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Deep vein thrombosis: be aware if taking a long haul flight ...
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Deep vein thrombosis ( DVT ), is the formation of blood clots in deep veins, most commonly in the limbs. Symptoms may include pain, swelling, redness, or warmth of the affected area. About half of cases have no symptoms. Complications may include pulmonary embolism, as a result of the release of clots moving to the lungs, and post-thrombotic syndrome.

Risk factors include recent surgery, cancer, trauma, immobilization, obesity, smoking, hormonal birth control, pregnancy and the period after birth, antiphospholipid syndrome, and certain genetic conditions. Genetic factors include antithrombin deficiency, protein C, and protein S, and a factor mutation V Leiden. The underlying mechanism usually involves some combination of decreased blood flow rate, increased clumping tendency, and injury to the blood vessel wall.

Individuals suspected of having DVT may be assessed using clinical prediction rules such as Wells score. D-dimer tests may also be used to help exclude the diagnosis or to imply the need for further testing. Diagnosis is most often confirmed by ultrasound of the suspected veins. Together, DVT and pulmonary embolism are known as venous thromboembolism (VTE).

Anticoagulation (blood thinners) is standard treatment. Common drugs include low molecular weight heparin, warfarin, or direct oral anticoagulants. Using compression stockings that pass may reduce the risk of post-thrombotic syndrome. Prevention may include early and frequent walking, calf exercises, aspirin, anticoagulants, stratified compression stockings, or intermittent pneumatic compression. DVT levels rise from childhood to old age; in adulthood, about one in 1,000 adults are affected per year. About 5% of people are affected by VTE at some point in time.

Video Deep vein thrombosis



Signs and symptoms

Common signs and symptoms of DVT include pain or pain, swelling, warmth, redness or discoloration, and surface venous distention, although about half of them with this condition show no symptoms. Signs and symptoms alone are not sensitive enough or specific to make a diagnosis, but when considered along with known risk factors, may help determine the likelihood of DVT. In most suspected cases, DVT is excluded after evaluation, and symptoms are more often caused by other causes, such as cellulitis, Baker's cyst, musculoskeletal injury, or lymphedema. Other differential diagnoses include hematoma, tumor, venous or arterial aneurysm, and connective tissue disorders.

Phlegmasia cerulea dolens is a very large and dangerous type of DVT. It is characterized by an acute and nearly total occlusion of the entire outer extremity, including the iliac and femoral veins. The legs are usually painful, stained with blue, and swollen, which can cause venous gangrene.

Maps Deep vein thrombosis



Cause

Three factors of stasis of Virchow veins, hypercoagulability, and changes in endothelial vessel lining (such as physical damage or endothelial activation) - contribute to DVT and are used to explain its formation. Other related causes include activation of the immune system components, the state of the microparticles in the blood, the concentration of oxygen, and possible platelet activation. Various risk factors contribute to DVT, although many at high risk never develop it.

Risk factors include a strong risk factor from older age, which changes the blood composition to support clotting. Other risk factors that are acquired include major surgery and trauma, both of which can increase the risk due to tissue factors from outside the vascular system entering the blood. In orthopedic surgery, venous stasis can be provoked temporarily by the cessation of blood flow as part of the procedure. Cancer can grow in and around the veins, causing venous stasis, and can also stimulate increased levels of tissue factor. Pregnancy causes blood to prefer blood clotting, and in the postpartum, the release of the placenta releases a substance that benefits clotting. Oral contraceptives and hormone replacement therapy increase the risk through a variety of mechanisms, including changes in blood clotting protein levels and reduced fibrinolysis.

The vein of thromboembolism (VTE) disease includes the development of either DVT or pulmonary embolism (PE). Genetic factors that increase the risk of VTE include a deficiency of three proteins that normally prevent blood from clotting - C protein, S protein, and antithrombin - other than the non-O blood group and mutations in factor V and prothrombin genes. Deficiencies in antithrombin, protein C, and S protein are rare but strong, or strong enough, risk factors. Thrombophilia increases the risk of VTE by about 10 times. Factor V Leiden, which makes factor V resistant to inactivation by activated protein C, and the genetic variant prothrombin G20210A, which causes an increase in prothrombin levels, largely expressed in Caucasian race. They simply increase the risk of VTE, three to eight times for factor V Leiden and two to three times for prothrombin G20210A. Having a non-O blood type roughly doubles the risk of VTE. Non-O blood type is common in all races, making it an important risk factor. Individuals without blood type O have higher levels of von Willebrand and factor VIII compared with blood type O, thus increasing the chances of blood clotting.

Several risk factors affect the location of DVT in the body. In isolated distal DVT, the risk factor profile looks different from the proximal DVT. Temporary factors, such as surgery and immobilization, appear to dominate, while thrombophilias and age do not appear to increase the risk. In upper limb DVTs, the most important risk factors are having central venous catheter, and chest outlet syndrome also increases risk.

Risk factors


Deep Vein Thrombosis DVT : Causes, Diagnosis, Symptoms, Treatment ...
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Pathophysiology

DVT often develops in the calf veins and "grows" toward the venous flow, towards the heart. When DVT does not grow, it can be cleaned naturally and dissolves into the blood (fibrinolysis). Veins in the calf or thigh are most commonly affected, including femoral vein, popliteal veins, and iliofemoral veins (as with May-Thurner syndrome). Extensive lower extremity DVT may reach the pelvic iliac vein or inferior cava vena. Sometimes the artery veins are affected, such as after central venous catheter placement and with a rare Paget-Schrötter disease.

The mechanisms behind arterial thrombosis, as with heart attacks, are more established than the steps that cause venous thrombosis. With arterial thrombosis, damage to blood vessel walls is necessary, as it initiates coagulation, but clots in the blood vessels mostly occur without such damage. The onset of venous thrombosis is thought to be caused by tissue factors, leading to the conversion of prothrombin to thrombin, followed by fibrin deposition. Red blood cells and fibrin are the main components of venous thrombus, and fibrin appears to be attached to the blood vessel wall (endothelium), a surface that usually acts to prevent clotting. Platelets and white blood cells are also components. Platelets are not so prominent in a vein because they are in the arteries, but they may play a role. Inflammation is associated with VTE, and white blood cells play a role in the formation and resolution of venous clots.

Often, DVT begins in the venous valves. The pattern of blood flow in the valve can cause low oxygen concentration in the blood (hypoxemia) of the sinus valve. Hypoxemia, exacerbated by venous stasis, activates pathways that include induced hypoxia-1 factors and early growth response proteins 1. Hypoxemia also produces the production of reactive oxygen species, which can activate this pathway, as well as nuclear factor-? B, which regulates hypoxia-inducible hypoxia-factor transcription. Hypoxia-inducible factor-1 and the initial growth-response protein 1 contribute to the monocyte association with endothelial proteins, such as P-selectin, inducing monocytes to release microvesicles filled by tissue factors, which may begin to clot after binding to the endothelial surface.

Deep venous thrombosis occurs in the upper extremity of about 4-10% of cases, generally in people with underlying serious illness, especially cancer.

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Diagnosis

DVT diagnosis requires the use of imaging devices such as ultrasound. Clinical assessments, which predict the likelihood of DVT, may help determine if a D-dimer test is useful. In those without DVT, normal D-dimer results may rule out the diagnosis.

Classification

Increased DVT occurs with regard to risk factors, such as surgery, oral contraceptives, trauma, immobility, obesity, or cancer; cases without the conditions obtained are called unwarranted or idiopathic. Acute DVT is characterized by pain and swelling and is usually occlusive, which means that it blocks blood flow, whereas non-occlusive DVTs are less symptomatic. The "chronic" label has been applied to symptomatic DVTs lasting longer than 10 to 14 days. DVTs that have no symptoms, but are only found by screening, labeled asymptomatic or incidental.

DVT in the legs is proximal (or iliofemoral) when above the knee and distal (or calf) when below the knee. DVT under the popliteal veins, the proximal veins behind the knee, are classified as distal and have limited clinical significance compared to the proximal DVT. Early episodes of DVT are called incidents and each subsequent DVT is called repeated. Bilateral DVT refers to freezing on both legs, while unilaterally means only one leg is affected.

Probability

In those suspected of DVT, clinical judgment may be useful for determining the tests to be performed. The most widely studied clinical prediction rule is the Wells score.

Wells score/criteria : (possible score -2 through 9)

  1. Active cancer (treatment within last 6 months or palliative): 1 point
  2. Swelling of the calf> = 3Ã, cm compared to asymptomatic calves (measured 10 cm below tibial tuberosity): point 1
  3. Unilateral superficial vein swelling (non-varicose veins, on the symptomatic leg): 1 point
  4. Unilateral pitting edema (at the symptomatic foot): 1 point
  5. The previously documented DVT: Point 1
  6. Whole-foot swelling: Point 1
  7. Localized softness along the deep vein system: point 1
  8. Paralysis, paresis, or immobilization of the last cast on the lower extremity: point 1
  9. Recently bedridden> = 3 days, or major surgery requiring regional or general anesthesia in the last 12 weeks: 1 point
  10. Alternative diagnosis is at least possible: -2 points

Those who had a Wells score of two or more had a 28% chance of having DVTs, those with a lower score were 6% more likely. Or, the Wells score can be categorized as high if greater than two, moderate if one or two, and low if less than one, with possibilities of 53%, 17%, and 5%, respectively.

D-dimer

D-dimers are the product of fibrin degradation, and an increased rate can be produced from plasmin dissolving clots - or other conditions. Inpatient patients often experience improvement for several reasons. When individuals are at high probability of having DVTs, diagnostic imaging is preferred over the D-dimer test. For those with low or moderate DVT probabilities, a D-dimer level may be obtained, which excludes a diagnosis if the results are normal. A higher level requires further investigation with diagnostic imaging to confirm or exclude the diagnosis.

For an alleged first-foot DVT in low probability situations, the American College of Chest Physicians recommend testing D-dimer levels with moderate or high sensitivity or ultrasound compression of the proximal veins. These options are recommended through whole-leg ultrasound, and D-dimer testing is an overall recommended preference. The UK National Institute for Health and Nursing Excellence (NICE) recommends testing D-dimers before proximal venous ultrasound.

For an alleged first-foot DVT in medium-probability scenarios, high-sensitivity D-dimers are recommended as recommended options through ultrasound imaging, with both legs intact and ultrasound compression possible. The NICE guidance uses the two-point Wells score and does not refer to moderate probability groups.

Imaging

Venous imaging tests are used in the diagnosis of DVT, most often also proximal ultrasound or ultrasound ultrasound. Each technique has its disadvantages: a single proximal scan can lose a distal DVT, while scanning the entire foot can cause distal DVT overtreatment. Doppler ultrasound, CT scan venography, MRI venography, or MRI thrombus are also likely.

Ultrasound for alleged deep vein thrombosis has a 97% sensitivity in detecting DVT in the proximal leg.

The gold standard for assessing imaging methods is venographic contrast, which involves injecting peripheral veins from affected limbs with contrast agents and taking X-rays, to reveal whether the venous supply has been blocked. Because of its cost, invasive, availability, and other limitations, these tests are rarely performed. In one study, he found DVT in an additional 20% of patients with pulmonary embolism in which ultrasound was negative.

Previous fibrinogen retrieval tests are used to detect deep vein thrombosis. << >> moved to the history section? ]

Do You Know The Signs Of Deep Vein Thrombosis? | Cascade In-Home Care
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Prevention

Depending on the risk for DVT, different precautions are recommended. Walking and calf exercises reduce vein stasis because leg muscle contractions suppress the veins and pump blood to the heart. In immobile individuals, the method of physical compression increases blood flow. Anticoagulation, which increases the risk of bleeding, may be used in high-risk scenarios. The risk of major haemorrhage with long-term anticoagulation is about 3% per year, and the point at which the annual VTE risk is estimated to require anticoagulation long term is estimated at between 3 and 9%. Usually, only when an individual exceeds 9% of annual VTE risk, long-term anticoagulation is a common consideration. Antithrombin deficiency, a strong or moderately strong risk factor, carries a VTE annual risk of only 0.8-1.5%; thus, asymptomatic individuals with thrombophilia do not guarantee long-term anticoagulants.

Aside from anticoagulants, aspirin antiplatelet drugs may be used in some people after orthopedic surgery and in those with previous VTE. Statins can lower the risk for healthy people, but the evidence is unclear. After the completion of long-term aspirin warfarin is useful to prevent re-occurrence.

Hospital

In 2011, the American College of Physicians (ACP) issued a clinical practice guide that made three strong recommendations based on moderate quality evidence: that hospitalized patients were assessed for the risk of thromboembolism and bleeding before prophylaxis began; that heparin or related drugs are used if potential benefits are considered greater than potential hazards; and that compression stockings are not used. ACP also draws attention to the lack of support for performance measures that encourage doctors to apply universal prophylaxis without regard to the risks.

The 2014 Cochrane Review found that the use of heparin in medical patients did not alter the risk of death or pulmonary embolism. While its use lowers people's risk of DVT, it also increases the risk of people from major bleeding. As such, this review recommends the need to balance risks and benefits.

The ACCP 2012 guidelines for nonsurgical patients recommend anticoagulation for patients with acute pain in cases of increased risk when there is no bleeding or high risk of bleeding. Mechanical prophylaxis is recommended when the risk for bleeding and thrombosis is increased. For critical, pharmacological or mechanical prophylaxis is recommended depending on the risks. Heparin is advised in outpatients with cancers that have solid tumors and additional risk factors for VTE - listed as "previous venous thrombosis, immobilization, hormonal therapy, angiogenesis inhibitors, thalidomide, and lenalidomide" - and low risk of bleeding.

After operation

Primary orthopedic surgery - total hip replacement, total knee replacement, or hip fracture surgery - has a high risk of causing VTE. If prophylaxis is not used after this surgery, symptomatic VTE has about 4% chance of developing in 35 days. Options for the prevention of VTE in people following non-orthopedic surgery include early walking, mechanical prophylaxis (intermittent pneumatic compression or stratified compression stockings), and drugs (low molecular weight heparin and low-density heparin) depending on the risk of VTE , the risk of major bleeding, and one's preference. After major orthopedic surgery, ACCP recommends treatment with drugs that reduce the risk of clotting (such as fondaparinux and aspirin) with low molecular weight heparin (LMWH) is recommended as a preference. Intermittent pneumatic compression is also an option. Compression stockings pass effectively after general and orthopedic surgery.

Pregnancy

VTE risk increases in pregnancies about five times due to a more hypercoagulation state, the possibility of adaptation to fatal postpartum hemorrhage. In addition, pregnant women with genetic risk factors are subjected to about three to 30 times the increased risk for VTE. Preventive treatment for VTE-related pregnancies in hypercoagulation women is recommended by ACCP. Homozygous factor V Leiden carriers or G20210A prothrombin with a family history of VTE are recommended for LMWH antepartum and either LMWH or vitamin K (VKA) antagonists for six weeks after delivery. Those with other thrombofilia and family history but none of the previous VTEs are advised to wait wary during pregnancy and LMWH or - for those who lack C or S - VKA protein deficiency. The homozygous carrier of V Leiden factor or G20210A prothrombin without a personal or family history of VTE is advised to wait wary during pregnancy and LMWH or VKA for six weeks after labor. Those with other thrombofilia but no family or personal history of VTE suggested to wait just wait. Warfarin, a common VKA, can cause fetal damage and is not used for VTE prevention during pregnancy.

Travelers

The ACCP 2012 guidelines offer weak recommendations. For long-distance travel at risk - those who have "previous VTE, surgery or recent trauma, active malignancy, pregnancy, estrogen use, old age, limited mobility, severe obesity, or known thrombophilic disorders" - suggestions including calf exercises , frequent walks, and aisle seating on airplanes to make it easy to walk. The use of a stratified compression stocking that fits below the knee and gives 15-30 mm Hg pressure to the ankle is advised, while aspirin or anticoagulant is not. Compression stockings have sharply reduced the rate of asymptomatic DVTs on passenger aircraft, but the effect on VTE symptoms is unknown, as no individual studied developed VTE symptoms.

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Treatment

Anticoagulation

Anticoagulation, which prevents further coagulation, but does not act directly on existing clots, is the standard treatment for DVT. Balancing risk vs. important benefits in determining anticoagulation duration, and three months is usually the standard length of care. In those with an annual risk of VTE over 9%, because after an unintentional episode, extended anticoagulation is a possibility. Those who completed VKA treatment after idiopathic VTE with high D-dimer levels showed an increased risk of recurrent VTE (about 9% vs about 4% for normal results), and these results may be used in clinical decision-making. Thrombophilia test results rarely play a role in the duration of treatment.

For acute cases of the legs, ACCP recommends parenteral anticoagulants (such as LMWH, fondaparinux, or unfractionated heparin) for at least five days and VKA, oral anticoagulants, on the same day. LMWH and fondaparinux are recommended over unfractionated heparin, but both are maintained in those with impaired renal function, unlike unfractionated heparin. VKA is generally taken for a minimum of three months to maintain an international normalization ratio of 2.0-3.0, with 2.5 being the target. The benefits of taking VKA decreases with length of treatment, and the risk of bleeding increases with age.

ACCP recommends treatment for three months on those with proximal DVT triggered by surgery. A three-month course is also recommended for those with proximal DVT provoked by temporary risk factors, and three months are recommended during extended treatment when the risk of hemorrhage is low to moderate. Unprovoked DVT patients should have at least three months of anticoagulation and be considered for extended treatment. Those whose first VTE is a proximal DVT that is not recommended is recommended for anticoagulation more than three months unless there is a high risk of bleeding. In this case, three months is enough. Those with a second unproven VTE are recommended for extended treatment when the risk of low bleeding, is recommended for extended treatment when the risk of moderate bleeding, and is recommended for three months of anticoagulation in high-risk scenarios.

Stockings, runs and re-imagery

ACCP recommends home care at home rather than hospitalization for those with acute foot DVT. This is true as long as the individual feels ready for it, and those with severe foot symptoms or comorbidities will not qualify. An appropriate home environment is needed: a home that can provide a quick return to the hospital if necessary, support from family or friends, and telephone access.

In addition to anticoagulation, ACCP recommends stratified compression stockings - which apply higher pressure (30-40 mm Hg) in the ankle and lower pressure around the knee - for those with symptomatic DVT. Use should start as soon as possible after anticoagulation. However, the evidence does not support that this stocking reduces the risk of post-chrombotic syndrome nor does it show a recurrent VTE decline. Use is recommended for two years, although discomfort and discomfort may reduce compliance. Walking is also recommended for those who do not suffer from severe pain or edema.

Unless a person has a medical problem that impedes movement, once a person has started anti-coagulation therapy, bed rest should not be used to treat acute venous thrombosis. There are clinical benefits associated with walking and there is no evidence that walking is dangerous, but people with DVT are disadvantaged by bed rest unless medically necessary.

Instead of anticoagulation, advanced imaging tests (usually ultrasound) about a week post-diagnosis are the choice for those with acute isolated acute DVT without high risk for extension; if the clot does not grow, ACCP does not recommend anticoagulation. This technique can be beneficial for those at high risk of bleeding. Patients may choose anticoagulation through serial imaging, however, to avoid the inconvenience of other scans if the concern about the risk of bleeding is not significant. When applied to symptomatic patients with initial negative ultrasound results, serial testing is inefficient and ineffective.

IVC filter, thrombolysis, and thrombectomy

Inferior vena cava filters (IVC filters) are used on the assumption that they reduce PE, although their effectiveness and safety profiles are not well established. In general, they are only recommended in some high-risk scenarios. ACCP recommends them to those who have contraindications to anticoagulant treatment but not in addition to anticoagulation, except for an individual with IVC filters but without the risk of bleeding developing acute proximal DVT. In this case, both anticoagulation and IVC filters are recommended. NICE recommends a kava filter in settings where a person with acute proximal DVT or PE can not receive anticoagulants, and that the filter is removed when anticoagulation can be started safely. While IVC filters themselves are associated with long-term risk of DVT, they are not reason enough to maintain an extended anticoagulant.

Thrombolysis is the administration of an enzyme (intravenously or directly into the affected vein via a catheter), which serves to break down enzymatic clots. This can reduce the risk of post-chromatosis syndrome to one-third, and may reduce the risk of foot ulcers, but is associated with an increased risk of bleeding. The current ACCP suggests anticoagulants rather than thrombolysis, but patients may choose thrombolysis if the prevention of post-thrombotic syndrome outweighs concerns over the complexity, risk of bleeding, and cost of procedures. NICE recommends that thrombolysis be considered in those who have symptoms less than two weeks, usually well, have a good life expectancy and a low risk of bleeding.

A mechanical thrombectomy device can eliminate venous clots, although ACCP considers it an option only when the following conditions apply: "iliofemoral DVT, symptoms for <7 days (criteria used in a single randomized trial), good functional status, life expectancy> = 1 year, and both resources and expertise are available. "Anticoagulation alone is recommended rather than thrombectomy.

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Prognosis

The most frequent complication of proximal DVT is postchrombotic syndrome, which is caused by reduced venous blood flow to the heart. Some of the symptoms of post-chrombosis syndrome are pain, edema, paresthesias, and in severe cases, foot ulcers. It is estimated that 20-50% of those with DVT will develop it, and 5-10% will develop a severe form. PE is the most serious complication of proximal DVT, and the risk of PE is higher when clots appear in the thighs and pelvis. Distal DVT alone is almost never associated with post-thrombosis or PE syndrome. Untreated untreated limb dTT has a PE 3% mortality rate, whereas DVT-related deaths of the upper extremities are very rare. The presence of residual thrombus after DVT often occurs in a small proportion of people, and increases the risk of recurrence, albeit at a lower rate than high D-dimers. Within 10 years after DVT, about one-third of individuals will have recurrent episodes.

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Epidemiology

About 1 in 1,000 adults per year have DVT, but in 2011, the available data was dominated by North American and European populations. VTE is rare in children, with an incidence of about 1 in 100,000 per year. From childhood to old age, incidence increased by a factor of about 1000, with nearly 1% of parents experiencing VTE each year. During pregnancy and after childbirth, acute VTE occurs about once per 1000 births. After surgery with preventive care, VTE develops in about 10 out of 1000 people after total or partial knee replacement, and in about 5 out of 1000 after total or partial hip replacement. About 300,000-600,000 Americans develop VTE every year, with about 60,000-100,000 deaths caused by PE. In the UK, an estimated 25,000 a year die from hospital-linked VTE. For reasons that are not clear, people of Asian descent have a lower risk of VTE than whites.

In North American and European populations, about 4-8% of people have thrombophilia, most commonly V factor leiden and prothrombin G20210A. For populations in China, Japan, and Thailand, protein deficiency S, protein C, and antithrombin predominate. The non-O blood type is present in about 50% of the general population and varies with ethnicity, and is present in about 70% of those with VTE. Overall, global data is incomplete.

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History

The earliest DVT case was described by Sushruta in his book Sushruta Samhita around 600-900 BC. Other documented cases are expected to occur in the 13th century, at the foot of a 20-year-old man. At some point, the increased incidence of DVT in women after childbirth is known, and by the late 1700s, public health recommendations were issued to encourage women to breastfeed as a means of preventing this phenomenon; DVT is called "milk leg", as it is thought to result from milk formation in the legs.

In 1856, German physician and pathologist Rudolf Virchow published what he called the Virchow triad, the three main causes of thrombosis. The triad provides a theoretical framework for explanation of current venous thrombosis, although it is focused on foreign body effects in the venous system and the conditions necessary for clot propagation.

Several pharmacological treatments for DVT were introduced in the 20th century: oral anticoagulants in 1940, LDUH subcutaneously in 1962 and subcutaneous LMWH in 1982. Diagnosis was generally done by impedance pletismography in the 1970s and 1980s, but the use of ultrasound techniques Doppler, with their increased sensitivity and specificity, largely supersedes this method.

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Economy

The initial DVT cost for the average US hospitalized patient is about $ 7,700- $ 10,800. The follow-up costs of VTE at three months, six months, and one year are about $ 5,000, $ 10,000, and $ 33,000 respectively; in Europe, the number three and six months around EUR1.800 and EUR3,200. Post-thrombotic syndrome is a significant contributor to DVT follow-up costs. The annual DVT charge in the US is about $ 5 billion or more than $ 8 billion, and the average annual cost per treated individual is estimated at about $ 20,000. For example, if 300,000 symptomatic DVT patients were treated at an average cost of $ 20,000 each year, it would cost $ 6 billion annually.

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Direction of research

In 2011, three large randomized controlled trials - the Norwegian CaVent trial, the North American ATTRAK trial, and the Dutch CAVA trial - were studying the effectiveness and safety of catheter-directed thrombolysis. In 2012, two studies found clinical benefit in taking aspirin to prevent recurrent VTE.

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Note




References

The cited library



External links


  • Cochrane Peripheral Vascular Diseases Review Group
  • Clinical prediction site - Wells score for deep vein thrombosis

Source of the article : Wikipedia

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