डिप भेन थ्रोम्बोसिस
|यो एउटा अनाथ (एक्लो) पृष्ठको रुपमा रहेको छ, यो पृष्ठ कुनै पनि पृष्ठसित जोडिएको छैन अथवा एक-दुईवटा लेखहरूसँग मात्र जोडिएको हुन सक्छ। कृपया सम्बन्धित लेखहरूलाई; यस पृष्ठसित लिङ्क जोड़्न सहायता गर्नुहोस् उपयोगी जानकारी यहाँ उपलब्ध हुनसक्छ। (जुन २०११)|
|Deep vein thrombosis|
|वर्गीकरण एवं बाह्य साधन|
A deep vein thrombosis in the right leg, note the swelling and redness
Deep vein thrombosis or deep venous thrombosis (DVT) is a blood clot in a deep vein. A clot inside a blood vessel is called a thrombus. DVT predominantly occurs in the legs. When symptoms are present, non-specific signs include pain, swelling, redness, warmness, and engorged superficial veins. The most serious complication is a pulmonary embolism, which may be life-threatening, the result of a thrombus detaching (embolizing) and traveling to the lungs. (DVT and pulmonary embolism are parts of the same disease process called venous thromboembolism.) Another complication is post-thrombotic syndrome, a significant contributor to health care costs. About 1 in 1000 adults develop DVT annually, and aging increases its rate of occurrence.
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, or during long-haul 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; the 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.
- १ Signs and symptoms
- २ Causes
- ३ Pathophysiology
- ४ Diagnosis
- ५ Prevention
- ६ Treatment
- ७ Prognosis
- ८ Epidemiology
- ९ Economics
- १० History
- ११ Research directions
- १२ List of notable individuals
- १३ Notes
- १४ References
- १५ External links
Signs and symptoms[सम्पादन गर्ने]
Approximately half of people with DVT are asymptomatic. When present, common symptoms include pain and tenderness, swelling, warmth, redness or discoloration, and distention of surface veins. However, signs and symptoms are neither sufficiently sensitive nor specific to make a diagnosis. When taken together with the risk factors (see below), they are useful in determining the likelihood of DVT, but most of those initially suspected are found not to have it after evaluation and most symptomatic individuals have another condition, such as cellulitis, Baker's cyst, musculoskeletal injury, and lymphedema.
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.
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. These three factors represent Virchow's triad of which changes to the vessel wall are the least understood. 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.
Acquired risk factors include the strong risk factor of older age, 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. In orthopedic surgery, venous stasis may be temporarily provoked by a cessation of blood flow as part of the procedure. 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.ढाँचा:Which
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. These three causes of thrombophilia[note १] are present in about 0.02%, 0.2%, and 0.03% to 0.13% of people, respectively. They increase 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 increased prothrombin levels, are present in about 3 to 5% and 1 to 3% of people, respectively. Both are predominantly expressed in Caucasians. They moderately increase risk for VTE, by three to eight times for factor V Leiden and two to three times for prothrombin G20210A. Having a non-O blood type approximately doubles VTE risk. Non-O blood types are present in all races and common, thus making non-O blood type an important risk factor. 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.
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. In upper extremity DVT, the most important risk factor is having a central venous catheter. Thoracic outlet syndrome also increases risk.
DVT usually develops first in the calf veins, and when it extends, it "grows" in the direction of venous flow, towards the knees. When DVT does not grow, it can be cleared naturally and dissolved into the blood. DVT most commonly affects the leg veins of the thigh or lower leg such as the femoral vein, the popliteal vein, or the iliofemoral vein (as with May–Thurner syndrome). Occasionally the veins of the arm are affected, as after central venous catheter placement and with the rare Paget–Schrötter disease. Extensive lower extremity DVT can reach into the iliac vein of the pelvis or the inferior vena cava. Rarely, DVT can occur in mesenteric (intestinal) veins.
The mechanism behind arterial thrombosis, as with heart attacks, is more established than the steps that cause venous thrombosis. With arterial thrombosis, blood vessel wall damage is required for thrombosis formation, as it initiates coagulation, but clotting in the veins mostly occurs without any blood vessel damage. 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. Red blood cells and fibrin are the main components of venous thrombi, and the fibrin appears to attach to the blood vessel wall lining (endothelium), a surface that normally acts to prevent clotting. 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. Inflammation and white blood cells play a key role in both the formation and resolution of venous clots.
Often, DVT begins in the valves of veins. 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. 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.
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 ३] can rule out a diagnosis.
In 2012, the American College of Chest Physicians (ACCP) released its 9th edition of clinical practice guidelines, which included recommendations on DVT diagnosis. Each recommendation was given a grade, indicating its strength and evidence quality (see table below). Grades of 2B and 2C suggest that the best practices are subject to debate. When this article cites a 2012 ACCP recommendation, the grade will appear in parentheses.
|Grade||Description of 2012 ACCP grade[note ४]|
|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|
The disease term venous thromboembolism (VTE) includes both DVT and pulmonary embolism (PE). DVT can be lower extremity (from the legs), upper extremity (from the arms), abdominal, or pelvic in origin. They can also occur in the neck. DVT in the legs is called proximal (or iliofemoral) when above the knee and distal (or calf) when below the knee. DVT below the popliteal vein, a proximal vein behind the knee, is in distal calf veins. Distal DVT has limited clinical significance compared to proximal DVT. An incident DVT is an initial episode and any subsequent DVT is recurrent. Bilateral DVT refers to clots in both legs while unilateral means only a single leg is affected.
DVT that has no symptoms, but is only found by screening, is labeled asymptomatic.Acute DVT is characterized by pain and swelling and is usually occlusive, which means they obstruct blood flow, whereas nonocclusive DVT is less symptomatic. The label ofchronic has been applied to symptomatic DVT that persists longer than 10 or 14 days. 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."
Wells score or criteria: (possible score −2 to 9)
- Active cancer (treatment within last 6 months or palliative): +1 point
- Calf swelling ≥ 3 cm compared to asymptomatic calf (measured 10 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 days, or major surgery requiring regional or general anesthetic in the past 12 weeks: +1 point
- Alternative diagnosis at least as likely: −2 points
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. 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%.
In high-probability cases D-dimers are to be skipped in favor of diagnostic imaging. For those with a low- or moderate-probability of DVT, a D-dimer level is 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. Hospitalized patients often have elevated levels for multiple reasons.
For a suspected first leg DVT in a low-probability situation, testing D-dimer levels with either moderate (2B) or high sensitivity (2C) is suggested by the ACCP, though compression ultrasound of the proximal veins is also an option. For a suspected first leg DVT in a moderate-probability scenario, a high-sensitivity D-dimer is suggested over ultrasound imaging (2C). An elevated D-dimer level means diagnostic imaging is necessary. A normal D-dimer result in either suggested scenario makes imaging unnecessary.
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. Doppler ultrasound, CT scan venography, MRI venography, or MRI of the thrombosis are also possibilities. 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, and other limitations this test is rarely performed.
Depending upon the risk for DVT, different preventative measures are used. Walking and calf exercises are possibilities; 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. 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%, and the point where annual VTE risk is thought to warrant long-term anticoagulation is estimated to be between 3 to 9%. Usually, only when individuals exceed a 9% annual VTE risk is long-term anticoagulation a common consideration. Antithrombin deficiency, a strong or moderately strong risk factor, carries an annual risk of VTE of only 0.8 to 1.5%; as such, asymptomatic individuals with thrombophilia do not warrant long-term anticoagulation (1C). Moderate alcohol consumption is associated with a reduction in DVT.
Post surgery[सम्पादन गर्ने]
Those who have major orthopedic surgery—total hip replacement, total knee replacement or hip fracture surgery—are at a high risk of VTE. After any of those surgeries, without prophylaxis, the risk of symptomatic VTE in the 35 days post surgery is estimated to be about 4%. 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. In major orthopedic surgery patients, the ACCP recommended additional drug options such as fondaparinux and aspirin (1B), though LMWH is suggested (2B or 2C). IPC is also an option.
The risk of VTE is increased in pregnancy by about five-fold because of a more hypercoaguable state, a likely adaptation against fatal postpartum hemorrhage. Additionally, pregnant women with genetic risk factors are subject to an approximate three- to thirty-fold increased risk for VTE. 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 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 have clinical vigilance during pregnancy and LMWH or—for those without protein C or S deficiency—a VKA suggested (2C). Homozygous carriers of factor V Leiden or prothrombin G20210A with no personal or family history of VTE were suggested to be subject to clinical vigilance during pregnancy and LMWH or a VKA for six weeks after childbirth (2B). Those with another thrombophilia but no family or personal history of VTE were suggested to receive clinical vigilance (2C). Warfarin, a common VKA, can cause harm to the fetus and is not used for VTE prevention during pregnancy.
The 2012 ACCP guidelines offered grade 2C 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. 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. 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.
In hospital[सम्पादन गर्ने]
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.
The 2012 ACCP guidelines for non-surgical patients[note ५] recommend anticoagulation for the acutely ill in cases of elevated risk when there is no bleeding nor a high risk of bleeding (1B). Mechanical prophylaxis is suggested when risks for both bleeding and thrombosis are elevated (2C). For the critically ill, either pharmacological or mechanical prophylaxis is suggested depending upon the risk (2C). 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 (2B).
Anticoagulation, which prevents further coagulation but does not act on existing clots, is the standard treatment for DVT. 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 (1B). The parenteral anticoagulant should be taken until the international normalized ratio (INR) is ≥ 2.0 for 24 hours minimum (1B). If the INR is > 3.0, the parental anticoagulant treatment can stop early. LMWH (2B) and fondaparinux (2C) are suggested over unfractionated heparin, but both are retained in those with compromised kidney function, unlike unfractionated heparin. The VKA is generally taken for a minimum of three months to maintain an INR of 2.0 to 3.0, with 2.5 as the target. The benefit of taking a VKA declines as the duration of treatment extends, and the risk of bleeding increases with age.
Balancing risk vs. benefit is important in determining the duration of anticoagulation. In those with an annual risk of VTE in excess of 9%, as after an unprovoked episode, long-term anticoagulation is a possibility. 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). This result might be used in clinical decision making. Thrombophilia test results rarely play a role in the length of treatment.
The ACCP recommended treatment for 3 months in those with proximal DVT provoked by surgery (1B). A three month course is also recommended for those with proximal DVT provoked by a transient risk factor (1B), and three months is suggested over lengthened treatment when bleeding risk is low to moderate (2B). Unprovoked DVT patients should have at least three months of anticoagulation (1B) and be considered for extended treatment. Those whose first VTE is an unprovoked proximal DVT are suggested for anticoagulation longer than 3 months (2B) unless there is a high risk of bleeding. In that case, three months is sufficient (1B). Those with a second unprovoked VTE are recommended for extended treatment when bleeding risk is low (1B), suggested for extended treatment when bleeding risk is moderate (2B), and suggested for three months of anticoagulation in high-risk scenarios (2B).
Definitive randomized controlled trial evidence of anticoagulation versus placebo for VTE treatment is nonexistent, but studying this is unlikely to be ethically approved because anticoagulation is accepted clinical practice. Evidence for clinical practice is derived from other studies. One small randomized controlled trial comparing anticoagulation versus NSAIDs for the treatment for DVT was identified in a review article published by the Cochrane Collaboration. In that study, the comparison between the 90 patients who met the inclusion criteria did not show any significant difference, as the small sample size limited statistical power. Thus, the data from randomized controlled trials on anticoagulation is inconclusive in regards to efficacy and safety.
Home treatment[सम्पादन गर्ने]
The ACCP recommended initial home treatment for those with acute leg DVT (1B). 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 the hospital if necessary, support from family or friends, and phone access.
Graduated compression stockings and walking[सम्पादन गर्ने]
In addition to anticoagulation treatment, 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—for those with symptomatic DVT (2B). Use should begin as soon as possible after anticoagulation. Existing randomized controlled trials give moderate quality evidence that GCSs reduce the risk of post-thrombotic syndrome (PTS). An estimate on the number needed to treat says about four people need GCS to prevent one PTS case. Trials do not indicate a reduction in recurrent VTE. The suggested duration of use is for two years, though inconvenience and discomfort can reduce compliance. Walking is also suggested over bed rest for those without severe pain or edema (2C).
Inferior vena cava filter[सम्पादन गर्ने]
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. In general, they are only recommended in some high-risk scenarios. The ACCP recommended them for 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). While IVC filters are associated with a long term risk of DVT, they are not reason enough to maintain extended anticoagulation.
Serial imaging[सम्पादन गर्ने]
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, the ACCP does not recommend anticoagulation (1B). 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. When applied to symptomatic patients with a negative initial ultrasound result, serial testing is inefficient and not cost effective.
Thrombolysis and thrombectomy[सम्पादन गर्ने]
Thrombolysis, which acts to break up clots, can be systemic or catheter-directed, but the ACCP suggested anticoagulation instead (2C); however, patients may choose thrombolysis if prevention of PTS outweighs concerns over the complexity, bleeding risk, and cost of the procedure. 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." Anticoagulation alone is suggested over thrombectomy (2C).
The most frequent complication of proximal DVT is post-thrombotic syndrome (PTS). 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. Distal DVT itself is hardly if ever associated with PTS or PE. 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. In the 10 years following a VTE, approximately ⅓ of individuals will have a recurrent episode.
DVT occurs in about 1 in 1000 adults per year. An estimated 300,000 to 600,000 Americans suffer from VTE each year, with about 60,000 to 100,000 deaths attributable to PE. 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. With pregnancy and postpartum, acute VTE incidence is about 1 per 1000 deliveries. 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.
In the U.S. population, about 5 to 8% of people have a thrombophilia. Among those who develop VTE, 30 to 50% have an 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. 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.
Initial DVT costs for an average hospitalized patient in the U.S. are around $7,700 to $10,800. 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. PTS is a significant contributor to DVT follow-up costs. Annual DVT costs in the U.S. are an estimated $5 billion or in excess of $8 billion, and the average annual cost per treated individual is thought to be about $20,000. As an example, if 300,000 symptomatic DVT patients were treated at costs averaging $20,000 annually, that would cost $6 billion a year.
The first documented DVT is thought to have occurred in the 13th century, in the leg of a 20-year-old male. 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.
In 1856, German physician and pathologist Rudolf Virchow published what is referred to as Virchow's triad: the three major causes of thrombosis. The triad provides the theoretical framework for how venous thrombosis formation is currently explained. 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.
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. 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.
Research directions[सम्पादन गर्ने]
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. In 2012, results from the ASPIRE study are expected. ASPIRE is similar to a study that demonstrated a reduction in recurrent VTE with aspirin use.
List of notable individuals[सम्पादन गर्ने]
- David Bloom, a US NBC TV journalist who died in Iraq from DVT/PE
- Heavy D, a US rapper who died from DVT/PE
- 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.
- Factor V Leiden increases the risk of DVT more than it does for PE, a phenomenon referred to as the factor V Leiden paradox.
- An elevated level is greater than 250 ng/mL D-dimer units (DDU) or greater than 0.5 μg/mL fibrinogen equivalent units (FEU). A normal level is below these values.
- For more detailed descriptions of the grades, including benefits vs. the risks and burdens, the methodologic strength of supporting evidence, and implications, see Table 4 of Guyatt et al. on p. 62S.
- 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."
- "What are the signs and symptoms of deep vein thrombosis?", 28 October 2011
- Scarvelis D, Wells P (2006), "Diagnosis and treatment of deep-vein thrombosis", CMAJ 175(9): 1087–92, PMID 17060659, doi 10.1503/cmaj.060366 
- Bates SM, Jaeschke R, Stevens SM, et al. (2012), "Diagnosis of DVT: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines", Chest 141(suppl 2): e351S–e418S, PMID 22315267, doi 10.1378/chest.11-2299
- Hargett CW, Tapson VF (2008), "Clinical probability and D-dimer testing: how should we use them in clinical practice?", Semin Respir Crit Care Med 29(1): 15–24, PMID 18302083, doi 10.1055/s-2008-1047559
- John T. Owings (2005), "Management of venous thromboembolism", ACS Surgery, American College of Surgeons
- Barham K, Shah T (2007), "Images in clinical medicine: phlegmasia cerulea dolens", N Engl J Med 356(3): e3, PMID 17229945, doi: 10.1056/NEJMicm054730 , <http://www.nejm.org/doi/full/10.1056/NEJMicm054730>
- Bates SM, Greer IA, Middeldorp S, et al. (2012), "VTE, thrombophilia, antithrombotic Therapy, and pregnancy: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines", Chest 141(suppl 2): e691S–e736S, PMID 22315276, doi 10.1378/chest.11-2300
- Martinelli I, Bucciarelli P, Mannucci PM (2010), "Thrombotic risk factors: basic pathophysiology", Crit Care Med 38(suppl 2): S3–S9, PMID 20083911, doi 10.1097/CCM.0b013e3181c9cbd9
- Bovill EG, van der Vliet A (2011), "Venous valvular stasis-associated hypoxia and thrombosis: what is the link?", Annu Rev Physiol 73: 527–45, PMID 21034220, doi 10.1146/annurev-physiol-012110-142305
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Cited literature[सम्पादन गर्ने]
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