Deep vein thrombosis pathophysiology

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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

Deep Vein Thrombosis Microchapters


Patient Information





Differentiating Deep vein thrombosis from other Diseases

Epidemiology and Demographics

Risk Factors



Natural History, Complications and Prognosis


Diagnostic Approach

Assessment of Clinical Probability and Risk Scores

Assessment of Probability of Subsequent VTE and Risk Scores

History and Symptoms

Physical Examination

Laboratory Findings





Other Imaging Findings


Treatment Approach

Medical Therapy

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Cost-Effectiveness of Therapy

Future or Investigational Therapies

Special Scenario

Upper extremity DVT




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Case #1

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Deep vein thrombosis (DVT) results from the formation of a blood clot in the deep veins. Three mechanisms predispose to DVT, they are 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.


Virchow's Triad

Figure 1. Virchow's triad conceptually encompasses three broad categories of factors that are thought to contribute to venous thrombosis.

Shown below is a table depicting the elements of Virchow's triad and their modern counterparts.

Virchow's[3] Modern Notes
Phenomena of interrupted blood-flow "Stasis" or "venous stasis"[4] The first category, alterations in normal blood flow, refers to several situations. These include turbulence, stasis, mitral stenosis, and varicose veins. The equivalence of Virchow's version and the modern version has been disputed.[5]
Phenomena associated with irritation of the vessel and its vicinity "Endothelial injury" or "vessel wall injury" The second category, injuries and/or trauma to endothelium includes damage to the veins arising from shear stress or hypertension.
Phenomena of blood-coagulation "Hypercoagulability" The last category, alterations in the constitution of blood,[6] has numerous possible risk factors such as hyperviscosity, deficiency of antithrombin III, nephrotic syndrome, changes after severe trauma or burn, disseminated cancer, late pregnancy and delivery, race, age, whether the patient is a smoker, and obesity. All of these risk factors lead to hypercoagulability.

Thrombus Formation

Shown below is an image depicting a thrombus formed in the deep vein of the leg.

Thrombus in the deep vein of the leg
Source: Wikipedia [7]

Venous Insufficiency

Special Conditions

Video: The Process of Thrombosis



Pathophysiology in Upper Extremity DVT

  • While approximately 80% of upper extremity DVT are secondary, only 20% of the cases are primary.[8]


  1. April Wang Armstrong; David E. Golan; Armen H. Tashjian; Ehrin Armstrong (2008). Principles of pharmacology: the pathophysiologic basis of drug therapy. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 396. ISBN 0-7817-8355-0.
  2. Bagot CN, Arya R (2008). "Virchow and his triad: a question of attribution". Br. J. Haematol. 143 (2): 180–90. doi:10.1111/j.1365-2141.2008.07323.x. PMID 18783400. Unknown parameter |month= ignored (help)
  3. Agutter, Paul S. (2008). The Aetiology of Deep Venous Thrombosis: A Critical, Historical and Epistemological Survey. Berlin: Springer. p. 84. ISBN 1-4020-6649-X.
  4. Lowe GD (2003). "Virchow's triad revisited: abnormal flow". Pathophysiol. Haemost. Thromb. 33 (5–6): 455–7. doi:10.1159/000083845. PMID 15692260.
  5. "Further reflections on Virchow's triad. - Free Online Library". Retrieved 2009-02-10.
  6. Chung I, Lip GY (2003). "Virchow's triad revisited: blood constituents". Pathophysiol. Haemost. Thromb. 33 (5–6): 449–54. doi:10.1159/000083844. PMID 15692259.
  7. staff (2014). "Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. - Obra do próprio
  8. 8.0 8.1 8.2 Kucher N (2011). "Clinical practice. Deep-vein thrombosis of the upper extremities". N Engl J Med. 364 (9): 861–9. doi:10.1056/NEJMcp1008740. PMID 21366477.

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