Management of Superficial Vein Thrombosis

Superficial vein thrombosis (SVT), indicating thrombosis of the superficial vein system, is less well-studied than deep vein thrombosis (DVT) because it has been considered a minor, self-limiting disease, easily diagnosed on clinical grounds, and deserving only symptomatic relief. The most frequently affected area of the superficial vein system are the lower limbs, especially the long and short saphenous vein, mostly in relation to varicose veins. The incidence of SVT of the lower limbs is estimated to be approximately 0.64 out of 1,000 per year in primary care, which is a lower incidence than that of venous thromboembolism (VTE), which is estimated to be 1 out of 1,000 per year. Lower limb SVT shares the same risk factors as DVT, such as advanced age, obesity, active cancer, previous thromboembolic episodes, pregnancy, oral contraceptives, hormone replacement therapy, recent surgery, and auto-immune diseases (particularly Behçet’s and Buerger’s diseases).It can propagate into the deep veins and have a complicated course with pulmonary embolism.Clinical diagnosis may not be accurate and presently ultrasonography is indicated for both confirmation and evaluation of SVT extension and exclusion of concomitant DVT. No validated diagnostic algorithms are available for SVT of the lower limbs. As a result, the approach to SVT diagnosis in clinical routine is variable and dependent on local sources; unlike DVT diagnosis, objective testing may still be considered neither mandatory nor urgent. Studies conducted on D-dimer diagnostic accuracy for SVT are few, with a high false negative rate. Treatment aims are symptom relief and prevention of VTE in relation to the thrombotic burden. SVT of the long saphenous vein within 3 cm of the sapheno-femoral junction (SFJ) is considered equivalent to DVT and thus deserving therapeutic anticoagulation. Less severe forms of SVT of the lower limbs not involving the SFJ have been included in randomised clinical trials of surgery, compression hosiery, non-steroidal anti-inflammatory agents, unfractionated heparin, and low molecular weight heparins (LMWH) with inconclusive results. The largest randomised clinical trial available, including 3,004 patients with lower limb SVT not involving SFJ, showed that fondaparinux 2.5 mg once daily for 6 weeks is more effective than placebo in reducing the risk of the composite endpoint of death from any cause and symptomatic VTE (0.9% versus 5.9%). The second largest study, STEFLUX, in 664 patients showed that LMWH, parnaparin, at 8,500 UI aXa (anti-factor Xa activity) once daily for 10 days followed by 6,400 UI aXa once daily for 20 days is effective and safe for the treatment of lower limb SVT. Inherited thrombophilic alterations have a similar frequency in SVTs when compared with DVT, however there are no data to indicate that the presence of thrombophilia should alter the management or influence rates of SVT recurrence or progression. No data are available on the best treatment of Trousseau’s syndrome, which is a recurrent and migratory pattern of inflammation of superficial veins in cancer. No studies are available either on the optimal treatment of cancer-associated SVT or screening for an occult malignancy after SVT. Pregnant women have usually been excluded from studies of SVT treatment, but pregnancy is a risk factor for both VTE and SVT. Unfractionated heparin and LMWH do not cross the placenta and are the agents of choice for treatment in pregnancy. Further studies are needed to define the optimal management strategies of SVT of the lower limbs and other possible SVT sites, such as the upper limbs, abdominal or thoracic wall, penis, or neck.