History and exam
Key diagnostic factors
common
presence of risk factors
Key risk factors include varicose veins, thrombophilic disorders, and autoimmune diseases.
previous superficial vein thrombosis (SVT), deep vein thrombosis, or pulmonary embolism
Commonly reported by patients with SVT.
redness/erythema of overlying skin
May extend for some distance into the surrounding tissue, making the distinction from cellulitis difficult.[Figure caption and citation for the preceding image starts]: Greater saphenous vein superficial vein thrombophlebitisLucia MA, Ely EW. N Engl J Med. 2001:344;1214; used with permission [Citation ends].
hot/warm overlying skin
May extend for some distance into the surrounding tissue, making the distinction from cellulitis difficult.
painful/tender over affected vein
In a patient with pre-existing varicose veins, there is a tender 'worm-like' mass deep to the skin.
In a patient without varicose veins, a palpable, sometimes nodular, cord may have associated tenderness.
swelling/oedema of surrounding area
There is often oedema of the surrounding area without generalised swelling of the whole limb.
cord-like mass palpable
An important sign that can distinguish superficial vein thrombosis (SVT) from other causes of leg swelling and redness. Remains palpable for several weeks to months after the initial episode of SVT.
development of symptoms over hours to days
Symptoms of superficial vein thrombosis typically develop over hours to days and resolve in days to weeks.
signs/symptoms of concomitant DVT or PE
The prevalence of concomitant deep vein thrombosis (DVT) varies widely in the literature from 2.6% to 65.0%; one meta-analysis of 4358 patients with superficial vein thrombosis (SVT) reported a concomitant DVT in 18.1% of cases.[40] Where present, DVT is thought to be contiguous with SVT in 50% to 75% of cases. Concomitant DVT may not be contiguous with the SVT and may be in the contralateral limb.[42] When the DVT is non-contiguous, the mechanism of DVT occurrence is probably related to a hypercoagulable state.
Concomitant symptomatic pulmonary embolism (PE) can occur in 0.5% to 4.0% of patients with SVT and symptoms of PE.[43] Hence it is important to elicit history for PE symptoms such as dyspnoea, chest pain, and syncope. Asymptomatic PE may be more common (detected in 20% to 33% of patients with SVT in the thigh in one small study).[58]
Other diagnostic factors
common
varicose veins
history of thrombophilic disorders
Abnormalities of coagulation are associated with superficial vein thrombosis (SVT), especially among patients with spontaneous SVT without varicose veins.
autoimmune diseases (e.g., Behcet's and Buerger's disease)
Behcet's disease and Buerger's disease are frequently associated with superficial vein thrombosis. The proposed pathogenic mechanism in both disorders involves mainly immune-mediated endothelial cell dysfunction.
recent vein instrumentation (e.g., sclerotherapy)
recent vein cannulation and intravenous drug administration
Superficial vein thrombosis can occur as a result of cannulation of superficial veins of the upper or lower limbs, and by irritant drugs or solutions delivered through the catheter.
low-grade fever
May be present in some cases.
pigmentation changes
Pigmentation changes of the skin overlying the superficial vein thrombosis are often observed.
Risk factors
strong
varicose veins
Varicose veins are the most frequent cause of superficial vein thrombosis (SVT). Up to 80% of patients with SVT of the lower limbs have pre-existing varicose veins with or without chronic venous insufficiency.[8][13][14]
The great saphenous vein is involved in 60% to 80% of cases, and the small saphenous vein is involved in 10% to 20%.[15] SVT is more frequently found in varicose tributaries of the saphenous veins rather than the saphenous trunk.[13] The incidence of SVT in the anterior accessory saphenous vein is higher than in the great saphenous vein at 6.41% and 2.17%, respectively.[16]
Venous stasis is thought to be important in the development of SVT in varicose veins.
thrombophilic disorders
Abnormalities of coagulation are associated with superficial vein thrombosis (SVT), especially among patients with spontaneous SVT without varicose veins, or involving the greater saphenous vein trunk. Clinically diagnosed SVT is weakly associated with thrombophilia.[17]
One observational study found that 76.6% of patients with SVT in non-varicose veins had a thrombophilia.[18] Factor V Leiden mutation is the most common thrombophilia associated with SVT, with a prevalence of 51.6% in one study.[18] Factor II (prothrombin) mutation, MTHFR mutation, and deficiencies in protein C, protein S, and antithrombin have also been associated with SVT.[18][19][20]
The presence of anticardiolipin antibodies, increased levels of factor VIII, and factor II mutations have been linked to an increased risk of recurrent SVT.[21][22][23]
autoimmune diseases (e.g., Behcet's and Buerger's disease)
Behcet's disease and Buerger's disease are frequently associated with superficial vein thrombosis (SVT). The proposed pathogenic mechanism in both disorders involves mainly immune-mediated endothelial cell dysfunction.
Behcet's disease is an autoimmune vasculitis disorder that is frequently associated with venous vascular complications. Among patients with Behcet's disease, up to 53% of patients will experience an SVT episode.[24] It is usually observed within 5 years of the diagnosis of Behcet's, and rarely precedes the diagnosis.
Buerger's disease is a non-atherosclerotic vascular disease (also known as thromboangiitis obliterans) and is characterised by segmental vascular inflammation, vaso-occlusive phenomena, and involvement of small- and medium-sized arteries and veins of the upper and lower extremities.[9] SVT and, more commonly, migratory SVT, are thought to occur in up to 27% to 50% of patients with Buerger's disease.[9]
prior history of superficial vein thrombosis (SVT)
Risk of recurrence is dependent on patient-specific factors such as the presence of malignancy or a persistent risk factor, such as varicose veins. After a first thrombotic episode of confirmed lower limb SVT in patients with no history of deep vein thrombosis (DVT), varicose veins, malignancy, or autoimmune disorders, up to 32% of patients developed DVT at a median elapsed interval of 4 years and 24% had recurrent episodes of SVT.[25]
female sex
sclerotherapy
Sclerotherapy, through the injection of a sclerosant or foam into varicose veins, provokes direct vessel wall damage, causing transmural wall damage, the subsequent generation of a local thrombus, and eventual transformation of the thrombosed vein into a fibrous cord. The endpoint of this process is functionally analogous to surgical removal of a vein. As a result, superficial vein thrombosis (SVT) is a normal and expected occurrence following sclerotherapy. However, in rare instances post-sclerotherapy thrombophlebitis may develop, usually occurring within 1 to 2 weeks after the treatment of larger vessels (typically >1 mm in diameter).[26]
The incidence of post-sclerotherapy SVT varies according to technique and type of sclerosant and has been reported to be as high as 6%.[27]
SVT and deep vein thrombosis have also been described following endovenous thermal and chemical ablation of varicose veins.[28]
intravenous catheterisation
Largely exclusive to upper-limb superficial vein thrombosis (SVT) rather than lower-limb SVT. Nonetheless, SVT can occur as a result of cannulation of superficial veins of the lower limbs, and by irritant drugs or solutions delivered through the catheter.
malignancy
One prospective study of consecutive ambulatory cancer patients (n=150, free of venous thromboembolism symptoms at baseline) reported superficial vein thrombosis (SVT) incidence of 9% during 9-month follow-up, despite low molecular weight heparin therapy.[29] Small retrospective cohort studies report that, among patients with SVT, 10% to 15% may have a diagnosis of malignancy.
Trousseau's syndrome (migratory superficial vein thrombophlebitis) is rare and is characterised by recurrent and migratory SVT, frequently in unusual sites such as the arm or chest (also called Mondor's disease when involving chest wall veins). It is most often associated with adenocarcinomas, especially pancreatic, lung, gastric, and prostate cancer.
Malignancy-mediated activation of the coagulation cascade and malignancy-derived procoagulant factors are thought to be important in the development of SVT.
weak
pregnancy
There is limited information on the association of pregnancy and superficial vein thrombosis (SVT). A nationwide cohort study in Denmark reported an SVT incidence of 0.6 per 1000 person-years from conception to 12 weeks postpartum, with the highest incidence (1.6 per 1000 person-years) during the postnatal period.[30] Increased age, parity, and hypertension are predisposing risk factors.[9][12][31]
Pregnancy-related changes such as increase in procoagulant factors and reduced fibrinolytic activity may explain the increased risk during pregnancy, particularly in the puerperium. In addition, the pronounced vein dilation (and resulting stasis), particularly in the third trimester, is also a predisposing factor for SVT during pregnancy.
use of oral contraceptives (OCPs) and hormonal replacement therapy
There appears to be a 2- to 6-fold increased relative risk of venous thrombotic events (including superficial vein thrombosis [SVT]) among OCP users and a 2- to 4-fold increased risk among oral HRT users.[32] Moreover, there is a suggestion that, among women who take an OCP, the risk of deep vein thrombosis is higher in those women with a history of SVT than those without.[33]
OCPs that contain third-generation progestins are associated with a greater risk than those that contain second-generation progestins.
older age
Incidence increases with age, with a rate of 0.73 per 1000 person-years among those aged below 40 years and 2.95 per 1000 person-years among those aged >80 years in one study.[4]
history of prior venous thromboembolism (VTE), including deep vein thrombosis and PE
In one study of patients with confirmed first spontaneous VTE (and without varicose veins, malignancy, or autoimmune disorders), superficial vein thrombosis (SVT) developed in 7.3% of patients over an average follow-up of 30 months.[21] Patients with a first spontaneous VTE and subsequent SVT were at 2-fold increased risk of recurrent VTE compared with patients with a first spontaneous VTE without subsequent SVT.[21]
obesity
Being overweight is recognised as a weak risk factor for the development of VTE.[34][35][36] With regard to superficial vein thrombosis (SVT), a 2.6-fold increased risk of SVT has been reported in overweight (BMI ≥28 kg/m²) patients when compared with patients with a BMI <28 kg/m², independent of the presence of varicose veins.[37]
Obesity predisposes to venous stasis and is associated with haemostatic changes.[38]
prolonged immobilisation (e.g., long-haul air travel)
The role of long-haul flight in the development of superficial vein thrombosis (SVT) is unclear and it is probably associated with only a small percentage of SVTs.
blood type
In one study, patients with a non-O blood group had a 1.3-fold increased risk for superficial vein thrombosis when compared to type O patients.[17]
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