Editing Deep vein thrombosis

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{{Redirect|DVT}}
{{Infobox disease
 | Name           = Deep vein thrombosis
 | Image          = DVT2010.JPG
 | Caption        = A deep vein thrombosis in the right leg. Note the swelling and redness.
 | DiseasesDB     = 3498
 | ICD10          = {{ICD10|I|80|2|i|80}}
 | ICD9           = {{ICD9|453.40}}
 | ICDO           =
 | OMIM           =
 | MedlinePlus    = 000156
 | eMedicineSubj  = med
 | eMedicineTopic = 2785
 | MeshID         = D020246
}}

A '''deep vein thrombosis''' ('''DVT''') is a [[blood clot]] in a [[deep vein]]. A clot inside a blood vessel is called a ''[[thrombosis]]''. DVTs predominantly occur in the legs and may have no [[symptoms]]. The non-specific signs of DVT include pain, [[Swelling (medical)|swelling]], redness, warmness, and engorged [[superficial veins]] in the leg. A DVT may go away naturally, but the most serious complication is when a thrombosis dislodges ([[embolize]]s) and travels to the [[lungs]] to become a life-threatening [[pulmonary embolism]] (PE). DVT and PE are the two manifestations of the disease [[venous thromboembolism]] (VTE). A late complication of DVT is the [[post-thrombotic syndrome]], which can manifest itself as [[edema]], pain or discomfort and skin problems. About 1 in a 1000 adults develop a DVT annually.

According to [[Virchow's triad]], described initially in 1856 by the German pathologist [[Rudolph Virchow]], venous thrombosis occurs due to three factors: decreased flow rate of the blood ([[venous stasis]]), damage or [[Endothelial activation|activation]] of the [[endothelium|blood vessel wall]], and an increased tendency of the blood to clot ([[hypercoagulability]]). DVT formation typically begins in the calves, inside vein valves, where the blood is relatively oxygen deprived. Several medical conditions increase the risk for DVT, such as cancer, [[physical trauma|trauma]], and [[antiphospholipid syndrome]]. Other [[risk factor]]s include older age (the strongest), surgery, immobilization (as with bed-rest, [[orthopedic cast]]s, or during long-haul flights), [[oral contraceptives]] and inborn tendencies to form clots known as [[thrombophilia]] (for example, in carriers of [[factor V Leiden]]). Women have an increased risk during pregnancy (due to altered blood protein levels) and in the [[puerperium|postnatal period]], partially due to substances released by the [[placenta]]. However, some of those who develop DVT have no recognized risk factors.

Individuals suspected of having a DVT may receive a probability assessment, such as the Wells score, and a [[D-dimer]] test, which may exclude the diagnosis or signal further testing is needed. Diagnosis of DVT is most commonly done with [[Medical ultrasonography|ultrasound]] of the affected veins. Treatment for DVT is dominated by [[anticoagulation]] (which prevents further coagulation) with a [[heparin]] and a [[vitamin K antagonist]]. If anticoagulation is not possible, management may involve [[inferior vena cava filter]] placement to presumably prevent PE. A complication of DVT, post-thrombotic syndrome, appears to be reduced by wearing [[graduated compression stocking]]s (GCS). [[Prophylaxis|Prevention]] of DVT is advised in at-risk medical and surgical inpatients with options such as early and frequent walking, anticoagulants, GCS or [[intermittent pneumatic compression]] (IPC).
{{TOC limit|3}}

==Classification==
[[Image:Gray582.png|thumb|50px|The popliteal vein is at the top of the image.]]
DVT and [[pulmonary embolism]] (PE) are the two manifestations of ''[[venous thromboembolism]]'' (VTE), a term which represents a distinct disease state.<ref name="ACP CPG">{{cite journal| author=Qaseem A, Chou R, Humphrey LL, ''et al''.| title=Venous thromboembolism prophylaxis in hospitalized patients: a clinical practice guideline from the American College of Physicians | journal=Ann Intern Med | year= 2011 | volume= 155 | issue= 9 | pages= 625–32 | pmid=22041951 | doi=10.1059/0003-4819-155-9-201111010-00011 | url=http://www.annals.org/content/155/9/625.long }}</ref> DVTs can be lower extremity (from the lower [[Limb (anatomy)|limbs]]), upper extremity, abdominal or pelvic in origin;<ref name="CC"/> they can also occur in the neck.<ref name="Young"/> DVTs in the legs are called ''proximal'' (or ''iliofemoral'')<ref name="Catheter">{{cite journal| author=Hofmann LV, Kuo WT| title=Catheter-directed thrombolysis for acute DVT | journal=Lancet | year= 2012 | volume= 379 | issue= 9810 | pages= 3–4 | pmid=22172245 | doi=10.1016/S0140-6736(11)61875-8 }}</ref> when above the knee and ''distal'' (or ''calf'') when below the knee.<ref name="single negative">{{cite journal| author=Johnson SA, Stevens SM, Woller SC, ''et al''.| title=Risk of deep vein thrombosis following a single negative whole-leg compression ultrasound: a systematic review and meta-analysis | journal=JAMA | year= 2010 | volume= 303 | issue= 5 | pages= 438–45 | pmid=20124539 | doi=10.1001/jama.2010.43 }}</ref>{{sfn|Welch|2010|p=2}} DVTs below the [[popliteal vein]], a proximal vein behind the knee, are in distal calf veins.<ref name="Scarvelis">{{cite journal | author = Scarvelis D, Wells P | title = Diagnosis and treatment of deep-vein thrombosis | journal = CMAJ | volume = 175 | issue = 9 | pages = 1087–92 | year = 2006 | pmid = 17060659 | doi = 10.1503/cmaj.060366 | pmc = 1609160 }} [http://www.cmaj.ca/content/177/11/1392.2.full.pdf+html Erratum]</ref> Distal DVT has limited [[clinical significance]] compared to proxmial DVT.<ref name="Galanaud">{{cite journal| author=Galanaud JP, Bosson JL, Quéré I | title=Risk factors and early outcomes of patients with symptomatic distal vs. proximal deep-vein thrombosis | journal=Curr Opin Pulm Med | year= 2011 | volume= 17 | issue= 5 | pages= 387-91 | pmid=21832920 | doi=10.1097/MCP.0b013e328349a9e3}}</ref> An ''incident'' DVT is an initial episode and any subsequent DVTs are termed ''recurrent''.<ref name="Predictors">{{cite journal| author=Heit JA, Mohr DN, Silverstein MD, ''et al''.| title=Predictors of recurrence after deep vein thrombosis and pulmonary embolism: a population-based cohort study | journal=Arch Intern Med | year= 2000 | volume= 160 | issue= 6 | pages= 761–8 | pmid=10737275 | url=http://archinte.ama-assn.org/cgi/content/full/160/6/761| doi=10.1001/archinte.160.6.761 }}</ref> ''Bilateral'' DVT refers to a presence of thromboses in both legs while ''unilateral'' means only a single leg is affected.<ref name="Casella">{{cite journal| author=Casella IB, Bosch MA, Sabbag CR| title=Incidence and risk factors for bilateral deep venous thrombosis of the lower limbs | journal=Angiology | year= 2009 | volume= 60 | issue= 1 | pages= 99–103 | pmid=18504268 | doi=10.1177/0003319708316897}}</ref>

DVTs that have no symptoms, but are found only by screening, are labeled ''[[asymptomatic]]''.<ref name="Prevent asymptomatic">{{cite journal| author=Lloyd NS, Douketis JD, Moinuddin I, ''et al''.| title=Anticoagulant prophylaxis to prevent asymptomatic deep vein thrombosis in hospitalized medical patients: a systematic review and meta-analysis | journal=J Thromb Haemost | year= 2008 | volume= 6 | issue= 3 | pages= 405–14 | pmid=18031292 | doi=10.1111/j.1538-7836.2007.02847.x }}</ref> Pain and swelling are symptoms of ''[[Acute (medicine)|acute]]'' DVT.<ref name="Conklin">{{cite journal| author=Conklin P, Soares GM, Dubel GJ, ''et al''.| title=Acute deep vein thrombosis (DVT): evolving treatment strategies and endovascular therapy | journal=Med Health R I | year= 2009 | volume= 92 | issue= 12 | pages= 394–7 | pmid=20066826 | url=http://rimed.org/medhealthri/2009-12/2009-12-394.pdf }}</ref> Acute DVTs are usually ''occlusive'',<ref name="Scarvelis"/> meaning they obstruct blood flow, whereas ''nonocclusive'' DVTs are more asymptomatic.<ref name="ACS">{{cite web |url=http://www.acssurgery.com/acs/chapters/ch0606.htm |title=Management of Venous Thromboembolism |author=John T. Owings |date=December 2005 |work=ACS Surgery |publisher=American College of Surgeons |accessdate=16 January 2012}}</ref> The label of ''[[Chronic (medicine)|chronic]]'' has been applied to symptomatic DVTs which persist longer than 10 or 14 days.<ref name="Pharmacomechanical">{{cite journal| author=Rao AS, Konig G, Leers SA, ''et al''.| title=Pharmacomechanical thrombectomy for iliofemoral deep vein thrombosis: an alternative in patients with contraindications to thrombolysis | journal=J Vasc Surg | year= 2009 | volume= 50 | issue= 5 | pages= 1092–8 | pmid=19782528 | doi=10.1016/j.jvs.2009.06.050 }}</ref> A DVT may also be called ''[[idiopathic]]'' when it "occurs in the absence of a known precipitating factor, such as oral contraceptives, surgery, trauma, or cancer."<ref name="EGAPP">{{cite journal| author=Evaluation of Genomic Applications in Practice and Prevention (EGAPP) Working Group| title=Recommendations from the EGAPP Working Group: routine testing for Factor V Leiden (R506Q) and prothrombin (20210G>A) mutations in adults with a history of idiopathic venous thromboembolism and their adult family members | journal=Genet Med | year= 2011 | volume= 13 | issue= 1 | pages= 67–76 | pmid=21150787 | doi=10.1097/GIM.0b013e3181fbe46f |url=http://journals.lww.com/geneticsinmedicine/Fulltext/2011/01000/Recommendations_from_the_EGAPP_Working_Group_.11.aspx }}</ref>

==Signs and symptoms==
Approximately half of people with DVT have symptoms. They include pain and tenderness in the leg, swelling, warmth in the leg that is swollen or painful, redness or discoloration, and dilation of surface veins.<ref name="NIH SS">{{cite web |url=http://www.nhlbi.nih.gov/health/health-topics/topics/dvt/signs.html |title=What Are the Signs and Symptoms of Deep Vein Thrombosis? |date=28 October 2011 |publisher=National Institutes of Health |accessdate=15 April 2012}}</ref> However, signs and symptoms cannot be used to diagnose DVT. When taken together with the risk factors (see below), they are useful in determining the likelihood of DVT,<ref name="Scarvelis"/> but most of those with suspected DVT do not have it after evaluation.<ref name="Diagnosis">{{cite journal| author=Bates SM, Jaeschke R, Stevens SM, ''et al''.| title=Diagnosis of DVT: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines | journal=Chest | year= 2012 | volume= 141 | issue= suppl 2 | pages= e351S–418S | pmid=22315267 | doi=10.1378/chest.11-2299}}</ref> Most symptomatic individuals have another condition, and those possibilities include "[[cellulitis]], [[Baker's cyst]], musculoskeletal injury, [and] [[lymphedema]]".<ref name="Hargett">{{cite journal| author=Hargett CW, Tapson VF | title=Clinical probability and D-dimer testing: how should we use them in clinical practice? | journal=Semin Respir Crit Care Med | year= 2008 | volume= 29 | issue= 1 | pages= 15–24 | pmid=18302083 | doi=10.1055/s-2008-1047559}}</ref>

In [[phlegmasia alba dolens]], which usually results from acute occlusion of the iliac and femoral veins, the leg is pale and cool with a diminished arterial pulse caused by spasm. A severe and uncommon form of DVT, [[phlegmasia cerulea dolens]], often develops on top of a life-threatening illness.<ref name="ACS"/><ref>{{Cite journal|title=Images in Clinical Medicine: Phlegmasia Cerulea Dolens|author=Barham K, Shah T|year=2007|journal=N Engl J Med |volume=356|issue=3|pages=e3|pmid=17229945|doi=10.1056/NEJMicm054730|url=http://www.nejm.org/doi/full/10.1056/NEJMicm054730}}</ref> It is characterized by an acute and nearly total venous occlusion of the entire extremity outflow, including the iliac and femoral veins. The leg is usually painful, [[Cyanosis|cyanosed]] (blue from lack of oxygen) and [[edema]]tous (filled with fluid). Venous gangrene may develop as a result.

In women, [[recurrent miscarriage]] may be a sign of DVT risk, as it is associated with [[antiphospholipid syndrome]], a risk factor for DVT.<ref name="Bates"/>

==Causes==
[[Image:Coagulation full.svg|right|thumb|The [[coagulation]] system, often described as a [[Biochemical cascade|"cascade"]], consists of a group of proteins that interact in the formation of a fibrin-rich clot. DVT risk is increased by certain alterations in the cascade.]]
Venous thrombi are recognized to be caused mainly by a combination of [[venous stasis]] and [[hypercoagulability]]—but to a lesser extent endothelial damage and [[Endothelial activation|activation]].<ref name="Basic patho"/> These three factors represent [[Virchow's triad]], and changes to the vessel wall are the least understood.<ref name="Whatis"/> Various risk factors increase the likelihood of any one individual developing a thrombosis. Risk factors do not predict all DVTs, however. Some of those with DVT have no risk factors present, and many individuals with multiple risk factors never have one.<ref name="Lijfering"/>

The strongest acquired risk factor is older age<ref name="Whatis"/> due to changes in blood composition which favor clotting. Major surgery and [[Physical trauma|trauma]] may increase DVT risk due to [[tissue factor]] from outside the vascular system mixing with blood. Cancer can grow in and around veins, causing venous stasis, and it can also stimulate increased levels of tissue factor. [[Hypercoagulability in pregnancy|Pregnancy causes blood to favor clotting]], and in the [[postpartum]], hemoconcentration along with [[placenta]]l tearing (which releases substances that favor clotting) increase risk. [[Oral contraceptives]] and [[hormonal replacement therapy]] increase risk through a variety of mechanisms.<ref name="Basic patho"/> Inherited thrombophilias (deficiencies in the anticoagulation factors [[protein C]], [[protein S]], [[antithrombin]], or mutations in the [[factor V]] and [[prothrombin]] genes) are present in about 30 to 50% of those with VTE.<ref name="Varga">{{cite journal| author=Varga EA, Kujovich JL| title=Management of inherited thrombophilia: guide for genetics professionals | journal=Clin Genet | year= 2012 | volume= 81 | issue= 1 | pages= 7–17 | pmid=21707594 | doi=10.1111/j.1399-0004.2011.01746.x }}</ref> [[Factor V Leiden]] and [[prothrombin G20210A]], both predominantly expressed in [[Caucasian race|Caucasians]], are the most commonly inherited risk factors;<ref name="Basic patho"/> they moderately increase risk, by factors of about three to eight and two to three, respectively.<ref name="Varga"/><ref name="RosendaalReitsma"/> Deficiencies in antithrombin, protein C and S are "rare but strong risk factors for venous thrombosis."<ref name="Basic patho"/> These three thrombophilias increase relative risks for VTE or venous thrombosis by up to 10- or 20-fold.<ref name="Lijfering"/><ref name="Varga"/><ref>Lijfering ''et al''. report that the relative risk (RR) of venous thrombosis for each is 15 to 20 while Varga and Kujovich report the RR of VTE for antithrombin deficiency, protein C deficiency and protein S deficiency to be 10 to 20, 7 to 10 and 5 to 10, respectively.</ref>

Depending upon their location in the body, DVTs are influenced by varying risk factors. In isolated distal DVT, the profile of risk factors appears distinct from proximal DVT; transient factors, such as surgery and immobilization, appear to dominate whereas thrombophilias and age do not seem to increase risk.<ref name="Palareti">{{cite journal| author=Palareti G, Schellong S| title=Isolated distal deep vein thrombosis: what we know and what we are doing | journal=J Thromb Haemost | year= 2012 | volume= 10 | issue= 1 | pages= 11–9 | pmid=22082302 | doi=10.1111/j.1538-7836.2011.04564.x }}</ref> In upper extremity DVT, [[central venous catheters]] are a dominant risk factor.<ref name="Lee">{{cite journal| author=Lee JA, Zierler BK, Zierler RE| title=The risk factors and clinical outcomes of upper extremity deep vein thrombosis | journal=Vasc Endovascular Surg | year= 2012 | volume= 46 | issue= 2 | pages= 139–44 | pmid=22328450 | doi=10.1177/1538574411432145 }}</ref>

===Risk factors===
{{Multicol}}
*'''Acquired'''
**Older age<ref name="Whatis"/>
**Major surgery and orthopedic surgery<ref name="RosendaalReitsma"/>
**Cancers, most particularly [[Pancreatic cancer|pancreatic]], but not cancers of the lip, oral cavity, and pharynx<ref name="Cancer">{{cite journal| author=Stein PD, Beemath A, Meyers FA, ''et al''.| title=Incidence of venous thromboembolism in patients hospitalized with cancer | journal=Am J Med | year= 2006 | volume= 119 | issue= 1 | pages= 60–8 | pmid=16431186 | doi=10.1016/j.amjmed.2005.06.058 }}</ref>
**Immobilization, as in [[orthopedic cast]]s<ref name="RosendaalReitsma"/> the sitting position, and travel, particularly by air<ref name="Basic patho">{{cite journal| author=Martinelli I, Bucciarelli P, Mannucci PM| title=Thrombotic risk factors: basic pathophysiology | journal=Crit Care Med | year= 2010 | volume= 38 | issue= suppl 2 | pages= S3–9 | pmid=20083911 | doi=10.1097/CCM.0b013e3181c9cbd9 }}</ref>
**Pregnancy and the postpartum period<ref name="Basic patho"/><ref name="Jackson">{{cite journal| author=Jackson E, Curtis KM, Gaffield ME| title=Risk of venous thromboembolism during the postpartum period: a systematic review | journal=Obstet Gynecol | year= 2011 | volume= 117 | issue= 3 | pages= 691–703 | pmid=21343773 | doi=10.1097/AOG.0b013e31820ce2db }}</ref>
**[[Antiphospholipid syndrome]]<ref name="RosendaalReitsma"/> (such as [[lupus anticoagulant]])<ref name="Basic patho"/><ref name="Whatis">{{cite journal| author=Bovill EG, van der Vliet A| title=Venous valvular stasis-associated hypoxia and thrombosis: what is the link? | journal=Annu Rev Physiol | year= 2011 | volume= 73 | pages= 527–45 | pmid=21034220 | doi=10.1146/annurev-physiol-012110-142305 }}</ref>
**Trauma<ref name="Basic patho"/> and minor leg injury<ref name="Varga"/>
**Previous VTE<ref name="Turpie"/>
**Oral contraceptives<ref name="RosendaalReitsma"/>
**Hormonal replacement therapy<ref name="RosendaalReitsma"/>
**Central venous catheters<ref name="RosendaalReitsma"/>
**Some [[autoimmune disease]]s<ref name="Zöller">{{cite journal| author=Zöller B, Li X, Sundquist J, ''et al''.| title=Risk of pulmonary embolism in patients with autoimmune disorders: a nationwide follow-up study from Sweden | journal=Lancet | year= 2012 | volume= 379 | issue= 9812 | pages= 244–9 | pmid=22119579 | doi=10.1016/S0140-6736(11)61306-8 }}</ref>
**[[Nephrotic syndrome]]<ref name="Lijfering">{{cite journal| author=Lijfering WM, Rosendaal FR, Cannegieter SC| title=Risk factors for venous thrombosis – current understanding from an epidemiological point of view | journal=Br J Haematol | year= 2010 | volume= 149 | issue= 6 | pages= 824–33 | pmid=20456358 | doi=10.1111/j.1365-2141.2010.08206.x}}</ref>
**Obesity<ref name="RosendaalReitsma">{{cite journal |author=Rosendaal FR, Reitsma PH |title=Genetics of venous thrombosis |journal=J. Thromb. Haemost. |volume=7 |issue=suppl 1 |pages=301–4 |year=2009 |month=July |pmid=19630821 |doi=10.1111/j.1538-7836.2009.03394.x |url=http://onlinelibrary.wiley.com/doi/10.1111/j.1538-7836.2009.03394.x/full}}</ref>
**Infection<ref name="Lijfering"/>
**HIV<ref name="Lijfering"/>
**[[Polycythemia vera]]<ref name="RosendaalReitsma"/>
**[[Chemotherapy]]<ref name="Whatis"/>
{{Multicol-break}}
*'''Inherited'''
**[[Antithrombin deficiency]]<ref name="Basic patho"/>
**[[Protein C deficiency]]<ref name="Basic patho"/>
**[[Protein S deficiency]] (type I)<ref name="Lijfering"/>
**Factor V Leiden<ref name="Basic patho"/>
**Prothrombin G20210A<ref name="Basic patho"/>
**[[Dysfibrinogenemia]]<ref name="RosendaalReitsma"/>
**Non O-[[blood type]]<ref name="RosendaalReitsma"/>
{{Multicol-break}}
*'''Mixed'''
**Low free protein S<ref name="Lijfering"/>
**[[Activated protein C resistance]]<ref name="Lijfering"/>
**High [[factor VIII]] levels<ref name="Basic patho"/>
**[[Hyperhomocysteinemia]]<ref name="Basic patho"/>
**High [[fibrinogen]] levels<ref name="Basic patho"/>
**High [[factor IX]] levels<ref name="Basic patho"/>
**High [[factor XI]] levels<ref name="Basic patho"/>
 
[[Image:Protein F5 PDB 1czs.png|thumb|The factor V protein is mutated in carriers of factor V Leiden, which is the most common inherited DVT risk factor.<ref name="Rosendaal2005">{{cite journal |author=Rosendaal FR |title=Venous thrombosis: the role of genes, environment, and behavior |journal=Hematology Am. Soc. Hematol. Educ. Program |volume= 2005|issue= 1|pages=1–12 |year=2005 |pmid=16304352 |doi=10.1182/asheducation-2005.1.1 |url=http://asheducationbook.hematologylibrary.org/cgi/content/full/2005/1/1}}</ref>]]
{{Multicol-end}}

==Pathophysiology==
[[Image:Gray586.png|thumb|The femoral vein (in the thigh), the iliac veins (in the pelvis), and the inferior vena cava (in the abdomen) are places of potential DVT extension.]] 
DVTs usually develop first in the calf veins, and when they extend, they "grow" in the direction of venous flow, towards the knees.<ref name="Distribution">{{cite journal| author=Chan WS, Spencer FA, Ginsbergm JS| title=Anatomic distribution of deep vein thrombosis in pregnancy | journal=CMAJ | year= 2010 | volume= 182 | issue= 7 | pages= 657–60 | pmid=20351121 | doi=10.1503/cmaj.091692 | pmc=2855912 }}</ref> When DVTs do not grow, they can be cleared naturally and dissolved into the blood.<ref name="Saha">{{cite journal| author=Saha P, Humphries J, Modarai B, ''et al''.| title=Leukocytes and the natural history of deep vein thrombosis: current concepts and future directions | journal=Arterioscler Thromb Vasc Biol | year= 2011 | volume= 31 | issue= 3 | pages= 506–12 | pmid=21325673 | doi=10.1161/ATVBAHA.110.213405 | pmc=3079895 }}</ref> There is a strong tendency for DVT to develop in the left leg (about 70 to 90% of the time) "possibly because of exacerbation of the compressive effects on the left iliac vein due to its being crossed by the right iliac artery."<ref name="Marik"/> DVT commonly affects the leg veins of the [[femoral vein]], the [[popliteal vein]], or the [[iliofemoral vein]] (as in [[May-Thurner syndrome]]). Occasionally the veins of the arm are affected, as with [[Paget-Schrötter disease]]. Very extensive lower extremity DVTs can extend into the [[iliac vein]]s or the [[inferior vena cava]]. Rarer DVTs can affect the upper extremities or the mesenteric (intestinal) and pelvic veins.<ref name="CC">{{cite web |author=Esther S.H. Kim and John R. Bartholomew | url = http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/venous-thromboembolism/ | title = Venous Thromboembolism| accessdate = 15 February 2011 |publisher=Cleveland Clinic}}</ref>

The mechanism behind arterial thrombosis, as with [[Myocardial_infarction#Pathophysiology|heart attacks]], is more established than the steps that cause venous thrombosis.<ref name="Lopez">{{cite journal| author=López JA, Chen J| title=Pathophysiology of venous thrombosis | journal=Thromb Res | year= 2009 | volume= 123 | issue= suppl 4 | pages= S30–4 | pmid=19303501 | doi=10.1016/S0049-3848(09)70140-9 }}</ref> With arterial thrombosis, blood vessel wall damage is required for thrombosis formation, as it initiates [[coagulation]],<ref name="Lopez"/> but the majority of venous thrombi form without any injured endothelium.<ref name="Basic patho" /> The initation of a venous thrombosis is thought to be caused by [[tissue factor]] effected thrombin production, which leads to fibrin deposition.<ref name="Whatis"/> [[Red blood cell]]s and [[fibrin]] are the main components of venous thrombi,<ref name="Basic patho"/> and the thrombi appear to attach to the blood vessel wall [[endothelium]], normally a non-thrombogenic surface, with fibrin.<ref name="Lopez"/> [[Platelet]]s are more prominent in arterial thrombi when compared to venous thrombi.<ref name="Basic patho"/> In venous thrombi platelets attach to downstream fibrin, while in arterial thrombi, they compose the core.<ref name="Lopez"/>

The valves of veins are a recognized site of VT initiation.<ref name="Saha"/> Due to the blood flow pattern, the base of the valve sinus is particularly deprived of oxygen ([[Hypoxia (medical)|hypoxic]]). Stasis exacerbates hypoxia, and this state is linked to the activation of white blood cells ([[leukocytes]]) and the [[Endothelial activation|endothelium]]. Specifically, the two pathways of [[hypoxia-inducible factor-1]] (HIF-1) and [[early growth response 1]] (EGR-1) are activated by hypoxia, and they contribute to [[monocyte]] and endothelial activation. Hypoxia also causes [[reactive oxygen species]] (ROS) production that can activate HIF-1, EGR-1 and [[nuclear factor-κB]] (NF-κB), which regulates HIF-1 transcription.<ref name="Whatis"/> HIF-1 and EGR-1 pathways lead to monocyte association with endothelial proteins, such as [[P-selectin]], prompting monocytes to release tissue factor filled [[microvesicles]], which presumably initiate fibrin deposition (via thrombin) after binding the endothelial surface.<ref name="Whatis"/>

==Diagnosis==
[[Image:Combinpedal.jpg|thumb|Swelling in the leg from fluid (edema) can result in "pitting" after pressure is applied.]]
[[File:DVTUS.PNG|thumb|An ultrasound image demonstrating a blood clot in the left common femoral vein.]]
[[Image:Iliac vein deep vein thrombosis.JPEG|thumb|Abdominal [[computed tomography|CT]] scan showing a [[common iliac vein]] thrombosis. The arrow indicates the filling defect in the vein visualised using [[radiocontrast]].]]
[[Image:Phlebographie mit Thrombose.jpg|thumb|[[Venography|Venogram]]s of DVT.]]

In 2012, the [[American College of Chest Physicians]] (ACCP) released their 9th edition of [[clinical guideline]]s,<ref>{{cite journal |title=Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines |journal=Chest |volume=141 |issue=suppl 2 |year=2012 |url=http://chestjournal.chestpubs.org/content/141/2_suppl.toc |publisher=American College of Chest Physicians}}</ref> which included recommendations on VTE diagnosis.<ref name="Diagnosis"/> The recommendations were given strengths with "grades", depending upon the evidence for them.

{| class="wikitable"
|-
! Grade
! Description of 2012 ACCP grade<ref>For more detailed text descriptions of the grades, including benefits vs. the risks and burdens, the methodologic strength of supporting evidence, and implications, see Table 4 of [http://chestjournal.chestpubs.org/content/141/2_suppl/53S.full.pdf+html Guyatt ''et al''.], p. 62S</ref>
|-
| 1A
| Strong recommendation, high-quality evidence
|-
| 1B
| Strong recommendation, moderate-quality evidence
|-
| 1C
| Strong recommendation, low- or very-low-quality evidence
|-
| 2A
| Weak recommendation, high-quality evidence
|-
| 2B
| Weak recommendation, moderate-quality evidence
|-
| 2C
| Weak recommendation, low- or very-low-quality evidence<ref name="Methodology">{{cite journal| author=Guyatt GH, Norris SL, Schulman S, ''et al''.| title=Methodology for the Development of Antithrombotic Therapy and Prevention of Thrombosis Guidelines: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines | journal=Chest | year=2012 | volume=141 | issue=suppl 2 | pages= 53S–70S | pmid=22315256 | doi=10.1378/chest.11-2288 |url=http://chestjournal.chestpubs.org/content/141/2_suppl/53S.full.pdf+html}}</ref>
|}

This article cites the 2012 ACCP recommendations, and it includes the grade in parentheses in this section and in the prevention and treatment sections below.

===Probability===

In those with suspected DVT, a clinical assessment of probability can be useful to determine which tests to perform.<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 16S: 3.1.</ref> The most studied [[clinical prediction rule]] is the Wells score.<ref name="Diagnosis"/>

'''Wells score or criteria''':
(Possible score −2 to 9)

#Active cancer (treatment within last 6 months or palliative): +1 point
#Calf swelling ≥ 3&nbsp;cm compared to asymptomatic calf (measured 10&nbsp;cm below tibial tuberosity): +1 point
#Swollen unilateral superficial veins (non-varicose, in symptomatic leg): +1 point
#Unilateral pitting edema (in symptomatic leg): +1 point
#Previous documented DVT: +1 point
#Swelling of entire leg: +1 point
#Localized tenderness along the deep venous system: +1 point
#Paralysis, [[paresis]], or recent cast immobilization of lower extremities: +1 point
#Recently bedridden ≥ 3&nbsp;days, or major surgery requiring regional or general anesthetic in the past 12 weeks: +1 point
#Alternative diagnosis at least as likely: −2 points<ref name="Hargett"/>

A Wells score can be interpreted in a binary (likely vs. unlikely) or ternary (low, moderate, or high probability) fashion. For a binary interpretation, scores of two or above are categorized as likely, while one and below means unlikely. For a ternary interpretation, scores of one and two are of moderate probability, while scores below or above are low and high probability, respectively.<ref name="Hargett"/> When people are segregated into binary groups, DVT prevalence is about 6% versus 28%. Ternary groups stratify prevalences into groups of about 5%, 17%, and 53%.<ref name="Diagnosis"/>

===D-dimer===
[[D-dimer]]s are a [[fibrin degradation product]], and a positive D-dimer test can result from the sensitive detection of a thrombosis being dissolved by [[plasmin]]. A positive test may also result from other conditions.<ref name="Diagnosis"/> Thus, a positive D-dimer test means further diagnostic testing should be done to determine if a DVT is present, while a negative result can exclude a DVT diagnosis.<ref name="Diagnosis"/> For suspected first lower extremity DVT in a low-probability situation, the typical next step is to test [[D-dimer]] levels with either moderate or high sensitivity.<ref name="G16S3.2."/> In a moderate-probability scenario, the ACCP recommends a high-sensitivity D-dimer over ultrasound imaging (2C),<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 16S: 3.3.</ref> and in high-probability cases D-dimers are to be skipped in favor of diagnostic imaging.<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 17S: 3.4.</ref>

===Imaging===

Imaging studies are used to diagnose DVT. Ultrasound on the veins is the most common method, and the two standard options include proximal compression ultrasound or whole-leg ultrasound. Drawbacks to each method exist. A single proximal scan may miss a distal DVT, while whole-leg scanning can lead to distal DVT overtreatment.<ref name="Diagnosis"/> [[Doppler ultrasound]],<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 19S: 5.3. & 6.1.</ref> [[CT scan]] venography, [[MRI]] venography or MRI of the thrombosis are also possibilities.<ref name="Diagnosis"/><ref name="G16S3.2.">[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 16S: 3.2.</ref> The [[gold standard (test)|gold standard]] for judging imaging methods is contrast [[venography]], which involves injecting a peripheral vein of the affected limb with a [[contrast agent]] and taking [[X-ray]]s, to reveal whether the venous supply has been obstructed. Because of its cost, invasiveness, and other limitations this test is rarely performed.<ref name="Diagnosis"/>

==Prevention==

Walking is a preventative measure, as are calf exercises.<ref>{{cite book|last=Perry|first=Anne Griffen|title=Clinical Nursing Skills and Techniques|year=2010|publisher=Mosby|location=St. Louis, MO|isbn=978-0-323-05289-4|page=243}}</ref> Both reduce venous stasis. Leg muscle contractions compress the veins to pump blood up towards the heart. Blood flow patterns can also be improved in at risk immobile individuals with physical compression methods. Anticoagulation, which increases the risk of bleeding, is standard when the benefits are thought to exceed the risks. The annual risk of major bleeding from long-term anticoagulation is about 3%,<ref name="Varga"/> and the point at which annual VTE risk is thought to warrant long-term anticoagulation is estimated to be between 3 to 9%.<ref name="Keeling"/> Usually, only when individuals exceed a 9% annual VTE risk is long-term anticoagulation a common consideration.<ref name="Keeling">{{cite journal |author=Keeling D, Baglin T, Tait C, ''et al.'' |title=Guidelines on oral anticoagulation with warfarin – fourth edition |journal=Br J Haematol |volume=154 |issue=3 |pages=311–24 |year=2011 |month=August |pmid=21671894 |doi=10.1111/j.1365-2141.2011.08753.x |url=http://www.bcshguidelines.com/documents/warfarin_4th_ed.pdf}}</ref> Antithrombin deficiency, a strong risk factor, only carries an annual risk of VTE of 0.8 to 1.5%;<ref name="Varga"/> as such, asymptomatic individuals with thrombophilia do not warrant long-term anticoagulation (1C).<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 11S: 7.1.</ref>

===Surgery patients===

Those who have major [[orthopedic surgery]]—such as [[total hip replacement]], [[total knee replacement]] or [[hip fracture]] surgery—are at a high risk of VTE.<ref name="Sobieraj">{{cite journal |author=Sobieraj DM, Lee S, Coleman CI, ''et al''. |title=Prolonged Versus Standard Duration Venous Thromboprophylaxis in Major Orthopedic Surgery: A Systematic Review |journal=Ann Intern Med |volume= |issue= |pages= |year=2012 |pmid=22412039 |doi=10.1059/0003-4819-156-10-201205150-00423 |url=http://www.annals.org/content/early/2012/03/09/0003-4819-156-10-201205150-00423.long}}</ref> After any one of those three surgeries, in the absence of prophylaxis, the risk of symptomatic VTE in the 35 days after surgery is estimated to be about 4%.<ref name="Falck-Ytter"/>

To prevent VTE in patients who have undergone non-orthopedic surgery, early ambulation (walking), mechanical prophylaxis ([[intermittent pneumatic compression]] [IPC] or [[graduated compression stockings]] [GCS]), and drugs ([[low-molecular-weight heparin]] [LMWH] and low-dose-unfractionated [[heparin]] [LDUH]) are potential treatments depending upon the risk of VTE, risk of major bleeding and patient preferences.<ref>{{cite journal |author=Gould MK, Garcia DA, Wren SM, ''et al''.|year=2012 |title=Prevention of VTE in Nonorthopedic Surgical Patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines |journal=Chest |volume=141 |issue= suppl 2 |pages=e227S–e277S |doi=10.1378/chest.11-2297 |pmid=22315263 }}</ref> In major orthopedic surgery patients, the ACCP recommended additional drug options such as [[fondaparinux]] and [[aspirin]], (1B), though LMWH is preferred (2B or 2C).<ref name="Falck-Ytter">{{cite journal |author=Falck-Ytter Y, Francis CW, Johanson NA, ''et al''. |year=2012 |title=Prevention of VTE in Orthopedic Surgery Patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines |journal=Chest |volume=141 |issue=suppl 2 |pages=e278S–e325S |doi=10.1378/chest.11-2404 |pmid=22315265 }}</ref> IPC is an option (1C).<ref name="Falck-Ytter"/><ref>{{cite journal |author=Kakkos SK, Caprini JA, Geroulakos G, ''et al''. |title=Combined intermittent pneumatic leg compression and pharmacological prophylaxis for prevention of venous thromboembolism in high-risk patients |journal=Cochrane Database Syst Rev |issue=4 |pages=CD005258 |year=2008 |pmid=18843686 |doi=10.1002/14651858.CD005258.pub2 |editor1-last=Kakkos |editor1-first=Stavros K }}</ref>

===Pregnancy===
{{See also|Hypercoagulability in pregnancy}}
[[Image:Warfarintablets5-3-1.jpg|thumb|Warfarin, a common VKA, is only recommended postpartum (after childbirth) in at risk women.]]
The risk of VTE is increased in pregnancy by about five-fold<ref name="Varga"/><ref name="Marik">{{cite journal| author=Marik PE, Plante LA| title=Venous thromboembolic disease and pregnancy | journal=N Engl J Med | year= 2008 | volume= 359 | issue= 19 | pages= 2025–33 | pmid=18987370 | doi=10.1056/NEJMra0707993 | url=http://www.nejm.org/doi/full/10.1056/NEJMra0707993 }}</ref> due to a more hypercoaguable state, a likely adaptation against fatal [[postpartum hemorrhage]].<ref name="Jackson" /> Additionally, pregnant women with genetic susceptibility to blood coagulation are subject to a further and approximate three- to thirty-fold increased risk for VTE, depending upon the risk factor(s).<ref name="Bates">{{cite journal|title= VTE, Thrombophilia, Antithrombotic Therapy, and Pregnancy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines |year=2012 |journal=Chest |volume=141 |issue=suppl 2 |pages= e691S–e736S |doi=10.1378/chest.11-2300 |pmid=22315276 |author=Bates SM, Greer IA, Middeldorp S, ''et al''.}}</ref> Only pregnant women with strong risk factors for VTE are suggested to receive targeted ([[Prothrombin time|INR]] of 2.0 to 3.0) preventative measures. Homozygous carriers of [[factor V Leiden]] or [[prothrombin G20210A]] with a family history of VTE were recommended by the ACCP to receive [[antepartum]] LMWH and either LMWH or a [[vitamin K antagonist]] (VKA) for the six weeks following childbirth (2B); those with another thrombophlia and a family history but no previous VTE were recommended to be subject to [[clinical vigilance]] during pregnancy and LMWH or (for those without [[Protein C deficiency|protein C]] or [[Protein S deficiency|S deficiency]]) a VKA (2C); homozygous carriers with no personal or family history of VTE were recommended to be subject to clinical vigilance during pregnancy and LMWH or a VKA for six weeks after childbirth (2B); and those with another thrombophilia but no family or personal history of VTE were suggested to receive clinical vigilance (2C).<ref name="Bates"/> [[Warfarin]], a common VKA, is known to have [[teratology|teratogenic effects]] on the fetus if administered in early pregnancy<ref name="Sathienkijkanchai-2005">{{cite journal | author=Sathienkijkanchai A, Wasant P | title=Fetal warfarin syndrome | journal=J Med Assoc Thai | year=2005 | volume=88 | issue=suppl 8 | pages=S246–50 | pmid=16856447}}</ref><ref name="Schaefer-2006">{{cite journal | author=Schaefer C, Hannemann D, Meister R, ''et al''.| title=Vitamin K antagonists and pregnancy outcome: A multi-centre prospective study | journal=Thromb Haemost | year=2006 | volume=95 | issue=6 | pages=949–57 | pmid=16732373 | doi=10.1160/TH06-02-0108}}</ref> and is not advised in pregnant women.

===Travellers===
[[Image:Kompressionsstrümpfe.jpg|thumb|110px|Graduated compression stockings are recommended in at-risk travelers and some hospital patients by the ACCP]]

In the 2012 ACCP clinical guidelines, grade 2C recommendations were offered. For at risk long-haul travelers—those with "previous VTE, recent surgery or trauma, active malignancy, pregnancy, estrogen use, advanced age, limited mobility, severe obesity, or known thrombophilic disorder"—recommendations for prevention included frequent walking, calf exercises, and aisle seating in airplanes to ease walking.<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 11S: 6.1.1. & 6.1.2.</ref><ref>{{cite web |url=http://www.chestnet.org/accp/article/new-dvt-guidelines-no-evidence-support-economy-class-syndrome |title=New DVT Guidelines: No Evidence to Support "Economy Class Syndrome"; Oral Contraceptives, Sitting in a Window Seat, Advanced Age, and Pregnancy Increase DVT Risk in Long-distance Travelers |date=7 February 2012 |publisher=American College of Chest Physicians |accessdate=10 February 2012}}</ref> The use of "properly fitted, below-knee GCS providing 15 to 30 mm Hg of pressure at the ankle during travel" was recommended though use of aspirin or anticoagulants were not.<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 11S: 6.1.2. & 6.1.3.</ref> Compression stockings have sharply reduced the levels of asymptomatic DVT in airline passengers, but the effect on symptomatic VTE is unknown as no individuals studied developed symptomatic VTE.<ref name="Clarke">{{cite journal| author=Clarke M, Hopewell S, Juszczak E, ''et al''.| title=Compression stockings for preventing deep vein thrombosis in airline passengers | journal=Cochrane Database Syst Rev | year= 2006 | issue= 2 | pages= CD004002 | pmid=16625594 | doi=10.1002/14651858.CD004002.pub2| editor1-last=Clarke| editor1-first=Mike J }}</ref>

===Hospital patients===

In 2011, the [[American College of Physicians]] (ACP) issued a [[clinical practice guideline]] with three strong recommendations on moderate-quality evidence: that hospitalized patients be assessed for their risk of thromboembolism and bleeding before prophylaxis is started; that heparin or a related drug is used if potential benefits are thought to outweigh potential harms; and that graduated compression stockings not be used. The ACP also stated a lack of support for any performance measures that incentivize physicians to apply universal prophylaxis without regard to the risks.<ref name="ACP CPG"/><ref name="Lederle">{{cite journal |author=Lederle FA, Zylla D, MacDonald R, ''et al''. |title=Venous thromboembolism prophylaxis in hospitalized medical patients and those with stroke: a background review for an american college of physicians clinical practice guideline |journal=Ann Intern Med |year=2011 |volume=155 |issue=9 |pages=602–15 |pmid=22041949 |doi=10.1059/0003-4819-155-9-201111010-00008|url=http://www.annals.org/content/155/9/602.long}}</ref>

The 2012 ACCP guidelines include recommendations for non-surgical patients.<ref name="Kahn">{{cite journal|author= Kahn SR, Lim W, Dunn AS, ''et al''.|title=Prevention of VTE in Nonsurgical Patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines |journal=Chest|volume=141|issue=suppl 2|pages= e195S–e226S|year=2012|pmid=22315261|doi=10.1378/chest.11-2296}}</ref><ref>Page e197S of Kahn ''et al''. specifies that the guideline does not apply to those with "trauma
and spinal cord injury" nor those "with ischemic and hemorrhagic stroke."</ref> Anticoagulation is recommended for the acutely ill in cases of elevated risk when there is no bleeding nor a high risk of bleeding (1B).<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 10S: 2.3., 2.4., & 2.7.1.</ref> When risks for both bleeding and thrombosis are elevated, mechanical prophylaxis is suggested (2C).<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 10S: 2.7.2.</ref> For the critically ill, prophylaxis is suggested, either pharmacological or mechanical depending upon the risk (2C).<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 10S–11S: 3.4.3. & 3.4.4.</ref> In outpatients with cancer who have solid tumors and additional risk factors for VTE—listed as "previous venous thrombosis, immobilization, hormonal therapy, [[angiogenesis inhibitor]]s, [[thalidomide]], and [[lenalidomide]]"—and a low risk of bleeding, heparin is recommended (2B).<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 11S: 4.2.2.</ref>

==Treatment==

===Anticoagulation===
{{double image|right|Heparin-2D-skeletal.png|165|Fondaparinux.svg|165|Structural representations of the backbone of heparins (''left''), which vary in the size of their chain, and the synthetic pentasaccaride (five-sugar) fondaparinux (''right'')||Heparin|Fondaparinux}}
[[Anticoagulation]], which prevents further coagulation, is the standard treatment for acute DVT of the leg. The ACCP recommends patients receive a [[parenteral]] anticoagulant (such as LMWH, [[fondaparinux]] or unfractionated heparin) for at least five days and to start [[vitamin K antagonist]] (VKA) treatment the same day (1B). The parenteral anticoagulant is recommended until the [[international normalized ratio]] (INR) is ≥ 2.0 for 24 hours minimum (1B); or, if the INR is > 3.0, the parental anticoagulant treatment can stop early.<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 20S: 2.4.</ref><ref name="Kearon2"/> LMWH and fondaparinux are recommended over unfractionated heparin (2B or C),<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 20S: 2.5.1.</ref> but unfractionated heparin does not present clearance issues in those with compromised kidney function.<ref name="Kearon2"/> The VKA is generally taken for a minimum of three months to maintain an INR of 2.0 to 3.0,<ref name="Strijkers"/><ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 20S–21S: 3.1.</ref> but the benefit of taking a VKA declines as the duration of treatment extends, while the risk of bleeding remains.<ref name="Hutten">{{cite journal |author=Hutten BA, Prins MH |title=Duration of treatment with vitamin K antagonists in symptomatic venous thromboembolism |journal=Cochrane Database Syst Rev |issue=1 |pages=CD001367 |year=2006 |pmid=16437432 |doi=10.1002/14651858.CD001367.pub2 |editor1-last=Prins |editor1-first=Martin H }}</ref> In those with an annual risk of venous thrombosis in excess of 9%, as after an unprovoked episode, long-term anticoagulation is a potential treatment.<ref name="Keeling"/> Guidelines for anticoagulant management have been published, but many facets are understudied.<ref>{{cite journal|author=Holbrook A, Schulman S, Witt DM, ''et al''. |title=Evidence-Based Management of Anticoagulant Therapy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines |journal=Chest |volume=141 |issue=suppl 2 |pages=e152S–e184S |year=2012 |pmid=22315259 |doi=10.1378/chest.11-2295}}</ref> In those who have a positive [[D-dimer]] level after the end of VKA treatment for idiopathic VTE, there is an increased risk of recurrent VTE (about 9% vs. about 4% for negative results) and this result may be used in clinical decision making.<ref name="Douketis">{{cite journal| author=Douketis J, Tosetto A, Marcucci M, ''et al''.| title=Patient-level meta-analysis: effect of measurement timing, threshold, and patient age on ability of D-dimer testing to assess recurrence risk after unprovoked venous thromboembolism | journal=Ann Intern Med | year= 2010 | volume= 153 | issue= 8 | pages= 523–31 | pmid=20956709 | doi=10.1059/0003-4819-153-8-201010190-00009 }}</ref>

A methodologically sound randomized controlled trial of anticoagulation versus placebo in the treatment of VTE has never been done, but it is unlikely to be performed due to ethical constraints. Evidence for clinical practice is derived from secondary evidence, such as "trials comparing anticoagulation versus placebo after initial anticoagulation."<ref name="Cundiff">{{cite journal| author=Cundiff DK, Manyemba J, Pezzullo JC| title=Anticoagulants versus non-steroidal anti-inflammatories or placebo for treatment of venous thromboembolism | journal=Cochrane Database Syst Rev | year= 2006 | issue= 1 | pages= CD003746 | pmid=16437461 | doi=10.1002/14651858.CD003746.pub2| editor1-last=Cundiff| editor1-first=David K }}</ref>

===Graduated compression stockings===
In addition to anticoagulation treatment, [[graduated compression stockings]] (GCSs)—which apply higher pressure (30 to 40&nbsp;mm Hg) at the ankles and a lower pressure around the knees<ref name="Kearon2"/>—are recommended by the ACCP for those with symptomatic DVT (2B).<ref name="G23S">[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 23S: 4.1.</ref> Use should begin as soon as possible after anticoagulation.<ref name="Kearon2"/> Randomized controlled trials indicate GCSs reduce the risk of [[post-thrombotic syndrome]] (PTS), although the "evidence is of moderate quality".<ref name="Kearon2"/><ref>{{cite journal |author=Musani MH, Matta F, Yaekoub AY, ''et al''.|title=Venous compression for prevention of postthrombotic syndrome: a meta-analysis |journal=Am. J. Med. |volume=123 |issue=8 |pages=735–40 |year=2010 |month=August |pmid=20670728 |doi=10.1016/j.amjmed.2010.01.027 |url=}}</ref> Trials do not indicate a reduction in recurrent VTE.<ref name="Kearon2"/> The [[number needed to treat]] is relatively high, at four to five patients needing to have been treated to prevent one case of PTS.<ref name="pmid17003920">{{cite journal |author=Kakkos S, Daskalopoulou S, Daskalopoulos M, ''et al''. |title=Review on the value of graduated elastic compression stockings after deep vein thrombosis |journal=Thromb Haemost |volume=96 |issue=4 |pages=441–5 |year=2006 |pmid=17003920}}</ref> The recommended duration of use is for two years, though inconvenience and discomfort can reduce patient [[Compliance (medicine)|compliance]].<ref name="G23S"/>

===Inferior vena cava filter===
[[Image:Inferior vena cava filter.jpg|thumb|An IVC filter]]
[[Inferior vena cava filter]]s (IVC filters) are used on the presumption that they reduce pulmonary embolism, though their effectiveness and safety profile is not well established.<ref name="Young">{{cite journal| author=Young T, Tang H, Hughes R| title=Vena caval filters for the prevention of pulmonary embolism | journal=Cochrane Database Syst Rev | year= 2010 | issue= 2 | pages= CD006212 | pmid=20166079 | doi=10.1002/14651858.CD006212.pub4| editor1-last=Young| editor1-first=Tim }}</ref> In general, they are recommended "to be restricted to certain high-risk situations until more information becomes available";<ref name="Young"/> the ACCP recommended them in those with a contraindication to anticoagulant treatment (1B), but not in addition to anticoagulation (1B) unless an individual with an IVC filter, but without a risk for bleeding, develops acute proximal DVT (2B).<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 21S: 2.13.1.–3.</ref> While IVC filters are "associated with an increased risk of DVT in the longer term"<ref name="Young"/> they are not considered to be reason enough to maintain extended anticoagulation.<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 21S: 2.13.</ref>

===Home vs. hospital===
Home treatment is recommended by the ACCP for the initial treatment of those with acute leg DVT (1B) who feel "well enough to be treated at home (eg, [those without] severe leg symptoms or comorbidity)" as long as there is an adequate home environment, which is described as "well-maintained living conditions, strong support from family or friends, phone access, and ability to quickly return to the hospital if there is deterioration."<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 21S: 2.7.</ref>

===Serial imaging===
A follow-up imaging test (typically ultrasound) about one week post-diagnosis is an option for those with an acute isolated distal DVT without a high risk for extension (2C); if the thrombosis does not extend, no anticoagulation is recommended by the ACCP (1B).<ref name="Kearon2"/><ref name="G20S 2.3."/> This technique can benefit those at a high risk for bleeding. However, "patients who place a high value on avoiding the inconvenience of repeat imaging and a low value on the inconvenience of treatment and on the potential for bleeding are likely to choose initial anticoagulation over serial imaging."<ref name="G20S 2.3.">[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 20S: 2.3.</ref> When applied to symptomatic patients with a negative initial ultrasound result, serial testing is inefficient and "not cost effective."<ref name="Scarvelis"/>

===Thrombolysis and thrombectomy===
[[Thrombolysis]] can be systemic or, depending upon medical capabilities, catheter-directed, but anticoagulation alone is preferred by the ACCP (2C). Although, those "who are most likely to benefit" from thrombolysis—"who attach a high value to prevention of post-thrombotic syndrome (PTS), and a lower value to the initial complexity, cost, and risk of bleeding"—"are likely to choose [it] over anticoagulation alone."<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 21S: 2.9 & 2.10.</ref>

A mechanical thrombectomy device can remove a thrombus. However, it is only considered as an option by the ACCP when the following conditions apply: "iliofemoral DVT, symptoms for < 7 days (criterion used in the single randomized trial), good functional status, life expectancy of ≥ 1 year, and both resources and expertise are available."<ref name="Kearon2">{{cite journal|author=Kearon C, Akl EA, Comerota AJ, ''et al''. |title=Antithrombotic Therapy for VTE Disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines |journal=Chest |volume=141 |issue=suppl 2 |pages=e419S–e494S |year=2012 |pmid=22315268 |doi=10.1378/chest.11-2301}}</ref> In general, anticoagulation alone is preferred (2C).<ref>[[#CITEREFGuyatt2012|Guyatt ''et al''. 2012]], p. 21S: 2.11.</ref>

==Prognosis==

The most frequent complication of proximal DVT is the [[post-thrombotic syndrome]] (PTS). Some signs and symptoms of PTS are pain, [[paresthesia]] and (in severe cases) [[leg ulcer]]s. An estimated 20 to 50% of those with DVT will develop PTS, and 5 to 10% will develop severe PTS.<ref name="Kahn2009">{{cite journal|author=Kahn SR|title=How I treat postthrombotic syndrome|journal=Blood|volume=114|issue=21|year=2009|pages=4624–31|doi=10.1182/blood-2009-07-199174|pmid=19741190|url=http://bloodjournal.hematologylibrary.org/content/114/21/4624.long}}</ref> Distal DVT itself "is seldom if ever associated" with PTS or PE.<ref name="Diagnosis"/> PE is the most serious complication of DVT, and the risk of PE is higher in the presence of more extensive clots. Untreated lower extremity DVT has a 3% PE-related mortality rate. Deaths associated with upper extremity DVT are extremely rare.<ref name="Turpie">{{cite web | author = Turpie AGG | date = March 2008 | title = Deep Venous Thrombosis |work=The Merck's Manuals Online Medical Library | url = http://www.merck.com/mmpe/sec07/ch081/ch081b.html?qt=dvt&alt=sh#sec07-ch081-ch081b-1775}}</ref>

==Epidemiology==

DVTs occur in about 1 per 1000 adults per year.<ref name="Severinsen">{{cite journal| author=Severinsen MT, Johnsen SP, Tjønneland A, ''et al''.| title=Body height and sex-related differences in incidence of venous thromboembolism: a Danish follow-up study | journal=Eur J Intern Med | year= 2010 | volume= 21 | issue= 4 | pages= 268–72 | pmid=20603033 | doi=10.1016/j.ejim.2010.03.013 }}</ref> It is estimated that approximately 300,000 to 600,000 Americans suffer from VTE each year, with about 60,000 to 100,000 deaths attributable to PE.<ref>{{cite web |url=http://www.cdc.gov/ncbddd/dvt/data.html |title=Deep Vein Thrombosis/Pulmonary Embolism (DVT/PE) |publisher=Centers for Disease Control and Prevention |date=31 January 2012 |accessdate=20 March 2012}}</ref> Venous thrombosis is rare in the pediatric population, with an [[Incidence (epidemiology)|incidence]] of about 1 per 100,000 per year. From childhood to old age, incidence increases by a factor of about 1000, with almost 1% of the elderly population experiencing a venous thrombosis in a given year.{{sfn|Rosendaal|2009|p=5}} With pregnancy and postpartum, acute VTE incidence is about 1 per 1000 deliveries.<ref name="Bates"/> VTE develops in about 10 per 1000 people who receive preventative measures after total or partial knee replacement, and in about 5 per 1000 after total or partial hip replacement.<ref name="Januel">{{cite journal| author=Januel JM, Chen G, Ruffieux C, ''et al''.| title=Symptomatic in-hospital deep vein thrombosis and pulmonary embolism following hip and knee arthroplasty among patients receiving recommended prophylaxis: a systematic review | journal=JAMA | year= 2012 | volume= 307 | issue= 3 | pages= 294–303 | pmid=22253396 | doi=10.1001/jama.2011.2029 }}</ref>

With those who develop VTE, 30 to 50% have an inherited thrombophilia. The [[prevalence]] estimates for individual states are as follows: 0.5 to 9% for antithrombin deficiency, 3 to 9% for protein C deficiency, 1 to 3% for protein S deficiency, 12 to 20% for heterozygous factor V Leiden, 6 to 8% for heterozygous prothrombin G20210A, 0.2 to 4% for the homozygous case, and 2 to 4.5% for individuals doubly heterozygous for factor V Leiden and prothrombin G20210A.<ref name="Varga"/>

==History==
[[Image:Rudolf Virchow older portrait.jpg|thumb|Rudolf Virchow]]
The first documented DVT is thought to have occurred in the 13th century, "in the right leg of a 20-year-old man."<ref name="Lijfering"/> At some point, the increased incidence of DVT in women after childbirth was noticed, and in the late 1700s, a public health recommendation was issued to encourage women to breast feed as a means to prevent this phenomenon; the DVT was called "milk leg", as it was thought to result from milk building up in the leg.{{sfn|Rosendaal|2009|p=3}}

In 1856, German physician and pathologist [[Rudolf Virchow]] published what is referred to as [[Virchow's triad]], the three major causes of thrombosis.<ref name="Lijfering"/>{{sfn|Rosendaal|2009|p=3}} The triad provides the theoretical framework for how venous thrombosis formation is currently explained.<ref name="Lijfering"/> While the medical literature can attribute the triad as explaining causation, the triad was focused on the effect of a foreign body in the venous system and the conditions required for clot propagation.<ref name="Bagot2008">{{cite journal|author=Bagot CN, Arya R |title=Virchow and his triad: a question of attribution |journal=Br J Haematol |year=2008 |volume=143 |issue=2 |pages=180–189 |doi=10.1111/j.1365-2141.2008.07323.x |url=http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2141.2008.07323.x/full |pmid=18783400}}</ref>

Multiple pharmacological therapies for DVT were introduced in the 20th century. Oral anticoagulants were introduced in the 1940s, [[Subcutaneous injection|subcutaneous]] LDUH in 1962, and subcutaneous LMWH in 1982. Randomized clinical trials demonstrating the effectiveness of oral anticoagulation and subcutaneous LDUH were done in 1959 and 1972, respectively.{{sfn|Dalen|2003|p=2}} Diagnoses were commonly performed by [[impedance plethysmography]] in the 1970s and 1980s, but the use of Doppler ultrasound techniques, with their increased sensitivity and specificity, largely superseded this method.{{sfn|Dalen|2003|p=3}}

==Research directions==

As of 2011, three large randomized clinical trials (the Norwegian CaVent trial, the North American ATTRACT trial, and the Dutch CAVA trial) "on the effectiveness and safety of catheter directed thrombolysis" were underway.<ref name="Strijkers">{{cite journal| author=Strijkers RH, Cate-Hoek AJ, Bukkems SF, ''et al''.| title=Management of deep vein thrombosis and prevention of post-thrombotic syndrome | journal=BMJ | year= 2011 | volume= 343 | pages= d5916 | pmid=22042752 | doi=10.1136/bmj.d5916 | url=http://www.bmj.com/content/343/bmj.d5916 }}</ref>

==List of notable individuals==
* [[David Bloom]], a US NBC TV journalist who died in Iraq after getting DVT and a PE<ref>{{cite news |title=My husband should be living today |author=Melanie Bloom |url=http://msnbc.msn.com/id/7074940/site/todayshow/ns/today-today_health/t/my-husband-should-be-living-today/ |publisher=msnbc.com |date=3 March 2005 |accessdate=5 June 2012}}</ref>
* [[Heavy D]], a US rapper who died after a DVT and PE<ref>{{cite news |title=Rapper Heavy D killed by DVT, coroner says |url=http://www.bbc.co.uk/news/entertainment-arts-16346934 |publisher=BBC News |date=28 December 2011 |accessdate=5 June 2012}}</ref>

==Notes==
{{reflist|colwidth=30em}}

==References==
{{refbegin}}
*{{cite book|last=Dalen|first=James E.|title=Venous Thromboembolism|url=http://books.google.com/books?id=u-3Fiw7yE5kC&pg=PA1|year=2003|publisher=CRC Press|isbn=978-0-8247-5645-1|ref=harv}}
*{{cite journal |last=Guyatt |first=GH |coauthors=Akl EA; Crowther M; ''et al''. |title=Executive Summary: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines |journal=Chest |year=2012 |volume=141 |issue=suppl 2 |pages=7S–47S |pmid=22315257 |doi=10.1378/chest.1412S3 |url=http://chestjournal.chestpubs.org/content/141/2_suppl/7S.full.pdf+html |ref=harv}}
*{{cite book |last=Rosendaal |first=Frits R. |editor1-last=van Beek |editor1-first=Edwin J. R. |editor2-last=Büller |editor2-first=Harry R. |editor3-last=Oudkerk |editor3-first=Mathijs |title=Deep Vein Thrombosis and Pulmonary Embolism|url=http://books.google.com/books?id=6dVVv0v5cUwC&pg=PA3|year=2009|publisher=John Wiley & Sons|isbn=978-0-470-74499-4|ref=harv}}
*{{cite book|last=Welch|first=Ellen|title=Venous Thromboembolism: A Nurse's Guide to Prevention and Management|url=http://books.google.com/books?id=POGKxm9VdMQC&pg=PA2|year=2010|publisher=John Wiley & Sons|isbn=978-0-470-51189-3|ref=harv}}
{{refend}}

==External links==

* [http://www.isth.org/ International Society on Thrombosis and Haemostasis]
* [http://www.NATFonline.org North American Thrombosis Forum]
* [http://www.clotconnect.org/ Clot Connect]

[[Category:Coagulopathies]]
[[Category:Diseases of veins, lymphatic vessels and lymph nodes]]

[[ar:خثار وريدي عميق]]
[[es:Trombosis venosa profunda]]
[[fa:ترومبوز سیاهرگی عمقی]]
[[fr:Thrombose veineuse profonde]]
[[it:Trombosi venosa profonda]]
[[nl:Diep-veneuze trombose]]
[[pl:Zakrzepica żył głębokich]]
[[pt:Trombose venosa profunda]]
[[ru:Тромбоз глубоких вен]]
[[vi:Huyết khối tĩnh mạch sâu]]
[[zh:深静脉血栓]]

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Greek: Ά ά Έ έ Ή ή Ί ί Ό ό Ύ ύ Ώ ώ Α α Β β Γ γ Δ δ Ε ε Ζ ζ Η η Θ θ Ι ι Κ κ Λ λ Μ μ Ν ν Ξ ξ Ο ο Π π Ρ ρ Σ σ ς Τ τ Υ υ Φ φ Χ χ Ψ ψ Ω ω {{Polytonic|}}
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deep vein thrombosis: Sitelink, Statement: P1395, Statement: P1461, Title, Statement: P5806, Description: en

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