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80-419: SVT may refer to: Medicine [ edit ] Superficial vein thrombosis , a type of problematic blood clot Supraventricular tachycardia , an abnormal heart condition Music [ edit ] SVT (band) , an early-1980s American rock band Seventeen (South Korean band) Organisations [ edit ] Soqosoqo ni Vakavulewa ni Taukei or

160-483: A prediction rule such as the Wells score . A D-dimer test can also be used to assist with excluding the diagnosis or to signal a need for further testing. Diagnosis is most commonly confirmed by ultrasound of the suspected veins. VTE becomes much more common with age. The condition is rare in children, but occurs in almost 1% of those ≥ age 85 annually. Asian, Asian-American, Native American, and Hispanic individuals have

240-431: A stroke in the presence of a heart defect . This is called a paradoxical embolism because the clot abnormally travels from the pulmonary circuit to the systemic circuit while inside the heart. The defect of a patent foramen ovale is thought to allow clots to travel through the interatrial septum from the right atrium into the left atrium. In most suspected cases, DVT is ruled out after evaluation. Cellulitis

320-413: A "palpable cord". Migratory thrombophlebitis ( Trousseau's syndrome) is a noted finding in those with pancreatic cancer and is associated with DVT. A pulmonary embolism (PE) occurs when a blood clot from a deep vein (a DVT) detaches from a vein ( embolizes ), travels through the right side of the heart, and becomes lodged as an embolus in a pulmonary artery that supplies deoxygenated blood to

400-542: A 50% reduction in PE, a 70% increase in DVT, and an 18% increase in 30 day mortality when compared to no IVC placement. Other studies including a systematic review and meta-analysis did not find a difference in mortality with IVC placement. If someone develops a PE despite being anticoagulated, care should be given to optimize anticoagulation treatment and address other related concerns before considering IVC filter placement. Patients with

480-426: A D-dimer value. With this prediction rule, three points or less means a person is at low risk for DVT. A result of four or more points indicates an ultrasound is needed. Instead of using a prediction rule, experienced physicians can make a DVT pre-test probability assessment using clinical assessment and gestalt, but prediction rules are more reliable. Compression ultrasonography for suspected deep vein thrombosis

560-739: A background genetic risk comparable to the factor V Leiden and prothrombin G20210A mutations. Blood alterations including dysfibrinogenemia , low free protein S, activated protein C resistance , homocystinuria , hyperhomocysteinemia , high fibrinogen levels, high factor IX levels, and high factor XI levels are associated with increased risk. Other associated conditions include heparin-induced thrombocytopenia , catastrophic antiphospholipid syndrome , paroxysmal nocturnal hemoglobinuria , nephrotic syndrome , chronic kidney disease , polycythemia vera , essential thrombocythemia , intravenous drug use, and smoking. Some risk factors influence

640-453: A blood thinner or aspirin combined with intermittent pneumatic compression . Symptoms classically affect a leg and typically develop over hours or days, though they can develop suddenly or over a matter of weeks. The legs are primarily affected, with 4–10% of DVT occurring in the arms. Despite the signs and symptoms being highly variable, the typical symptoms are pain, swelling , and redness. However, these symptoms might not manifest in

720-669: A healthcare professional. A more specific evaluation can be made by ultrasound . An ultrasound can be useful in situations in which an SVT occurs above the knee and is not associated with a varicose vein, because ultrasounds can detect more serious clots like DVTs. The diagnostic utility of D-dimer testing in the setting of SVTs has yet to be fully established. SVTs can be classified as either varicose vein (VV) or non-varicose (NV) associated. NV-SVTs are more likely to be associated with genetic procoagulable states compared to VV-SVTs. SVTs can also be classified by pathophysiology . That is, primary SVTs are characterized by inflammation that

800-846: A high risk of VTE recurrence are typically anticoagulated as if they had proximal DVT. Those at a low risk for recurrence might receive a four- to six-week course of anticoagulation, lower doses, or no anticoagulation at all. In contrast, those with proximal DVT should receive at least 3 months of anticoagulation. Some anticoagulants can be taken by mouth, and these oral medicines include warfarin (a vitamin K antagonist ), rivaroxaban (a factor Xa inhibitor ), apixaban (a factor Xa inhibitor), dabigatran (a direct thrombin inhibitor ), and edoxaban (a factor Xa inhibitor). Other anticoagulants cannot be taken by mouth. These parenteral (non-oral) medicines include low-molecular-weight heparin , fondaparinux , and unfractionated heparin . Some oral medicines are sufficient when taken alone, while others require

880-442: A history of DVT might be managed by primary care , general internal medicine , hematology , cardiology , vascular surgery , or vascular medicine . Patients suspected of having an acute DVT are often referred to the emergency department for evaluation. Interventional radiology is the specialty that typically places and retrieves IVC filters, and vascular surgery might do catheter directed thrombosis for some severe DVTs. For

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960-477: A life expectancy of 1 year or more, and a low risk of bleeding." A mechanical thrombectomy device can remove DVT clots, particularly in acute iliofemoral DVT (DVT of the major veins in the pelvis), but there is limited data on its efficacy. It is usually combined with thrombolysis, and sometimes temporary IVC filters are placed to protect against PE during the procedure. Catheter-directed thrombolysis with thrombectomy against iliofemoral DVT has been associated with

1040-696: A lower VTE risk than Whites or Blacks. Populations in Asia have VTE rates at 15 to 20% of what is seen in Western countries. Using blood thinners is the standard treatment. Typical medications include rivaroxaban , apixaban , and warfarin . Beginning warfarin treatment requires an additional non-oral anticoagulant, often injections of heparin . Prevention of VTE for the general population includes avoiding obesity and maintaining an active lifestyle. Preventive efforts following low-risk surgery include early and frequent walking. Riskier surgeries generally prevent VTE with

1120-595: A non-O blood type roughly doubles VTE risk. Non-O blood type is common globally, making it 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. Those homozygous for the common fibrinogen gamma gene variant rs2066865 have about a 1.6 times higher risk of VTE. The genetic variant prothrombin G20210A , which increases prothrombin levels, increases risk by about 2.5 times. Additionally, approximately 5% of people have been identified with

1200-468: A parenteral anticoagulant together with warfarin is given, which is followed by warfarin-only therapy. Warfarin is taken to maintain an international normalized ratio (INR) of 2.0–3.0, with 2.5 as the target. The benefit of taking warfarin declines as the duration of treatment extends, and the risk of bleeding increases with age. Periodic INR monitoring is not necessary when first-line direct oral anticoagulants are used. Overall, anticoagulation therapy

1280-481: A positive D-dimer test. While the Wells score is the predominant and most studied clinical prediction rule for DVT, it does have drawbacks. The Wells score requires a subjective assessment regarding the likelihood of an alternate diagnosis and performs less well in the elderly and those with a prior DVT. The Dutch Primary Care Rule has also been validated for use. It contains only objective criteria but requires obtaining

1360-652: A prior DVT increases the risk of a subsequent DVT. Major surgery and trauma increase risk because of tissue factor from outside the vascular system entering the blood. Minor injuries, lower limb amputation, hip fracture , and long bone fractures are also risks. In orthopedic surgery , venous stasis can be temporarily provoked by a cessation of blood flow as part of the procedure. Inactivity and immobilization contribute to venous stasis, as with orthopedic casts , paralysis, sitting, long-haul travel, bed rest, hospitalization, catatonia , and in survivors of acute stroke . Conditions that involve compromised blood flow in

1440-500: A reduction in the severity of post-thrombotic syndrome at an estimated cost-effectiveness ratio of about $ 138,000 per gained QALY . Phlegmasia cerulea dolens might be treated with catheter-directed thrombolysis and/or thrombectomy. In DVT in the arm, the first (topmost) rib can be surgically removed as part of the typical treatment when the DVT is due to thoracic outlet syndrome or Paget–Schroetter syndrome . This treatment involves initial anticoagulation followed by thrombolysis of

1520-607: A risk of bleeding, complexity, and the cost of the procedure. Although, while anticoagulation is the preferred treatment for DVT, thrombolysis is a treatment option for those with the severe DVT form of phlegmasia cerula dorens ( bottom left image ) and in some younger patients with DVT affecting the iliac and common femoral veins. Of note, a variety of contraindications to thrombolysis exist. In 2020, NICE kept their 2012 recommendations that catheter-directed thrombolysis should be considered in those with iliofemoral DVT who have "symptoms lasting less than 14 days, good functional status,

1600-424: A role in venous thrombi formation. NET components are pro-thrombotic through both the intrinsic and extrinsic coagulation pathways. NETs provide "a scaffold for adhesion" of platelets, red blood cells, and multiple factors that potentiate platelet activation. In addition to the pro-coagulant activities of neutrophils, multiple stimuli cause monocytes to release tissue factor. Monocytes are also recruited early in

1680-424: A role. In cancer, tissue factor is produced by cancer cells. Cancer also produces unique substances that stimulate factor Xa , cytokines that promote endothelial dysfunction , and plasminogen activator inhibitor-1 , which inhibits the breakdown of clots (fibrinolysis). Often, DVT begins in the valves of veins. The blood flow pattern in the valves can cause low oxygen concentrations in the blood ( hypoxemia ) of

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1760-413: A second ultrasound some days later to rule out the diagnosis. Whole-leg ultrasound is the option that does not require a repeat ultrasound, but proximal compression ultrasound is frequently used because distal DVT is only rarely clinically significant. Ultrasound methods including duplex and color flow Doppler can be used to further characterize the clot and Doppler ultrasound is especially helpful in

1840-428: A triple-lumen PICC line), cancer, and recent surgery. Blood has a natural tendency to clot when blood vessels are damaged ( hemostasis ) to minimize blood loss. Clotting is activated by the coagulation cascade and the clearing of clots that are no longer needed is accomplished by the process of fibrinolysis . Reductions in fibrinolysis or increases in coagulation can increase the risk of DVT. DVT often develops in

1920-630: A valve sinus. Hypoxemia, which is worsened by venous stasis, activates pathways—ones that include hypoxia-inducible factor-1 and early-growth-response protein 1 . Hypoxemia also results in the production of reactive oxygen species , which can activate these pathways, as well as nuclear factor-κB , which regulates hypoxia-inducible factor-1 transcription . Hypoxia-inducible factor-1 and early-growth-response protein 1 contribute to monocyte association with endothelial proteins, such as P-selectin , prompting monocytes to release tissue factor-filled microvesicles , which presumably begin clotting after binding to

2000-418: A variety of causes. Diagnosis is often based on symptoms. There are multiple possible treatments, with the goal of providing symptomatic relief and preventing complications. SVT is recognized by the presence of pain, warmth, redness, and tenderness over a superficial vein. The SVT may present as a "cord-like" structure upon palpation. The affected vein may be hard along its entire length. SVTs tend to involve

2080-419: Is phlegmasia cerulea dolens . It is life-threatening, limb-threatening, and carries a risk of venous gangrene . Phlegmasia cerulea dolens can occur in the arm but more commonly affects the leg. If found in the setting of acute compartment syndrome , an urgent fasciotomy is warranted to protect the limb. Superior vena cava syndrome is a rare complication of arm DVT. DVT is thought to be able to cause

2160-665: Is post-thrombotic syndrome , which can cause pain, swelling, a sensation of heaviness, itching, and in severe cases, ulcers . Recurrent VTE occurs in about 30% of those in the ten years following an initial VTE. The mechanism behind DVT formation typically involves some combination of decreased blood flow , increased tendency to clot , changes to the blood vessel wall , and inflammation. Risk factors include recent surgery, older age, active cancer , obesity , infection, inflammatory diseases, antiphospholipid syndrome , personal history and family history of VTE, trauma, injuries, lack of movement, hormonal birth control , pregnancy , and

2240-457: Is a frequent mimic of DVT, with its triad of pain, swelling, and redness. Symptoms concerning for DVT are more often due to other causes, including cellulitis, ruptured Baker's cyst , hematoma , lymphedema , and chronic venous insufficiency . Other differential diagnoses include tumors, venous or arterial aneurysms , connective tissue disorders , superficial vein thrombosis , muscle vein thrombosis, and varicose veins . DVT and PE are

2320-541: Is a possibility. Those who finish warfarin 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. Thrombophilia test results rarely play a role in the length of treatment. Treatment for acute leg DVT is suggested to continue at home for uncomplicated DVT instead of hospitalization. Factors that favor hospitalization include severe symptoms or additional medical issues. Early walking

2400-578: Is also used for intermediate risk SVTs that are greater than 3 cm from the saphenofemoral junction or are greater than 4–5 cm in length. Anticoagulation for high risk SVTs includes the use of vitamin K antagonists or novel oral anticoagulants (NOACs) for 3 months. Anticoagulation for intermediate risk SVTs includes fondaparinux 2.5 mg daily for 45 days or the use of intermediate to therapeutic dose low molecular weight heparin for 4–6 weeks. NSAIDs (non-steroidal anti-inflammatory drugs) can be used in both oral or topical formulations for

2480-434: Is classified as recurrent. Bilateral DVT refers to clots in both limbs while unilateral means only a single limb is affected. DVT in a leg above the knee is termed proximal DVT ( proximal ). DVT in a leg below the knee is termed distal DVT ( distal ), also called calf DVT when affecting the calf, and has limited clinical significance compared to proximal DVT. Calf DVT makes up about half of DVTs. Iliofemoral DVT

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2560-641: Is complex, and many circumstances can affect how these therapies are managed. The duration of anticoagulation therapy (whether it will last 4 to 6 weeks, 6 to 12 weeks, 3 to 6 months, or indefinitely) is a key factor in clinical decision making . When proximal DVT is provoked by surgery or trauma a 3-month course of anticoagulation is standard. When a first VTE is proximal DVT that is either unprovoked or associated with transient non-surgical risk factor, low-dose anticoagulation beyond 3 to 6 months might be used. In those with an annual risk of VTE in excess of 9%, as after an unprovoked episode, extended anticoagulation

2640-467: Is considered "likely" (about a 28% chance), while those with a lower score are considered "unlikely" to have DVT (about a 6% chance). In those unlikely to have DVT, a diagnosis is excluded by a negative D-dimer blood test. In people with likely DVT, ultrasound is the standard imaging used to confirm or exclude a diagnosis. Imaging is also needed for hospital inpatients with suspected DVT and those initially categorized as unlikely to have DVT but who have

2720-619: Is described as involving either the iliac , or common femoral vein ; elsewhere, it has been defined as involving at a minimum the common iliac vein , which is near the top of the pelvis. DVT can be classified into provoked and unprovoked categories. For example, DVT that occurs in association with cancer or surgery can be classified as provoked. However, the European Society of Cardiology in 2019 urged for this dichotomy to be abandoned to encourage more personalized risk assessments for recurrent VTE. The distinction between these categories

2800-536: Is frequently associated with secondary antiphospholipid syndrome. Cancer can grow in and around veins, causing venous stasis, and can also stimulate increased levels of tissue factor. Cancers of the blood, lung, pancreas, brain, stomach, and bowel are associated with high VTE risk. Solid tumors such as adenocarcinomas can contribute to both VTE and disseminated intravascular coagulation . In severe cases, this can lead to simultaneous clotting and bleeding. Chemotherapy treatment also increases risk. Obesity increases

2880-583: Is localized to the veins. Secondary SVTs are characterized by systemic inflammatory processes. A subclass of SVTs are septic thrombophlebitis , which are SVTs that occur in the setting of an infection. The goal of treatment in SVT is to reduce local inflammation and prevent the SVT from extending from its point of origin. Treatment may entail the use of compression, physical activity, medications, or surgical interventions. The optimal treatment for many SVT sites (i.e. upper limbs, neck, abdominal and thoracic walls, and

2960-573: Is needed and should include a physical examination , a review of medical history , and universal cancer screening done in people of that age. A review of prior imaging is considered worthwhile, as is "reviewing baseline blood test results including full blood count , renal and hepatic function , PT and APTT ." It is not recommended practice to obtain tumor markers or a CT of the abdomen and pelvis in asymptomatic individuals. NICE recommends that further investigations are unwarranted in those without relevant signs or symptoms. Thrombolysis

3040-415: Is not always clear. Traditionally, the three factors of Virchow's triad — venous stasis , hypercoagulability , and changes in the endothelial blood vessel lining—contribute to VTE and were used to explain its formation. More recently, inflammation has been identified as playing a clear causal role. Other related causes include activation of immune system components, the state of microparticles in

3120-530: Is overweight or obese lose weight reduce DVT risk. Avoiding both smoking and a Western pattern diet are thought to reduce risk. Statins have been investigated for primary prevention (prevention of a first VTE), and the JUPITER trial , which used rosuvastatin , has provided some tentative evidence of effectiveness. Of the statins, rosuvastatin appears to be the only one with the potential to reduce VTE risk. If so, it appears to reduce risk by about 15%. However,

3200-594: Is rarely performed. Treatment for DVT is warranted when the clots are either proximal, distal and symptomatic, or upper extremity and symptomatic. Providing anticoagulation, or blood-thinning medicine, is the typical treatment after patients are checked to make sure they are not subject to bleeding . However, treatment varies depending upon the location of DVT. For example, in cases of isolated distal DVT, ultrasound surveillance (a second ultrasound after 2 weeks to check for proximal clots), might be used instead of anticoagulation. Although, those with isolated distal DVT at

3280-638: Is suggested over bedrest. Graduated compression stockings—which apply higher pressure at the ankles and a lower pressure around the knees can be trialed for symptomatic management of acute DVT symptoms, but they are not recommended for reducing the risk of post-thrombotic syndrome , as the potential benefit of using them for this goal "may be uncertain". Nor are compression stockings likely to reduce VTE recurrence. They are, however, recommended in those with isolated distal DVT. If someone decides to stop anticoagulation after an unprovoked VTE instead of being on lifelong anticoagulation, aspirin can be used to reduce

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3360-416: Is the injection of an enzyme into the veins to dissolve blood clots, and while this treatment has been proven effective against the life-threatening emergency clots of stroke and heart attacks, randomized controlled trials have not established a net benefit in those with acute proximal DVT. Drawbacks of catheter-directed thrombolysis (the preferred method of administering the clot-busting enzyme ) include

3440-399: Is the standard diagnostic method, and it is highly sensitive for detecting an initial DVT. A compression ultrasound is considered positive when the vein walls of normally compressible veins do not collapse under gentle pressure. Clot visualization is sometimes possible, but is not required. Three compression ultrasound scanning techniques can be used, with two of the three methods requiring

3520-485: The Wells score (see column in the table below) to determine if a potential DVT is "likely" or "unlikely" is typically the first step of the diagnostic process. The score is used in suspected first lower extremity DVT (without any PE symptoms) in primary care and outpatient settings, including the emergency department . The numerical result (possible score −2 to 9) is most commonly grouped into either "unlikely" or "likely" categories. A Wells score of two or more means DVT

3600-475: The period following birth . VTE has a strong genetic component, accounting for approximately 50 to 60% of the variability in VTE rates. Genetic factors include non-O blood type , deficiencies of antithrombin , protein C , and protein S and the mutations of factor V Leiden and prothrombin G20210A . In total, dozens of genetic risk factors have been identified. People suspected of having DVT can be assessed using

3680-447: The prevention of blood clots in the general population, incorporating leg exercises while sitting down for long periods, or having breaks from a sitting position and walking around, having an active lifestyle, and maintaining a healthy body weight are recommended. Walking increases blood flow through the leg veins. Excess body weight is modifiable unlike most risk factors, and interventions or lifestyle modifications that help someone who

3760-497: The subclavian vein and staged first rib resection to relieve the thoracic outlet compression and prevent recurrent DVT. The placement of an inferior vena cava filter (IVC filter) is possible when either the standard treatment for acute DVT, anticoagulation, is absolutely contraindicated (not possible), or if someone develops a PE despite being anticoagulated. However, a 2020 NICE review found "little good evidence" for their use. A 2018 study associated IVC filter placement with

3840-521: The 2012 American College of Chest Physicians guidelines and the 2012 British Committee for Standards in Haematology guidelines. The use of surgery for the treatment of SVT is controversial. SVT is often a mild, self-resolving medical condition. The inflammatory reaction may last up to 2–3 weeks, with possible recanalization of the thrombosed vein occurring in 6–8 weeks. The superficial vein may continue to be hyperpigmented for several months following

3920-768: The Fijian Political Party Special Vehicle Team , division of the Ford Motor Company Sudbury Valley Trustees , a regional land trust in eastern Massachusetts Sveriges Television , public broadcaster in Sweden Technology [ edit ] S-VT , sequential valve timing Ampeg SVT , a super valve technology amplifier SVT-40 , Samozaryadnaya Vintovka Tokareva, a WW2 semi-automatic rifle Transport [ edit ] DRG Class SVT 877 and DRG Class SVT 137, series of streamlined diesel trainsets of

4000-414: The SVT as well as for preventing the development of more serious complications (e.g. pulmonary embolism). Surgical interventions include ligation of the saphenofemoral junction, ligation and stripping of the affected veins, and local thrombectomy . Because of the risk of symptomatic pulmonary embolism with surgery itself, surgical interventions are not recommended for the treatment of lower limb SVTs by

4080-495: The SVT to elongate from its point of origin, increasing the risk for complications and clinical worsening. Medications used for the treatment of SVT include anticoagulants , NSAIDs (except aspirin ), antibiotics , and corticosteroids . SVTs that occur within the great saphenous vein within 3 cm of the saphenofemoral junction are considered to be equivalent in risk to DVTs. These high risk SVTs are treated identically with therapeutic anticoagulation. Anticoagulation

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4160-589: The affected area, but some DVTs have no symptoms. The most common life-threatening concern with DVT is the potential for a clot to embolize (detach from the veins), travel as an embolus through the right side of the heart, and become lodged in a pulmonary artery that supplies blood to the lungs . This is called a pulmonary embolism (PE). DVT and PE comprise the cardiovascular disease of venous thromboembolism (VTE). About two-thirds of VTE manifests as DVT only, with one-third manifesting as PE with or without DVT. The most frequent long-term DVT complication

4240-416: The blood, acts to temper the process of thrombus growth. This is the preferred process. Aside from the potentially deadly process of embolization, a clot can resolve through organization, which can damage the valves of veins, cause vein fibrosis, and result in non-compliant veins. Organization of a thrombus into the vein can occur at the third stage of its pathological development, in which collagen becomes

4320-431: The blood, the concentration of oxygen, and possible platelet activation. Various risk factors contribute to VTE, including genetic and environmental factors, though many with multiple risk factors never develop it. Acquired risk factors include the strong risk factor of older age, which alters blood composition to favor clotting. Previous VTE, particularly unprovoked VTE, is a strong risk factor. A leftover clot from

4400-506: The calf veins and "grows" in the direction of venous flow, towards the heart. DVT most frequently affects veins in the leg or pelvis including the popliteal vein (behind the knee), femoral vein (of the thigh), and iliac veins of the pelvis. Extensive lower-extremity DVT can even reach into the inferior vena cava (in the abdomen). Upper extremity DVT most commonly affects the subclavian, axillary, and jugular veins . The process of fibrinolysis, where DVT clots can be dissolved back into

4480-519: The characteristic component. The first pathological stage is marked by red blood cells, and the second is characterized by medium-textured fibrin. In arterial thrombosis, blood vessel wall damage is required, as it initiates coagulation , but clotting in the veins mostly occurs without any such mechanical damage. The beginning of venous thrombosis is thought to arise from "activation of endothelial cells, platelets, and leukocytes, with initiation of inflammation and formation of microparticles that trigger

4560-537: The coagulation system" via tissue factor. Vein wall inflammation is likely the inciting event. Importantly, the activated endothelium of veins interacts with circulating white blood cells (leukocytes). While leukocytes normally help prevent blood from clotting (as does normal endothelium), upon stimulation, leukocytes facilitate clotting. Neutrophils are recruited early in the process of venous thrombi formation. They release pro-coagulant granules and neutrophil extracellular traps (NETs) or their components, which play

4640-483: The endothelial surface. D-dimers are a fibrin degradation product , a natural byproduct of fibrinolysis that is typically found in the blood. An elevated level can result from plasmin dissolving a clot—or other conditions. Hospitalized patients often have elevated levels for multiple reasons. Anticoagulation , the standard treatment for DVT, prevents further clot growth and PE, but does not act directly on existing clots. A clinical probability assessment using

4720-418: The former Deutsche Reichsbahn-Gesellschaft Sturtevant (Amtrak station) 's train station code Savuti Airport 's IATA code Other uses [ edit ] Superfluid vacuum theory Topics referred to by the same term [REDACTED] This disambiguation page lists articles associated with the title SVT . If an internal link led you here, you may wish to change the link to point directly to

4800-474: The initial event. In a French population, SVT occurred in 0.64 per 1000 persons per year. SVTs have been historically considered to be benign diseases, for which treatment was limited to conservative measures. However, an increased awareness of the potential risks of SVTs developing into more serious complications has prompted more research into the diagnosis, classification, and treatment of SVTs. A Cochrane review recommends that future research investigate

4880-430: The intended article. Retrieved from " https://en.wikipedia.org/w/index.php?title=SVT&oldid=961786488 " Category : Disambiguation pages Hidden categories: Short description is different from Wikidata All article disambiguation pages All disambiguation pages Superficial vein thrombosis SVT has risk factors similar to those for other thrombotic conditions and can arise from

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4960-719: The legs are often due to varicose veins , though most people with varicose veins do not develop SVTs. SVTs of the arms are often due to the placement of intravenous catheters. Many of the risk factors that are associated with SVT are also associated with other thrombotic conditions (e.g. DVT). These risk factors include age, cancer , history of thromboembolism , pregnancy , use of oral contraceptive medications (containing estrogen), hormone replacement therapy , recent surgery, and certain autoimmune diseases (especially Behçet's and Buerger's diseases). Other risk factors include immobilization (stasis) and laparoscopy . Hypercoagulable states due to genetic conditions that increase

5040-408: The legs, though they can affect any superficial vein (e.g. those in the arms). SVT in the lower extremities can lead to a dangerous complication in which the clot travels to the lungs, called pulmonary embolism (PE). This is because lower limb SVTs can migrate from superficial veins into deeper veins. In a French population, the percent of people with SVTs that also suffered from PEs was 4.7%. In

5120-424: The likelihood of DVT, but they are not used alone for diagnosis. At times, DVT can cause symptoms in both arms or both legs, as with bilateral DVT. Rarely, a clot in the inferior vena cava can cause both legs to swell. Superficial vein thrombosis , also known as superficial thrombophlebitis , is the formation of a blood clot (thrombus) in a vein close to the skin . It can co-occur with DVT and can be felt as

5200-410: The location of DVT 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. Common risk factors for having an upper extremity DVT include having an existing foreign body (such as a central venous catheter, a pacemaker, or

5280-564: The lower limbs of those unable to walk. In those who are able to walk, DVT can reduce one's ability to do so. The pain can be described as throbbing and can worsen with weight-bearing, prompting one to bear more weight with the unaffected leg. Additional signs and symptoms include tenderness, pitting edema ( see image ), dilation of surface veins, warmth, discoloration, a "pulling sensation", and even cyanosis (a blue or purplish discoloration) with fever. DVT can also exist without causing any symptoms. Signs and symptoms help in determining

5360-571: The lungs for oxygenation. Up to one-fourth of PE cases are thought to result in sudden death. When not fatal, PE can cause symptoms such as sudden onset shortness of breath or chest pain , coughing up blood ( hemoptysis ), and fainting ( syncope ). The chest pain can be pleuritic (worsened by deep breaths) and can vary based upon where the embolus is lodged in the lungs. An estimated 30–50% of those with PE have detectable DVT by compression ultrasound . A rare and massive DVT that causes significant obstruction and discoloration (including cyanosis)

5440-450: The non-compressible iliac veins. CT scan venography , MRI venography, or a non-contrast MRI are also diagnostic 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, availability, and other limitations, this test

5520-425: The penis) has not been determined. Multiple compression bandages exist. Fixed compression bandages, adhesive short stretch bandages, and graduated elastic compression stockings have all be used in the treatment of SVTs. The benefit of compression stockings is unclear, though they are frequently used. Inactivity is contraindicated in the aftermath of an SVT. Uninterrupted periods of sitting or standing may cause

5600-425: The potential of blood to clot, as does pregnancy. 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 . Dozens of genetic risk factors have been identified, and they account for approximately 50 to 60% of

5680-417: The process. Tissue factor, via the tissue factor– factor VIIa complex, activates the extrinsic pathway of coagulation and leads to conversion of prothrombin to thrombin, followed by fibrin deposition. Fresh venous clots are red blood cell and fibrin rich. Platelets and white blood cells are also components. Platelets are not as prominent in venous clots as they are in arterial ones, but they can play

5760-516: The relief of SVT symptoms. The British Committee for Standards in Haematology guidelines recommend the use of NSAIDs for low-risk SVTs (thrombus <4–5 cm in length, no additional risk factors for thromboembolic events). NSAIDs are used for treatment durations of 8–12 days. Antibiotics are used in the treatment of septic SVT . Corticosteroids are used for the treatment of SVTs in the setting of vasculitic and autoimmune syndromes. Surgical interventions are used for both symptomatic relief of

5840-523: The risk of clotting may contribute to the development of SVT, such as factor V Leiden , prothrombin 20210A mutation, and protein C , S , and antithrombin III and factor XII deficiency . The mechanism for the development of an SVT depends upon the specific etiology of the SVT. For example, varicose veins and prolonged bed rest both may induce SVTs due to slowing the flow of blood through superficial veins. SVTs may be diagnosed based upon clinical criteria by

5920-412: The risk of recurrence, but it is only about 33% as effective as anticoagulation in preventing recurrent VTE. Statins have also been investigated for their potential to reduce recurrent VTE rates, with some studies suggesting effectiveness. An unprovoked VTE might signal the presence of an unknown cancer, as it is an underlying condition in up to 10% of unprovoked cases. A thorough clinical assessment

6000-488: The same population, deep vein thrombosis (DVT) was found in 24.6% of people with SVTs. However, because superficial veins lack muscular support, any clots that form are far less likely to be squeezed by muscle contraction, dislodged, and induce a PE. SVTs can recur after they resolve, which is termed "migratory thrombophlebitis." Migratory thrombophlebitis is a complication that may be due to more serious disorders, such as cancer and other hypercoagulable states. SVTs of

6080-579: The two manifestations of the cardiovascular disease venous thromboembolism (VTE). VTE can occur as DVT only, DVT with PE, or PE only. About two-thirds of VTE manifests as DVT only, with one-third manifesting as PE with or without DVT. VTE, along with superficial vein thrombosis, are common types of venous thrombosis. DVT is classified as acute when the clots are developing or have recently developed, whereas chronic DVT persists more than 28 days. Differences between these two types of DVT can be seen with ultrasound. An episode of VTE after an initial one

6160-416: The use of an additional parenteral blood thinner. Rivaroxaban and apixaban are the typical first-line medicines, and they are sufficient when taken orally. Rivaroxaban is taken once daily, and apixaban is taken twice daily. Warfarin, dabigatran, and edoxaban require the use of a parenteral anticoagulant to initiate oral anticoagulant therapy. When warfarin is initiated for VTE treatment, a 5-day minimum of

6240-452: The utility of oral, topical, and surgical treatments for preventing the progression of SVTs and the development of thromboembolic complications. Deep vein thrombosis Deep vein thrombosis ( DVT ) is a type of venous thrombosis involving the formation of a blood clot in a deep vein , most commonly in the legs or pelvis. A minority of DVTs occur in the arms. Symptoms can include pain, swelling, redness, and enlarged veins in

6320-554: The variability in VTE rates. As such, family history of VTE is a risk factor for a first VTE. Factor V Leiden , which makes factor V resistant to inactivation by activated protein C , mildly increases VTE risk by about three times. Deficiencies of three proteins that normally prevent blood from clotting— protein C , protein S , and antithrombin —contribute to VTE. These deficiencies in antithrombin , protein C , and protein S are rare but strong, or moderately strong, risk factors. They increase risk by about 10 times. Having

6400-570: The veins are May–Thurner syndrome , where a vein of the pelvis is compressed, and venous thoracic outlet syndrome , which includes Paget–Schroetter syndrome , where compression occurs near the base of the neck. Infections, including sepsis , COVID-19 , HIV , and active tuberculosis , increase risk. Chronic inflammatory diseases and some autoimmune diseases , such as inflammatory bowel disease , systemic sclerosis , Behçet's syndrome , primary antiphospholipid syndrome , and systemic lupus erythematosus (SLE) increase risk. SLE itself

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