelial dysfunction): Intrinsic or secondary to external trauma, such as catheterization, can cause intimal damage and stimulate clot formation. 3. Alterations in the constitution of blood (Hypercoagulability): Abnormal changes in coagulation can increase the propensity to develop thrombosis.