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==Overview==
'''Virchow's triad'''  describes the three broad categories of factors that are thought to contribute to [[thrombosis]].<ref name="isbn0-7817-8355-0">{{cite book
|author=April Wang Armstrong; David E. Golan; Armen H. Tashjian; Ehrin Armstrong
|title=Principles of pharmacology: the pathophysiologic basis of drug therapy
|publisher=Wolters Kluwer Health/Lippincott Williams & Wilkins
|location=Philadelphia
|year=2008
|pages=396
|isbn=0-7817-8355-0}}</ref>
*[[Hypercoagulability]]
*[[Hemodynamic]] changes (stasis, turbulence)
*[[Endothelial]] injury/dysfunction
It is named after the eminent [[Germany|German]] [[physician]] [[Rudolf Virchow]] (1821-1902). However, the elements comprising Virchow's triad were neither proposed by Virchow, nor did he ever suggest a triad to describe the pathogenesis of venous thrombosis. In fact, it was decades following Virchow's death before a consensus was reached proposing that thrombosis is the result of alterations in blood flow, vascular endothelial injury, or alterations in the constitution of the blood. Still, the modern understanding of the factors leading to embolism are similar to the description provided by Virchow. Its nebulous origins notwithstanding, Virchow's triad remains a useful concept for clinicians and pathologists alike in understanding the contributors to thrombosis.<ref name="pmid18783400">{{cite journal
|author=Bagot CN, Arya R
|title=Virchow and his triad: a question of attribution
|journal=Br. J. Haematol.
|volume=143
|issue=2
|pages=180–90
|year=2008
|month=October
|pmid=18783400
|doi=10.1111/j.1365-2141.2008.07323.x}}</ref>


'''Virchow's triad''' encompasses three broad categories of factors that are thought to contribute to [[venous thrombosis]]:
==The triad==
The triad consists of three components:


# Alterations in blood flow ([[stasis]])  
{| class="wikitable"
# Injury to the vascular [[endothelium]]  
|-
# Alterations in the constitution of blood ([[hypercoagulability]])
! Virchow's<ref name="isbn1-4020-6649-X">{{cite book
|author=Malone, P. Colm, Agutter, Paul S.
|title=The Aetiology of Deep Venous Thrombosis: A Critical, Historical and Epistemological Survey
|publisher=Springer
|location=Berlin
|year=2008
|pages=84
|isbn=1-4020-6649-X
|url=http://books.google.ie/books/about/The_Aetiology_of_Deep_Venous_Thrombosis.html?id=TUfRqCH0smoC&redir_esc=y}}</ref>
! Modern
! Notes
|-
| Phenomena of interrupted blood-flow
| '''[[stasis (medicine)|Stasis]]''' <ref name="pmid15692260">{{cite journal
|author=Lowe GD
|title=Virchow's triad revisited: abnormal flow
|journal=Pathophysiol. Haemost. Thromb.
|volume=33
|issue=5-6
|pages=455–7
|year=2003
|pmid=15692260
|doi=10.1159/000083845
|url=http://content.karger.com/produktedb/produkte.asp?doi=10.1159/000083845&typ=pdf}}</ref>
| The first category, alterations in normal blood flow, refers to several situations. These include [[venous stasis]], [[turbulence]], [[mitral stenosis]], and [[varicose veins]]. The equivalence of Virchow's version and the modern version has been disputed.<ref name="urlFurther reflections on Virchows triad. - Free Online Library">{{cite web
|url=http://www.thefreelibrary.com/Further+reflections+on+Virchow%27s+triad.(Letter+to+the+Editor)-a0128075135
|title=Further reflections on Virchow's triad. - Free Online Library
|format=
|work=
|accessdate=2009-02-10}}</ref>
|-
| 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 vessel piercings and damages arising from [[shear stress]] or [[hypertension]]. This category is ruled by [[Surface science|surface phenomena]] and contact with procoagulant surfaces, such as [[bacteria]], shards of foreign materials, [[biomaterials]] of [[Implant (medicine)|implants]] or [[medical devices]], [[cell membrane|membranes]] of activated [[platelets]], and membranes of [[monocytes]] in [[inflammation|chronic inflammation]].
|-
| Phenomena of blood-coagulation
| '''[[Hypercoagulability]]'''
| The last category, alterations in the constitution of blood,<ref name="pmid15692259">{{cite journal
|author=Chung I, Lip GY
|title=Virchow's triad revisited: blood constituents
|journal=Pathophysiol. Haemost. Thromb.
|volume=33
|issue=5-6
|pages=449–54
|year=2003
|pmid=15692259
|doi=10.1159/000083844
|url=http://content.karger.com/produktedb/produkte.asp?doi=10.1159/000083844&typ=pdf}}</ref> has numerous possible risk factors such as [[hyperviscosity]], deficiency of [[antithrombin]] III, [[nephrotic syndrome]], changes after severe [[Physical trauma|trauma]] or burn, disseminated [[cancer]], late pregnancy and delivery, race, age, whether the patient is a smoker, and [[obesity]].  All of these risk factors cause the situation called [[hypercoagulability]].
|}


The origin of the term "Virchow's triad" is of historical interest. [[Rudolf Virchow]] elucidated the etiology of pulmonary [[thromboembolism]], whereby thrombi occurring within the veins -- particularly those of the extremities -- become dislodged and migrate to the pulmonary vasculature.  In detailing the [[pathophysiology]] surrounding [[pulmonary embolism]], Virchow alluded to many of the factors known to contribute to [[venous thrombosis]]. While these factors had already been previously established in the medical literature by others, for unclear reasons they ultimately became known as Virchow's triad.
==Historical Perspective==
The origin of the term "Virchow's Triad" is of historical interest, and has been subject to reinterpretation in recent years.<ref>{{cite journal
|author=Dickson, B.C.
|title=Venous thrombosis: on the history of Virchow’s triad
|journal=University of Toronto Medical Journal
|year=2004
|volume=81
|pages=166-171
|url=http://utmj.org/archive/81-3/HIST.pdf}}</ref> While both Virchow's and the modern triads describe [[thrombosis]], the previous triad has been characterized as "the consequences of thrombosis", and the modern triad as "the causes of thrombosis".<ref name="urlResponse: further reflections on Virchows Triad. - Free Online Library">{{cite web |url=http://www.thefreelibrary.com/Response%3a+further+reflections+on+Virchow%27s+Triad.(Letter+to+the...-a0128075136
|title=Response: further reflections on Virchow's Triad. - Free Online Library
|format=
|work=
|accessdate=2009-02-10}}</ref>


Thus, the elements comprising Virchow's triad were neither proposed by Virchow, nor did he ever suggest a triad to describe the pathogenesis of venous thrombosis.  In fact, it was decades following Virchow's death before a consensus was reached proposing that thrombosis is the result of alterations in blood flow, vascular endothelial injury, or alterations in the constitution of the blood.  Moreover, the [[eponym]] Virchow's triad did not emerge in the literature until almost 150 years after his original work.
Rudolf Virchow elucidated the etiology of [[pulmonary embolism]], whereby [[thrombi]] occurring within the [[veins]], particularly those of the extremities, become dislodged and migrate to the pulmonary vasculature. He published his description in 1856 <ref>{{cite book
|author=Virchow, R.
|title=Gesammelte Abhandlungen zur wissenschaftlichen Medicin
|location= Frankfurt am Main
|publisher=Von Meidinger & Sohn
|year=1856
|chapter=Thrombose und Embolie. Gefässentzündung und septische Infektion
|pages=219–732
|language=German}}{{cite book
|author=Matzdorff AC, Bell WR
|title=Thrombosis and embolie (1846-1856)
|location=Canton, Massachusetts
|publisher=Science History Publications
|year=1998 |isbn=0-88135-113-X}}</ref>  In detailing the [[pathophysiology]] surrounding pulmonary embolism, he alluded to many of the factors known to contribute to venous thrombosis.  While these factors had already been previously established in the medical literature by others,<ref name="urlVirchows triad? - Free Online Library">{{cite web
|url=http://www.thefreelibrary.com/Virchow%27s+triad%3F-a0123332713
|title=Virchow's triad? - Free Online Library
|format=
|work=
|accessdate=2009-02-10}}</ref><ref>Wiseman R. Several Chirurgical Treatises. 2nd ed. London, Norton and Macock, 1686, pp. 64-66. </ref> for unclear reasons they ultimately became known as Virchow's triad.  This [[eponym]] did not emerge in the literature until long after Virchow's death. One estimate of the first use of the phrase dates it to the early 1950s.<ref name="isbn1-4020-6649-X" />


Its nebulous origins notwithstanding, Virchow's triad remains a useful concept for clinicians and pathologists alike in understanding the contributors to venous, and perhaps arterial, thrombosis.
Although the concept of the triad is usually attributed to Virchow, he did not include endothelial injury in his description.<ref>{{WhoNamedIt|synd|1223}}</ref> This has been attributed to a dispute Virchow had with [[Jean Cruveilhier]], who considered local trauma of primary importance in the development of pulmonary artery thrombosis.<ref name="urlVirchows triad revisited. - Free Online Library">{{cite web |url=http://www.thefreelibrary.com/Virchow%27s+triad+revisited.(Letters+to+the+Editor)(Letter+to+the...-a0114134751
|title=Virchow's triad revisited. - Free Online Library
|format=
|work=
|accessdate=2009-02-10}}</ref><ref>Aschoff L. Thrombosis, in Lectures on Pathology. New York, Paul B. Hoeber, Inc., 1924, pp 253-278. </ref>


<youtube v=X_POCRsy7i4/>
==Pathophysiology==
This video explains the process of thrombosis:
 
{{#ev:youtube|X_POCRsy7i4}}


==References==
==References==
# Dickson BC.  Venous thrombosis: on the history of Virchow’s triad.  UTMJ. 2004;81:166-171. [http://www.utmj.org/issues/81.3/Historical_Review_81-166.pdf]
{{reflist|2}}
# Owen CA. A History of Blood Coagulation. Rochester, Mayo Foundation for Medical Education and Research. 2001:169-180.
 
# Brotman DJ, Deitcher SR, Lip GY, Matzdorff AC. Virchow's triad revisited. South Med J. 2004;97:213-214. 
{{Eponymous medical signs for hematology and oncology}}
# Malone PC.  Further reflections on Virchow's triad.  South Med J. 2005;98:125.
 
# Dickson BC.  Virchow's triad?  South Med J. 2004;97:915-6.
[[Category:Hematology]]
# Virchow RLK. Gesammelte Abhandlungen zur Wissenschaftlichen Medicin. Frankfurt, Meidinger Sohn & Co., 1856. In, Virchow RLK. Thrombosis and Emboli (1846–1856). Matzdorff AC, Bell WR (transl). Canton, Science History Publications, 1998;5-11,110.


{{SIB}}
[[de:Virchow-Trias]]
[[es:Tríada de Virchow]]
[[fr:Triade de Virchow]]
[[pl:Triada Virchowa]]
[[pt:Tríade de Virchow]]


[[Category:Hematology]]
[[Category:Hematology]]

Latest revision as of 19:32, 21 September 2012

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Virchow's triad describes the three broad categories of factors that are thought to contribute to thrombosis.[1]

It is named after the eminent German physician Rudolf Virchow (1821-1902). However, the elements comprising Virchow's triad were neither proposed by Virchow, nor did he ever suggest a triad to describe the pathogenesis of venous thrombosis. In fact, it was decades following Virchow's death before a consensus was reached proposing that thrombosis is the result of alterations in blood flow, vascular endothelial injury, or alterations in the constitution of the blood. Still, the modern understanding of the factors leading to embolism are similar to the description provided by Virchow. Its nebulous origins notwithstanding, Virchow's triad remains a useful concept for clinicians and pathologists alike in understanding the contributors to thrombosis.[2]

The triad

The triad consists of three components:

Virchow's[3] Modern Notes
Phenomena of interrupted blood-flow Stasis [4] The first category, alterations in normal blood flow, refers to several situations. These include venous stasis, turbulence, 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 vessel piercings and damages arising from shear stress or hypertension. This category is ruled by surface phenomena and contact with procoagulant surfaces, such as bacteria, shards of foreign materials, biomaterials of implants or medical devices, membranes of activated platelets, and membranes of monocytes in chronic inflammation.
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 cause the situation called hypercoagulability.

Historical Perspective

The origin of the term "Virchow's Triad" is of historical interest, and has been subject to reinterpretation in recent years.[7] While both Virchow's and the modern triads describe thrombosis, the previous triad has been characterized as "the consequences of thrombosis", and the modern triad as "the causes of thrombosis".[8]

Rudolf Virchow elucidated the etiology of pulmonary embolism, whereby thrombi occurring within the veins, particularly those of the extremities, become dislodged and migrate to the pulmonary vasculature. He published his description in 1856 [9] In detailing the pathophysiology surrounding pulmonary embolism, he alluded to many of the factors known to contribute to venous thrombosis. While these factors had already been previously established in the medical literature by others,[10][11] for unclear reasons they ultimately became known as Virchow's triad. This eponym did not emerge in the literature until long after Virchow's death. One estimate of the first use of the phrase dates it to the early 1950s.[3]

Although the concept of the triad is usually attributed to Virchow, he did not include endothelial injury in his description.[12] This has been attributed to a dispute Virchow had with Jean Cruveilhier, who considered local trauma of primary importance in the development of pulmonary artery thrombosis.[13][14]

Pathophysiology

This video explains the process of thrombosis:

{{#ev:youtube|X_POCRsy7i4}}

References

  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. ↑ 3.0 3.1 Malone, P. Colm, 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. ↑ Dickson, B.C. (2004). "Venous thrombosis: on the history of Virchow's triad" (PDF). University of Toronto Medical Journal. 81: 166–171.
  8. ↑ "Response: further reflections on Virchow's Triad. - Free Online Library". Retrieved 2009-02-10.
  9. ↑ Virchow, R. (1856). "Thrombose und Embolie. Gefässentzündung und septische Infektion". Gesammelte Abhandlungen zur wissenschaftlichen Medicin (in German). Frankfurt am Main: Von Meidinger & Sohn. pp. 219–732.Matzdorff AC, Bell WR (1998). Thrombosis and embolie (1846-1856). Canton, Massachusetts: Science History Publications. ISBN 0-88135-113-X.
  10. ↑ "Virchow's triad? - Free Online Library". Retrieved 2009-02-10.
  11. ↑ Wiseman R. Several Chirurgical Treatises. 2nd ed. London, Norton and Macock, 1686, pp. 64-66.
  12. ↑ Template:WhoNamedIt
  13. ↑ "Virchow's triad revisited. - Free Online Library". Retrieved 2009-02-10.
  14. ↑ Aschoff L. Thrombosis, in Lectures on Pathology. New York, Paul B. Hoeber, Inc., 1924, pp 253-278.

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