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'''Editors-in-Chief:''' [[C. Michael Gibson, M.S., M.D.]]  '''Associate Editor-In-Chief''': [[User:Ujjwal Rastogi|Ujjwal Rastogi, MBBS]] [mailto:urastogi@perfuse.org]


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'''Editor(s)-In-Chief:''' {{ATI}}, [[C. Michael Gibson, M.S., M.D.]] [mailto:charlesmichaelgibson@gmail.com]; '''Associate Editor(s)-In-Chief:''' {{CZ}} ; [[User:Kashish Goel|Kashish Goel, M.D.]]; '''Assistant Editor(s)-In-Chief:''' [[User:Justine Cadet|Justine Cadet]]
{{Deep vein thrombosis}}
{{Deep vein thrombosis}}
==Overview==
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 [[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.


==Pathophysiology==
==Pathophysiology==
{{main|Thrombosis}}
=== Virchow's Triad ===
* [[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 |oclc= |doi= |accessdate=}}</ref><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>
** Alterations in [[blood]] flow
** [[Vascular]] [[endothelial]] injury
** Alterations in the constitution of the [[blood]]
 
[[File:VTE Pathophysisology Virchow's triad.JPG|400x400px|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.
 
{| class="wikitable"
|-
! Virchow's<ref name="isbn1-4020-6649-X">{{cite book |author=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 |oclc= |doi= |accessdate=}}</ref>
! Modern
! Notes
|-
| Phenomena of interrupted [[blood]]-flow
| "Stasis" or "[[venous 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 [[turbulence]], [[stasis (medicine)|stasis]], [[mitral stenosis]], and [[varicose veins]]. The equivalence of [[Virchow's triad|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 damage to the veins arising from [[shear stress]] or [[hypertension]].
|-
| 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]] lead to  [[hypercoagulability]].
|}
 
===Thrombus Formation===
* Normal [[homeostasis]] is maintained by the balance between the [[coagulation]] and [[fibrinolysis]] systems of the body.  A [[homeostatic]] imbalance leads to the formation of a [[thrombus]] or [[hemorrhage]].
* Factors that increase the risk for a homeostatic imbalance include:
**[[Thrombophilia]]
**Immobilization
**[[Trauma]]
* An insult to [[homeostatic]] balance can expose the sub-[[endothelium]] and lead to the collection of various [[coagulation factors]]. Accumulation of [[coagulation factors]] can lead to the formation of a [[thrombus]] of [[red blood cell|red blood cells]], [[leukocyte|leukocytes]], and [[fibrin]].
* A [[thrombus]] is characteristically found to first develop in the calf [[veins]] and progressively grow in the direction of [[blood]] flow (leading to the [[heart]]).
* An exceedingly extensive DVT can extend well into the [[iliac vein|iliac veins]] or [[inferior vena cava|the inferior vena cava]].
 
Shown below is an image depicting a [[thrombus]] formed in the deep [[vein]] of the leg.
 
[[image:Deep vein thrombosis thrombus formation.png|300px|left|thumb|Thrombus in the deep vein of the leg <br>Source: Wikipedia <ref> Blausen.com 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 </ref>]]
<br style="clear:left" />
 
===Venous Insufficiency===
* In patients with DVT, there is a potential to develop chronic [[venous insufficiency]], also known as [[post-phlebitic syndrome]].
* At 10 years of follow-up, the [[incidence]] of [[venous insufficiency]] is around 30%.
* Valvular incompetence is the mechanism responsible for [[venous insufficiency]] development. Valves within the deep [[veins]] may be involved early in the formation of a deep vein thrombus (DVT) and subsequently become damaged. This damage causes a lack of [[blood]] flow back into the involved [[veins]]. When the calf [[muscle]] is contracted, the [[blood]] moves to superficial [[veins]] and can ultimately lead to superficial [[venous insufficiency]].
 
===Special Conditions===
* [[May-Thurner syndrome]]: As a result of the right [[common iliac artery]] compressing the left common [[iliac vein]], DVTs occur more commonly in left leg [[vasculature]] than the right.
* [[Phlegmasia alba dolens]]: Following an acute episode of DVT, the leg may turn a milky white color. Causation is not clear but may be linked to [[edema]]-induced compartment syndrome resulting in [[Tissue (biology)|tissue]] [[ischemia]] and [[gangrene]].
* [[Phlegmasia cerulea dolens]]: Complete occlusion of the [[venous]] flow secondary to massive ilio-femoral [[thrombus]] and excessive [[edema]].
 
===Video: The Process of Thrombosis===
 
 
{{#ev:youtube|CETfozL0cQg}}
 
{{#ev:youtube|X_POCRsy7i4}}
 
==Pathophysiology in Upper Extremity DVT==
* While approximately 80% of upper extremity DVT are secondary, only 20% of the cases are primary.<ref name="pmid21366477">{{cite journal| author=Kucher N| title=Clinical practice. Deep-vein thrombosis of the upper extremities. | journal=N Engl J Med | year= 2011 | volume= 364 | issue= 9 | pages= 861-9 | pmid=21366477 | doi=10.1056/NEJMcp1008740 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21366477  }} </ref>


[[Virchow's triad]] is a group of 3 factors known to affect clot formation: rate of flow, the consistency (thickness) of the blood, and qualities of the vessel wall.  Virchow noted that more deep venous thrombosis occurred in the left leg than in the right and proposed compression of the left common iliac vein by the overlying right common iliac artery as the underlying cause (see [[May-Thurner syndrome]]).<ref>Virchow R. Ueber die Erweiterung kleinerer Gefäfse. Arch Pathol Anat Physiol Klin Med 1851;3:427-62. </ref>
* Primary upper extremity DVT occurs in the following conditions:<ref name="pmid21366477">{{cite journal| author=Kucher N| title=Clinical practice. Deep-vein thrombosis of the upper extremities. | journal=N Engl J Med | year= 2011 | volume= 364 | issue= 9 | pages= 861-9 | pmid=21366477 | doi=10.1056/NEJMcp1008740 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21366477 }} </ref>
** Venous [[thoracic outlet syndrome]] caused by compression of the [[subclavian vein]]
** [[Paget Schroetter syndrome]] caused by repetitive trauma to the [[subclavian vein]] due to repetitive overhead arm movement
** Idiopathic etiology


The most common risk factors are recent surgery or hospitalization.<ref name="pmid17646600">{{cite journal |author=Spencer FA, Lessard D, Emery C, Reed G, Goldberg RJ |title=Venous thromboembolism in the outpatient setting |journal=Arch. Intern. Med. |volume=167 |issue=14 |pages=1471-5 |year=2007 |pmid=17646600 |doi=10.1001/archinte.167.14.1471}}</ref> 40% of these patients did not receive heparin prophylaxis. Other risk factors include advanced age, obesity, infection, immobilization, female sex, use of combined (estrogen-containing) forms of [[hormonal contraception]], tobacco usage and air travel ("[[economy class syndrome]]", a combination of immobility and relative dehydration) are some of the better-known causes.<ref>{{cite journal | author = Tsai A, Cushman M, Rosamond W, Heckbert S, Polak J, Folsom A | title = Cardiovascular risk factors and venous thromboembolism incidence: the longitudinal investigation of thromboembolism etiology. | journal = Arch Intern Med | volume = 162 | issue = 10 | pages = 1182-9 | year = 2002 | id = PMID 12020191}}</ref>  [[Thrombophilia]] (tendency to develop thrombosis) often expresses itself with recurrent thromboses.
* Secondary upper extremity DVT occurs in the following conditions:<ref name="pmid21366477">{{cite journal| author=Kucher N| title=Clinical practice. Deep-vein thrombosis of the upper extremities. | journal=N Engl J Med | year= 2011 | volume= 364 | issue= 9 | pages= 861-9 | pmid=21366477 | doi=10.1056/NEJMcp1008740 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21366477  }} </ref>
** [[Catheter]] associated thrombosis
*** Indwelling [[central venous catheter]]
*** [[Pacemaker]]
*** [[Defibrillator]]
** [[Cancer]] and [[chemotherapy]]
** [[Surgery]] or [[trauma]] to the upper extremities that predisposes to [[thrombosis]] due to injury of the [[vein]]s, compression of the [[vein]]s, immobilization, or placement of plaster cast.
** [[Hormone]]-induced hypercoagulabity in [[pregnancy]] or due to [[oral contraceptive]] intake


It is recognized that thrombi usually develop first in the calf veins, "growing" in the direction of flow of the vein.  DVTs are distinguished as being above or below the [[popliteal]] vein.  Very extensive DVTs can extend into the [[iliac vein]]s or the [[inferior vena cava]].  The risk of pulmonary embolism is higher in the presence of more extensive clots.
==References==
{{reflist|2}}


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Latest revision as of 20:06, 6 March 2018

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Resident
Survival
Guide

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

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Overview

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.

Pathophysiology

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

{{#ev:youtube|CETfozL0cQg}}

{{#ev:youtube|X_POCRsy7i4}}

Pathophysiology in Upper Extremity DVT

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

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. ↑ 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. ↑ Blausen.com 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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