21 22 Genetic factors that increase the risk of 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 protein s are rare but strong, or moderately strong, risk factors. 15 17 These three thrombophilia c increase the risk of vte by about 10 times. 23 Factor v leiden, which makes factor V resistant to inactivation by activated protein c, 25 and the genetic variant prothrombin G20210a, which causes increased prothrombin levels, are predominantly expressed in caucasians. 15 d They moderately increase risk for vte, by three to eight times for factor v leiden and two to three times for prothrombin G20210A. 23 26 having a non-O blood type roughly doubles vte risk. 17 Non-O blood type is common in all races, making it an important risk factor. 27 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.

13 14 causes The incision for a completed knee replacement surgery, a procedure that can predispose people to a dvt the three factors of koortslip Virchow's triad — venous stasis, india hypercoagulability, and changes in the endothelial blood vessel lining (such as physical damage or endothelial activation. 15 16 Other related causes include activation of immune system components, the state of microparticles in the blood, the concentration of oxygen, and possible platelet activation. 17 Various risk factors contribute to dvt, though many at high risk never develop. 18 Acquired risk factors include the strong risk factor of older age, 16 18 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 entering the blood. 15 In orthopedic surgery, venous stasis may be temporarily provoked by a cessation of blood flow as part of the procedure. 17 Cancer can grow in and around veins, causing venous stasis, and 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 b and hormonal replacement therapy increase the risk through a variety of mechanisms, including altered blood coagulation protein levels and reduced fibrinolysis. 17 The disease term venous thromboembolism (VTE) includes the development of either dvt or pulmonary embolism (PE).

deep vein thrombosis risk factors
Deep vein Thrombosis, causes, risk

3 4 a d-dimer test may also be used best to assist with excluding the diagnosis or to signal a need for further testing. 2 diagnosis is most commonly confirmed by ultrasound of the suspected veins. 2 Together, dvt and pulmonary embolism are known as venous thromboembolism (VTE). 2 Anticoagulation (blood thinners) is the standard treatment. 2 Typical medications include low-molecular-weight heparin, warfarin, or a direct oral anticoagulant. 3 wearing graduated compression stockings may reduce the risk of post-thrombotic syndrome. 5 Prevention may include early and frequent walking, calf exercises, aspirin, anticoagulants, graduated compression stockings, or intermittent pneumatic compression. 5 The rate of dvts increases from childhood to old age; in adulthood, about one in 1000 adults are affected per year. 6 About 5 of people are affected by a vte at some point in time. 4 Contents Signs and symptoms Illustration depicting a deep vein thrombosis Common signs and symptoms of dvt include pain or tenderness, swelling, warmth, redness or discoloration, and distention of surface veins, although about half of those with the condition have no symptoms.

deep vein thrombosis risk factors
Deep vein thrombosis - symptoms

Deep vein thrombosis : Symptoms and risk factors


For other uses, see. Deep vein thrombosis dvt is the formation of a blood clot in a deep vein, most commonly the legs. 2 a, symptoms may include pain, swelling, redness, or warmth of the affected area. 2, about half of cases have no symptoms. 2, complications may include pulmonary embolism, as a result of detachment of a clot which travels to the lungs, and post-thrombotic syndrome. 2 3, risk factors include recent surgery, cancer, trauma, lack of movement, obesity, smoking, hormonal birth control, pregnancy and the period following birth, antiphospholipid syndrome, and certain genetic conditions. 2 3, genetic factors include deficiencies of antithrombin, protein c, and protein s, and factor v leiden mutation. 3 The underlying mechanism typically involves some combination of decreased blood flow rate, increased tendency to clot, doppler and injury to the blood vessel wall. 2 Individuals suspected of having dvt may be assessed using a clinical prediction rule such as the wells score.

Deep vein Thrombosis, dvt


Winters jp, callas pw, cushman m, repp ab, zakai. Central venous catheters and upper extremity deep vein thrombosis in medical inpatients: the medical Inpatients and Thrombosis (mith) Study. J thromb haemost 2015;13:2155-60. Verso m, agnelli. Venous thromboembolism associated with long-term use of central venous catheters in cancer patients. J clin Oncol 2003;21:3665-75. Van rooden cj, molhoek sg, rosendaal fr, schalij mj, meinders ae, huisman. Incidence and risk factors of early venous thrombosis associated with permanent pacemaker leads. J cardiovasc Electrophysiol 2004;15:1258-62.

deep vein thrombosis risk factors
Deep vein thrombosis - wikipedia

Symptoms can vary widely from complete lack of symptoms to limb threatening phlegmasia cerulea dolens. Clinical suspicion should arise in those with the development of unilateral edema or pain, particularly in young athletes, or those with central venous catheters. In the absence of contraindications, anticoagulation should be initiated with consideration for catheter-directed thrombolysis in those with severe symptoms or those with venous thoracic outlet syndrome prior to evaluation for surgical decompression. Catheter-associated uedvt does not necessitate removal of the central venous catheter if it continues to function properly and it is still needed. Anticoagulation should be initiated for as long as the catheter is in place and continued for 3 months after removal. Superior vena cava filters have little application in the therapy for uedvt with the risk outweighing the benefit in the majority of cases. References, munoz fj, mismetti p, poggio r,.

Clinical outcome of patients with upper-extremity deep vein recht thrombosis: results from the riete registry. Engelberger rp, kucher. Management of deep vein thrombosis of the upper extremity. Lee ja, zierler bk, zierler. The risk factors and clinical outcomes of upper extremity deep vein thrombosis. Vasc Endovascular Surg 2012;46:139-44.

Deep vein Thrombosis - orthoInfo


The most recent updates to the American College of Chest Physicians (accp) guidelines recommend anticoagulant therapy alone over thrombolysis. However, thrombolysis can be considered in patients in whom there are severe symptoms, extent of thrombus from subclavian to axillary vein, symptoms 14 days, good performance status, life expectancy 1 year, and low risk for bleeding.14 Angioplasty with stent placement at the costoclavicular junction. Surgical decompression involves resection of the first rib and costoclavicular ligament, anterior scalenectomy, and venolysis. The timing of surgical decompression is controversial; most advocate for surgical evaluation within 3 months of cdt, with some proponents recommending evaluation and treatment during first hospitalization. In cases of catheter-associated uedvt, recommendations from the accp are to remove the offending catheter only if the catheter is no longer needed or no longer working.

Overlap of therapeutic anticoagulation prior to removal of a catheter associated with thrombosis has not been validated in the literature, although is often advocated. This should be followed by a minimum of 3 months of anticoagulation. If the cvc is not removed, anticoagulation should continue as long as the cvc remains in place and continue for 3 months after its removal.14 cdt can be considered for those in whom there are severe symptoms and require the continued use of the cvc. The use of superior vena cava filters should only be considered in rare cases in those patients with contraindications for anticoagulant and pulmonary embolism. Given the substantially lower risk of clinically significant pulmonary embolism, as discussed above, the potential benefit must outweigh the significant risks of filter placement, including filter dislocation and development of the superior vena cava syndrome due to thrombus occlusion of the filter. In a review of the literature including 21 publications including 209 cases, there was 2 risk of pericardial tamponade and 1 risk of aortic perforation after the placement of a superior vena cava filter.10. In conclusion, the incidence of uedvt appears to be increasing with greater awareness and use of central venous catheters with subclinical dvt likely more common than previously understood.

Deep vein thrombosis - ebm

There are several clinically relevant complications resulting from uedvt. Compared to lower extremity dvt, uedvt has a lower risk of embolism to the pulmonary vasculature. Clinically apparent pulmonary embolism (PE) occurs in 5-8 of patients of uedvt with a mortality.7.1,10 Subclinical pe is far more common being seen in upwards of 36 of patients.11 The post-thrombotic syndrome which combines debilitating upper ligplaats extremity pain and swelling has been seen. The management of uedvt depends largely on the etiology; however, in the absence of a contraindication, the cornerstone of treatment is anticoagulation. Treatment should be aimed at obtaining early venous recanalization and attempts to restore vein patency. In primary uedvt, prompt anticoagulation should be initiated with consideration for more advanced therapeutics including catheter directed thrombolytics (CDT). A retrospective study of 30 patients with uedvt, 97 of patient treated with cdt showed at least 50 reduction in clot burden at the risk of 9 major bleeding.13 Anticoagulation should be continued for at least 3 months with either low molecular weight heparin (lmwh. Lmwh is the preferred method gel of anticoagulation in malignancy associated uedvt with therapy continuing beyond 3 months until cure or remission is achieved. Subsequent rheolytic or mechanical thrombectomy is often utilized to improve venous outflow.

deep vein thrombosis risk factors
Risk of dvt, deep vein thrombosis

Deep vein Thrombosis (dvt )

With increasing venous outflow obstruction, arterial compromise can occur leading to limb threatening phlegmasia cerulea dolens. The diagnosis of uedvt is made by correlating pancreas individual history and typical clinical findings with appropriate radiographic imaging. The most commonly use imaging modality in the diagnosis of uedvt is venous duplex ultrasonography. Duplex ultrasound typically shows loss of compressibility of the vein and lack of color Doppler flow within the venous lumen. Spectral analysis may show reduced or absent respiratory phasicity suggestive of proximal obstruction. Although direct visualization of the proximal subclavian vein can be difficult due to shadowing from the clavicle, duplex ultrasonography has a sensitivity and specificity approaching 100.9 Computed tomography (CT) and magnetic resonance imaging (MRI) can be helpful if Duplex ultrasonography is indeterminate, however must. Additionally, ct or mri may be useful in imaging anatomy to assess the proximal extent of dvt, and to assess for the possibility of compression of vascular structures.


Repetitive motion also results in venous microtrauma and subsequent perivenous fibrosis which leads to activation of the coagulation cascade. In chronic cases, venous webs can form. Secondary uedvt occurs due to thrombosis as a result of indwelling devices such as a central venous catheters (cvc pacemaker or defibrillator leads, and tunneled central access lines. Catheter-associated uedvt is the most common etiology comprising 93 of all uedvt in one retrospective analysis of 373 patients with the presence of a cvc increasing the risk of developing uedvt by up to 14-fold.3-4 The incidence of catheter-associated uedvt appears to be increasing, likely. Additionally, the synthetic material used to construct many central venous catheters may induce fibrin sheath formation along the outer lumen of the catheter which can occur within as early as 24 hours of insertion.7 Other factors including inherited or acquired thrombophilia and malignancy further increase. The severity of symptoms in uedvt parallels the degree of venous obstruction. Common symptoms include unilateral upper extremity pain, swelling, and arm fatigue. If the more proximal superior vena cava ligplaats (SVC) is involved, facial plethora and chest wall edema may be noted. Prominent superficial collateral veins may appear on the shoulder and anterior chest wall, known as Urschel's sign.

Nhs direct Wales - encyclopaedia

Upper extremity deep vein thrombosis (uedvt) accounts for approximately 5 to 10 percent of all cases of dvt with incidence increasing due to higher frequency of intravenous catheter use.1 veins considered to be "deep" classically have a corresponding named artery. In the waar upper extremity the deep veins include the paired radial veins, paired ulnar veins, paired brachial veins, axillary vein, and subclavian vein. The most common site of uedvt involves the axillary and subclavian veins; however, the more distal brachial vein may also be involved. Additionally, many also consider the internal jugular veins to be included in the deep veins given their proximity to the central venous system. Uedvt can occur in primary and secondary forms with the symptom severity and treatment options varying between the two types. Primary uedvt is less common than secondary uedvt and most typically is effort-induced, known as Paget-Schroetter syndrome (PSS).2 pss is a venous form of thoracic outlet syndrome (vtos) which classically occurs in the dominant arm of young athletes. The pathophysiology involves compression of the neurovascular bundle exiting the thoracic outlet. Compression is caused by repetitive motion of the upper extremity which, in the setting of anatomic abnormalities, such as hypertrophied scalene muscles, congenital presence of cervical ribs, and subclavius ligaments, place these individuals at a higher risk of uedvt. The subclavian vein is most commonly involved due to its anatomical location adjacent to the first rib which often causes compression.

Deep vein thrombosis risk factors
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