Deep vein thrombosis overview: Difference between revisions
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==Pathophysiology== | ==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 [[Congestive heart failure|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 [[Tunica intima|intimal]] damage and [[coagulation|stimulate clot formation]]. 3. Alterations in the constitution of blood ([[Hypercoagulability]]): Abnormal changes in coagulation can increase the propensity to develop thrombosis. | 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 [[Congestive heart failure|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 [[Tunica intima|intimal]] damage and [[coagulation|stimulate clot formation]]. 3. Alterations in the constitution of blood ([[Hypercoagulability]]): Abnormal changes in coagulation can increase the propensity to develop thrombosis. | ||
==Differentiating Deep Vein Thrombosis from Other Diseases== | |||
Only 25% of the patient evaluated for [[deep vein thrombosis]] (DVT) have the disease.<ref name="pmid3951515">{{cite journal| author=Huisman MV, Büller HR, ten Cate JW, Vreeken J| title=Serial impedance plethysmography for suspected deep venous thrombosis in outpatients. The Amsterdam General Practitioner Study. | journal=N Engl J Med | year= 1986 | volume= 314 | issue= 13 | pages= 823-8 | pmid=3951515 | doi=10.1056/NEJM198603273141305 | pmc= | url= }} </ref> DVT is characterized by pain and swelling of the limb, which is not specific. Numerous patients with DVT are asymptomatic. | |||
==References== | ==References== | ||
Revision as of 19:50, 29 January 2013
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.
Differentiating Deep Vein Thrombosis from Other Diseases
Only 25% of the patient evaluated for deep vein thrombosis (DVT) have the disease.[2] DVT is characterized by pain and swelling of the limb, which is not specific. Numerous patients with DVT are asymptomatic.
References
- ↑ Ramzi DW, Leeper KV (2004). "DVT and pulmonary embolism: Part I. Diagnosis". Am Fam Physician. 69 (12): 2829–36. PMID 15222648.
- ↑ Huisman MV, Büller HR, ten Cate JW, Vreeken J (1986). "Serial impedance plethysmography for suspected deep venous thrombosis in outpatients. The Amsterdam General Practitioner Study". N Engl J Med. 314 (13): 823–8. doi:10.1056/NEJM198603273141305. PMID 3951515.