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==Research directions==
==Research directions==


As of 2011, three large randomized controlled trials—the Norwegian CaVent trial, the North American ATTRACT trial, and the Dutch CAVA trial—were studying the effectiveness and safety of catheter directed thrombolysis.<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> In 2012, further data on the potential for aspirin to prevent recurrent VTE are expected.<ref name="Becker">{{cite journal| author=Becker RC| title=Aspirin and the prevention of venous thromboembolism | journal=N Engl J Med | year= 2012 | volume= 366 | issue= 21 | pages= 2028–30 | pmid=22621631 | doi=10.1056/NEJMe1201911}}</ref> A 2012 study demonstrated a reduction in recurrent VTE with aspirin use.<ref name="Becattini">{{cite journal| author=Becattini C, Agnelli G, Schenone A, ''et al''.| title=Aspirin for preventing the recurrence of venous thromboembolism | journal=N Engl J Med | year= 2012 | volume= 366 | issue= 21 | pages= 1959–67 | pmid=22621626 | doi=10.1056/NEJMoa1114238}}</ref>
As of 2011, three large randomized controlled trials—the Norwegian CaVent trial, the North American ATTRACT trial, and the Dutch CAVA trial—were studying the effectiveness and safety of catheter directed thrombolysis.<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> In 2012, two studies found a clinical benefit with taking aspirin to prevent recurrent VTE.<ref name="Becattini">{{cite journal| author=Becattini C, Agnelli G, Schenone A, ''et al''.| title=Aspirin for preventing the recurrence of venous thromboembolism | journal=N Engl J Med | year= 2012 | volume= 366 | issue= 21 | pages= 1959–67 | pmid=22621626 | doi=10.1056/NEJMoa1114238}}</ref><ref name="Brighton">{{cite journal| author=Brighton TA, Eikelboom JW, Mann K, ''et al''.| title=Low-dose aspirin for preventing recurrent venous thromboembolism | journal=N Engl J Med | year= 2012 | volume= | issue= | pages= | pmid= | doi=10.1056/NEJMoa1210384}}</ref>


==List of deaths==<!--This list is for the deaths of people that meet Wikipedia's notability guideline (the person or the death) or people whose deaths have been covered in detail by reliable sources for public health awareness reasons.-->
==List of deaths==<!--This list is for the deaths of people that meet Wikipedia's notability guideline (the person or the death) or people whose deaths have been covered in detail by reliable sources for public health awareness reasons.-->

Revision as of 22:41, 10 November 2012

"DVT" redirects here. For other uses, see DVT (disambiguation).

Deep vein thrombosis
SpecialtyCardiology Edit this on Wikidata

Deep vein thrombosis or deep venous thrombosis (DVT) is a blood clot in a deep vein.[note 1] A clot inside a blood vessel is called a thrombosis. DVT predominantly occurs in the legs. When symptoms are present, non-specific signs may include pain, swelling, redness, warmness, and engorged superficial veins. A potentially life-threatening complication is pulmonary embolism, caused by detachment (embolization) of a thrombosis which then travels to the lungs. Together, DVT and pulmonary embolism can be seen as a single disease process known as venous thromboembolism. Another complication is post-thrombotic syndrome, a significant contributor to health care costs. About 1 in 1000 adults develop DVT annually, and incidence increases with age.

In 1856, German pathologist Rudolph Virchow postulated the interplay of three processes resulting in venous thrombosis, now known as Virchow's triad: a decreased blood flow rate (venous stasis), increased tendency to clot (hypercoagulability), and changes to the blood vessel wall. DVT formation typically begins inside the valves of the calf veins, where the blood is relatively oxygen-deprived, activating certain biochemical pathways. Several medical conditions increase the risk for DVT, such as cancer, trauma, and antiphospholipid syndrome. Other risk factors include older age, surgery, immobilization (as with bed-rest, orthopedic casts, and sitting on long flights), oral contraceptives, pregnancy, the postnatal period, and genetic factors such as a non-O blood type.

Individuals suspected of having DVT may be assessed using a clinical prediction rule, such as the Wells score, to estimate the likelihood of disease. A D-dimer test may also be used to assist with excluding the diagnosis (because of its high sensitivity) or to signal a need for further testing. Diagnosis is most commonly done with ultrasound of the affected veins. Anticoagulation is the standard treatment; typical medications are a low-molecular-weight heparin and a vitamin K antagonist. Wearing graduated compression stockings appears to reduce the risk of post-thrombotic syndrome. Prevention options for at-risk individuals include early and frequent walking, calf exercises, anticoagulants, aspirin, graduated compression stockings, and intermittent pneumatic compression.

Signs and symptoms

Approximately half of people with DVT are asymptomatic. When present, common symptoms include unexplained pain or tenderness, swelling, warmth, redness or discoloration, and distention of surface veins.[1] However, signs and symptoms are neither sufficiently sensitive nor specific to make a diagnosis. When taken together with known risk factors, they are useful in determining the likelihood of DVT,[2] but most of those initially suspected are found not to have it after evaluation[3] and most symptomatic individuals have an alternative explanation, such as cellulitis, Baker's cyst, musculoskeletal injury, and lymphedema.[4]

A severe and uncommon form of DVT, phlegmasia cerulea dolens, tends to develop in association with a life-threatening illness. 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, cyanosed (blue from lack of oxygen), and edematous (filled with fluid). Venous gangrene may develop as a result.[5][6]

Causes

The coagulation system, often described as a "cascade", consists of a group of proteins that interact to form a blood clot. DVT risk is increased by abnormalities in the cascade. The regulators, antithrombin (ᾳTHR) and activated protein C (APC) are shown in green above the blood's clotting factors they affect.

Venous thrombosis is mainly caused by a combination of venous stasis and hypercoagulability, and to a lesser extent changes in the blood vessel wall (endothelium), such as physical damage or endothelial activation.[7] These three factors represent Virchow's triad of which changes to the vessel wall are the least understood.[8] Various risk factors increase the likelihood of developing a DVT. However, some with DVT have no risk factors present, and many with multiple risk factors never have one.[9]

Acquired risk factors include the strong risk factor of older age,[8][9] which alters blood composition to favor clotting. Other important acquired risk factors include major surgery and trauma, both of which may increase the risk because of tissue factor from outside the vascular system mixing with blood.[7] In orthopedic surgery, venous stasis may be temporarily provoked by a cessation of blood flow as part of the procedure.[10] Cancer can grow in and around veins, causing venous stasis, and it can also stimulate increased levels of tissue factor. Pregnancy causes blood to favor clotting, and in the postpartum, placental tearing releases substances that favor clotting. Oral contraceptives and hormonal replacement therapy increase the risk through a variety of mechanisms, including altered blood coagulation protein levels and reduced fibrinolysis.[10]

Genetic factors that increase the risk of venous thromboembolism (VTE) include deficiencies of three proteins that normally prevent blood from clotting—protein C, protein S, and antithrombin—in addition to non-O blood type and mutations in the factor V and prothrombin genes. Deficiencies in antithrombin, protein C, and S are rare but strong, or moderately strong, risk factors.[7][10] These three causes of thrombophilia[note 2] are present in about 0.02%, 0.2%, and 0.03% to 0.13% of people, respectively.[11] They increase the risk of VTE by about 10 times.[12] Factor V Leiden, which makes factor V resistant to inactivation by activated protein C,[13] and the genetic variant prothrombin G20210A, which causes increased prothrombin levels, are present in about 3 to 5% and 1 to 3% of people, respectively.[12] Both are predominantly expressed in Caucasians.[7] They moderately increase risk for VTE, by three to eight times for factor V Leiden and two to three times for prothrombin G20210A.[12][14] Having a non-O blood type approximately doubles VTE risk.[10] Non-O blood types are present in all races and common, thus making non-O blood type an important risk factor.[15] Individuals without O-blood type have higher blood levels of von Willebrand factor and factor VIII than those with O-blood type, increasing the likelihood of clotting.[15]

Some risk factors influence the location of where DVT occurs within the body. 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.[16] In upper extremity DVT, the most important risk factor is having a central venous catheter and thoracic outlet syndrome also increases risk.[17]

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The incision for a completed knee replacement surgery, a procedure that can cause DVT.

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Pathophysiology

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.

DVT usually develops first in the calf veins, and when it extends, it "grows" in the direction of venous flow, towards the heart.[26] When DVT does not grow, it can be cleared naturally and dissolved into the blood (fibrinolysis).[27] DVT most commonly affects the leg veins of the thigh or lower leg[28] such as the femoral vein, the popliteal vein, or the iliofemoral vein (as with May–Thurner syndrome). Extensive lower extremity DVT can reach into the iliac vein of the pelvis or the inferior vena cava.[29] Occasionally the veins of the arm are affected, as after central venous catheter placement and with the rare Paget–Schrötter disease.[21]

The mechanism behind arterial thrombosis, as with heart attacks, is more established than the steps that cause venous thrombosis.[30] With arterial thrombosis, blood vessel wall damage is required for thrombosis formation, as it initiates coagulation,[30] but clotting in the veins mostly occurs without any blood vessel damage.[7] The beginning of a venous thrombosis is thought to be caused by tissue factor, which leads to conversion of prothrombin to thrombin, followed by fibrin deposition.[8] Red blood cells and fibrin are the main components of venous thrombi,[7] and the fibrin appears to attach to the blood vessel wall lining (endothelium), a surface that normally acts to prevent clotting.[30] Platelets and white blood cells are also components. Platelets are not as prominent in venous clots when compared to arterial ones, but they may play a mechanistic role.[10] Inflammation and white blood cells play a key role in both the formation and resolution of venous clots.[27]

Often, DVT begins in the valves of veins.[27] The blood flow pattern in vein valves can cause low oxygen concentrations (hypoxia) in the blood of a valve sinus. Hypoxia (which is worsened by venous stasis) activates certain pathways—hypoxia-inducible factor-1 (HIF-1) and early growth response 1 (EGR-1)—that contribute to monocyte and endothelial activation. Hypoxia also causes reactive oxygen species production that can activate these two pathways, in addition to nuclear factor-κB, which regulates HIF-1 transcription.[8] 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 begin clotting after binding the endothelial surface.[8]

Diagnosis

Swelling in the leg from fluid (edema) can result in "pitting" after pressure is applied. (This person did not have DVT.)
An ultrasound image demonstrating a blood clot in the left common femoral vein.
An abdominal CT scan showing a common iliac vein thrombosis. The arrow indicates the filling defect in the vein visualized using radiocontrast.
Venograms of DVT

DVT diagnosis requires using imaging devices such as ultrasound. Clinical assessments, which predict DVT likelihood, can help determine if a D-dimer test is useful. In those not highly likely to have DVT, a normal D-dimer test[note 5] can rule out a diagnosis.

Classification

The disease term venous thromboembolism (VTE) includes both DVT and pulmonary embolism (PE).[17][32] DVT in the legs is called proximal (or iliofemoral)[33] when above the knee and distal (or calf) when below the knee.[34][35] DVT below the popliteal vein, a proximal vein behind the knee, is in distal calf veins.[2] Distal DVT has limited clinical significance compared to proximal DVT.[36] An initial episode of DVT is called incident and any subsequent DVT is termed recurrent.[37][38] Bilateral DVT refers to clots in both legs while unilateral means only a single leg is affected.[39]

DVT that has no symptoms, but is only found by screening, is labeled asymptomatic.[40] Acute DVT is characterized by pain and swelling[41] and is usually occlusive,[2] which means they obstruct blood flow, whereas nonocclusive DVT is less symptomatic.[5] The label of chronic has been applied to symptomatic DVT that persists longer than 10 or 14 days.[42] A DVT might also be called idiopathic when it "occurs in the absence of a known precipitating factor, such as oral contraceptives, surgery, trauma, or cancer."[43]

Probability

In those with suspected DVT, a clinical assessment of probability can be useful to determine which tests to perform.[44] The most studied clinical prediction rule is the Wells score.[3]

Wells score or criteria: (possible score −2 to 9)

  1. Active cancer (treatment within last 6 months or palliative): +1 point
  2. Calf swelling ≥ 3 cm compared to asymptomatic calf (measured 10 cm below tibial tuberosity): +1 point
  3. Swollen unilateral superficial veins (non-varicose, in symptomatic leg): +1 point
  4. Unilateral pitting edema (in symptomatic leg): +1 point
  5. Previous documented DVT: +1 point
  6. Swelling of entire leg: +1 point
  7. Localized tenderness along the deep venous system: +1 point
  8. Paralysis, paresis, or recent cast immobilization of lower extremities: +1 point
  9. Recently bedridden ≥ 3 days, or major surgery requiring regional or general anesthetic in the past 12 weeks: +1 point
  10. Alternative diagnosis at least as likely: −2 points[4]

A Wells score can be divided into two (likely vs. unlikely) or three (low, moderate, or high probability) groups. With two groups, a score of two or above is categorized as likely, while one and below means unlikely. If divided into three groups, a score of one and two are of moderate probability, while scores below or above are low and high probability, respectively.[4] When a score is segregated into two groups, DVT prevalence is about 6% or 28%. When divided into three groups, the value is estimated at 5%, 17%, or 53%.[3]

D-dimer

In high-probability cases a D-dimer is not recommended; instead, diagnostic imaging should begin.[45] For those with a low- or moderate-probability of DVT, a D-dimer level might be obtained because a negative level excludes the possibility of a diagnosis. D-dimers are a fibrin degradation product, and an elevated level can result from the sensitive detection of a thrombosis being dissolved by plasmin—or other conditions.[31] Hospitalized patients often have elevated levels for multiple reasons.[3][46]

For a suspected first leg DVT in a low-probability situation, testing D-dimer levels with either moderate or high sensitivity is suggested by the American College of Chest Physicians (ACCP), though compression ultrasound of the proximal veins is also an option.[47] For a suspected first leg DVT in a moderate-probability scenario, a high-sensitivity D-dimer is suggested over ultrasound imaging.[48] An elevated D-dimer level means diagnostic imaging is necessary. A normal D-dimer result in either suggested scenario makes imaging unnecessary.[47][48]

Imaging

Imaging tests are used to diagnose DVT. Ultrasound of the veins is the most common method, and the two options are proximal compression ultrasound and whole-leg ultrasound. Drawbacks to each method exist. A single proximal scan can miss a distal DVT, while whole-leg scanning can lead to distal DVT overtreatment.[3] Doppler ultrasound,[49] CT scan venography, MRI venography, or MRI of the thrombosis are also possibilities.[3][47]

The 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-rays, to reveal whether the venous supply has been obstructed. Because of its cost, invasiveness, availability, and other limitations this test is rarely performed.[3]

Prevention

The ACCP suggested graduated compression stockings for at-risk travelers and some hospital patients

Depending upon the risk for DVT, different preventative measures are used. Walking and calf exercises are possibilities;[50] both reduce venous stasis because leg muscle contractions compress the veins to pump blood up towards the heart. In immobile individuals, physical compression methods improve blood flow. Evidence suggests aspirin is effective.[51] Anticoagulation, which increases the risk of bleeding, is typical when the benefits are thought to exceed the risks. The annual risk of major bleeding from long-term anticoagulation is about 3%,[12] and the point where annual VTE risk is thought to warrant long-term anticoagulation is estimated to be between 3 to 9%.[52] Usually, only when individuals exceed a 9% annual VTE risk is long-term anticoagulation a common consideration.[52] Antithrombin deficiency, a strong or moderately strong risk factor, carries an annual risk of VTE of only 0.8 to 1.5%;[12] as such, asymptomatic individuals with thrombophilia do not warrant long-term anticoagulation.[53]

In hospital

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.[32][54]

The 2012 ACCP guidelines for non-surgical patients[55][note 6] recommend anticoagulation for the acutely ill in cases of elevated risk when there is no bleeding nor a high risk of bleeding.[56] Mechanical prophylaxis is suggested when risks for both bleeding and thrombosis are elevated.[57] For the critically ill, either pharmacological or mechanical prophylaxis is suggested depending upon the risk.[58] Heparin is suggested in outpatients with cancer who have solid tumors and additional risk factors for VTE—listed as "previous venous thrombosis, immobilization, hormonal therapy, angiogenesis inhibitors, thalidomide, and lenalidomide"—and a low risk of bleeding.[59]

Post surgery

Those who have major orthopedic surgery—total hip replacement, total knee replacement, or hip fracture surgery—are at a high risk of VTE.[60] After any of those surgeries, without prophylaxis, the risk of symptomatic VTE in the 35 days post surgery is estimated to be about 4%.[61] Options for VTE prevention in non-orthopedic surgery patients include early walking, mechanical prophylaxis (intermittent pneumatic compression [IPC] or graduated compression stockings [GCS]), and drugs (low-molecular-weight heparin [LMWH] and low-dose-unfractionated heparin) depending upon the risk of VTE, risk of major bleeding, and patient preferences.[62] In major orthopedic surgery patients, the ACCP recommends treatment with drugs that reduce the risk of clots (such as fondaparinux and aspirin) with LMWH suggested over the others.[61] IPC is also an option.[61][63]

Pregnancy

See also: Hypercoagulability in pregnancy
Warfarin, a common VKA, is suggested only postpartum (after childbirth) in some at-risk women.

The risk of VTE is increased in pregnancy by about five-fold[12][64] because of a more hypercoaguable state, a likely adaptation against fatal postpartum hemorrhage.[19] Additionally, pregnant women with genetic risk factors are subject to an approximate three to thirty times increased risk for VTE.[65] Preventative treatments for pregnancy related VTE in hypercoaguable women were suggested by the ACCP. Homozygous carriers of factor V Leiden or prothrombin G20210A with a family history of VTE were suggested for antepartum LMWH and either LMWH or a vitamin K antagonist (VKA) for the six weeks following childbirth. Those with another thrombophilia and a family history but no previous VTE were suggested for watchful waiting during pregnancy and LMWH or—for those without protein C or S deficiency—a VKA. Homozygous carriers of factor V Leiden or prothrombin G20210A with no personal or family history of VTE were suggested for watchful waiting during pregnancy and LMWH or a VKA for six weeks after childbirth. Those with another thrombophilia but no family or personal history of VTE were suggested for watchful waiting only.[66] Warfarin, a common VKA, can cause harm to the fetus and is not used for VTE prevention during pregnancy.[65][67]

Travelers

The 2012 ACCP guidelines offered weak recommendations. 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"—suggestions included calf exercises, frequent walking, and aisle seating in airplanes to ease walking.[68][69] The use of "properly fitted, below-knee GCS providing 15 to 30 mm Hg of pressure at the ankle during travel" was suggested—aspirin or anticoagulants were not.[70] 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.[71]

Treatment

Anticoagulation

Anticoagulation, which prevents further coagulation but does not act on existing clots, is the standard treatment for DVT.[72] Balancing risk vs. benefit is important in determining the duration of anticoagulation, and three months is typically a standard length of treatment. In those with an annual risk of VTE in excess of 9%, as after an unprovoked episode, extended anticoagulation is a possibility.[52] Those who finish VKA treatment after idiopathic VTE with an elevated D-dimer level show an increased risk of recurrent VTE (about 9% vs. about 4% for normal results), and this result might be used in clinical decision making.[73] Thrombophilia test results rarely play a role in the length of treatment.[74] The evidence used to support anticoagulation comes from studies other than definitive randomized controlled trials that demonstrate efficacy and safety for anticoagulation vs. placebo or using NSAIDs, and a trial of anticoagulation vs. placebo is unlikely to be ethically approved because harm to participants would be expected.[75]

For acute cases in the leg, the ACCP recommended a parenteral anticoagulant (such as LMWH, fondaparinux, or unfractionated heparin) for at least five days and a vitamin K antagonist (VKA), an oral anticoagulant, the same day. The parenteral anticoagulant should be taken until the international normalized ratio (INR) is ≥ 2.0 for 24 hours minimum. If the INR is > 3.0, the parental anticoagulant treatment can stop early.[76][77] LMWH and fondaparinux are suggested over unfractionated heparin, but both are retained in those with compromised kidney function, unlike unfractionated heparin.[77][78] The VKA is generally taken for a minimum of three months[79] to maintain an INR of 2.0 to 3.0, with 2.5 as the target.[80][81] The benefit of taking a VKA declines as the duration of treatment extends,[82] and the risk of bleeding increases with age.[17]

The ACCP recommended treatment for three months in those with proximal DVT provoked by surgery.[83] A three-month course is also recommended for those with proximal DVT provoked by a transient risk factor, and three months is suggested over lengthened treatment when bleeding risk is low to moderate.[84] Unprovoked DVT patients should have at least three months of anticoagulation and be considered for extended treatment.[85] Those whose first VTE is an unprovoked proximal DVT are suggested for anticoagulation longer than three months unless there is a high risk of bleeding.[86] In that case, three months is sufficient.[87] Those with a second unprovoked VTE are recommended for extended treatment when bleeding risk is low, suggested for extended treatment when bleeding risk is moderate,[88] and suggested for three months of anticoagulation in high-risk scenarios.[89]

Home treatment, stockings, and walking

The ACCP recommended initial home treatment for those with acute leg DVT. This applies as long as individuals feel ready for it, and those with severe leg symptoms or comorbidities would not qualify. An appropriate home environment is expected, one that can provide a quick return to the hospital if necessary, support from family or friends, and phone access.[90] In addition to anticoagulation, the ACCP suggested graduated compression stockings (GCSs)—which apply higher pressure (30 to 40 mm Hg) at the ankles and a lower pressure around the knees[77]—for those with symptomatic DVT.[91] Use should begin as soon as possible after anticoagulation.[77] Existing randomized controlled trials give moderate quality evidence that GCSs reduce the risk of post-thrombotic syndrome (PTS).[77][92] An estimate on the number needed to treat suggests about four people need GCS to prevent one PTS case.[93] Trials do not indicate a reduction in recurrent VTE.[77] The suggested duration of use is for two years, though inconvenience and discomfort can reduce compliance.[91] Walking is also suggested over bed rest for those without severe pain or edema.[94]

Inferior vena cava filter

An IVC filter

Inferior vena cava filters (IVC filters) are used on the presumption that they reduce PE, though their effectiveness and safety profile are not well established.[95] In general, they are only recommended in some high-risk scenarios.[95] The ACCP recommended them for those with a contraindication to anticoagulant treatment but not in addition to anticoagulation, unless an individual with an IVC filter but without a risk for bleeding develops acute proximal DVT. In this case, both anticoagulation and an IVC filter is suggested.[96] While IVC filters are associated with a long-term risk of DVT,[95] they are not reason enough to maintain extended anticoagulation.[97]

Serial imaging

Instead of anticoagulation, 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; if the thrombosis does not extend, the ACCP does not recommend anticoagulation.[77][98] This technique can benefit those at a high risk for bleeding. However, patients may choose anticoagulation over serial imaging to avoid the inconvenience of another scan if concerns about the risk of bleeding are not significant.[98] When applied to symptomatic patients with a negative initial ultrasound result, serial testing is inefficient and not cost effective.[2]

Thrombolysis and thrombectomy

Thrombolysis, which acts to break up clots, can be systemic or catheter-directed, but the ACCP suggested anticoagulation instead; however, patients may choose thrombolysis if prevention of PTS outweighs concerns over the complexity, bleeding risk, and cost of the procedure.[99] A mechanical thrombectomy device can remove a thrombosis. Although, the ACCP considers it an option only 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."[77] Anticoagulation alone is suggested over thrombectomy.[100]

Prognosis

The most frequent complication of proximal DVT is post-thrombotic syndrome (PTS),[101] which is caused by a reduction in the return of venous blood to the heart.[18] Some symptoms of PTS are pain, edema, paresthesia, and in severe cases, leg ulcers. An estimated 20 to 50% of those with DVT will develop PTS, and 5 to 10% will develop severe PTS.[101] PE is the most serious complication of proximal DVT, and the risk of PE is higher when clots are present in the thigh and pelvis.[95] Distal DVT itself is hardly if ever associated with PTS or PE.[3] Untreated lower extremity DVT has a 3% PE-related mortality rate, while deaths associated with upper extremity DVT are extremely rare.[20] The presence of a remaining thrombosis after a DVT frequently occurs in a minority of people, and it increases the risk of recurrence, though to a lesser extent than an elevated D-dimer.[18] In the 10 years following a VTE, approximately ⅓ of individuals will have a recurrent episode.[102]

Epidemiology

About 1 in 1000 adults per year have DVT,[103] but only limited data exists outside of North American and European populations.[104] VTE is rare in children, with an incidence of about 1 in 100,000 a year. From childhood to old age, incidence increases by a factor of about 1000, with almost 1% of the elderly experiencing VTE yearly.[105] With pregnancy and postpartum, acute VTE incidence is about 1 per 1000 deliveries.[65] After surgery with preventative treatment, VTE develops in about 10 of 1000 people after total or partial knee replacement, and in about 5 of 1000 after total or partial hip replacement.[106] An estimated 300,000 to 600,000 Americans get a VTE each year, with about 60,000 to 100,000 deaths attributable to PE.[102] In England, about 25,000 per year die from hospital-related VTE.[107] For unclear reasons, people of Asian decent have a lower VTE risk than that of whites.[104]

Around 4 to 8% of people have a thrombophilia of some form, and among people who develop VTE, 30 to 50% have thrombophilia. Prevalence estimates 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.[12] Non-O blood type is present in around 50% of the general population and varies with ethnicity, but it is present in about 70% of those with VTE.[15][108]

Economics

Initial DVT costs for an average hospitalized patient in the U.S. are around $7,700 to $10,800.[109] VTE follow-up costs at three months, six months, and a year are about $5,000, $10,000, and $33,000; in Europe, the three and six-month figures are about €1,800 and €3,200.[110] PTS is a significant contributor to DVT follow-up costs.[109] Annual DVT costs in the U.S. are an estimated $5 billion[111] or in excess of $8 billion,[112][113] and the average annual cost per treated individual is thought to be about $20,000.[112] As an example, if 300,000 symptomatic DVT patients were treated at costs averaging $20,000 annually, that would cost $6 billion a year.

History

Rudolf Virchow

The first documented DVT is thought to have occurred in the 13th century, in the leg of a 20-year-old male.[9] 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.[114]

In 1856, German physician and pathologist Rudolf Virchow published what is referred to as Virchow's triad: the three major causes of thrombosis.[9][114] The triad provides the theoretical framework for how venous thrombosis formation is currently explained.[9] 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.[115]

Multiple pharmacological therapies for DVT were introduced in the 20th century. Oral anticoagulants were introduced in the 1940s, subcutaneous LDUH in 1962, and subcutaneous LMWH in 1982.[116] 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.[117]

Research directions

As of 2011, three large randomized controlled trials—the Norwegian CaVent trial, the North American ATTRACT trial, and the Dutch CAVA trial—were studying the effectiveness and safety of catheter directed thrombolysis.[80] In 2012, two studies found a clinical benefit with taking aspirin to prevent recurrent VTE.[118][119]

List of deaths

  • Chris Staniforth, aged 20, died after DVT/PE thought to be associated with extended sitting (approximately 12 hours) for video game playing.[120]
  • David Bloom, who had factor V Leiden, was a NBC TV journalist that died in Iraq from DVT/PE.[121]
  • Heavy D, who was an obese US rapper, died from DVT/PE.[122]

Notes

  1. ^ Thromboses associated with the abdominal organs (viscera)—such as portal vein thrombosis, renal vein thrombosis, and Budd–Chiari syndrome—are separate diseases excluded from the scope of this definition.
  2. ^ The term thrombophilia as used here applies to the five inherited abnormalities of antithrombin, protein C, protein S, factor V, and prothrombin, as is done elsewhere.[11][12]
  3. ^ Third-generation combined oral contraceptives (COCs) have an approximate two to three times higher risk than second-generation COCs. The use of progesterone-only pills is not assocated with an increased VTE risk.[18]
  4. ^ Factor V Leiden increases the risk of DVT more than it does for PE, a phenomenon referred to as the factor V Leiden paradox.[24]
  5. ^ An elevated level is greater than 250 ng/mL D-dimer units (DDU) or greater than 0.5 μg/mL fibrinogen equivalent units (FEU).[31] A normal level is below these values.
  6. ^ Page e197S of Kahn et al.[55] specifies that the guideline does not apply to those with "trauma and spinal cord injury" nor those "with ischemic and hemorrhagic stroke."

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Cited literature

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