Approach
A diagnosis of superficial vein thrombosis (SVT) is established primarily on the basis of clinical signs: pain, tenderness, induration, warmth, erythema, and/or a palpable cord along the course of a superficial vein.[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].
Duplex ultrasound is recommended to exclude concurrent deep vein thrombosis (DVT), to confirm the clinical diagnosis of SVT, and to show thrombus extension and proximal thrombus location in reference to the saphenofemoral and saphenopopliteal junctions.[1] Doppler ultrasonography may also help in the presence of a difficult differential diagnosis that may include cellulitis, erythema nodosum, and lymphangitis.
History
Patients with SVT often report the gradual onset of localised pain followed by the appearance of an area of redness along the course of a superficial vein. Some report constitutional symptoms such as low-grade fever; high fever and purulent discharge suggest septic (infected) thrombophlebitis. Septic thrombophlebitis, which most often occurs as a result of bacterial entry from an intravenous catheter, may be associated with bacteraemia and severe systemic infection that can lead to shock.
Symptoms of SVT typically develop over hours to days and resolve in days to weeks. Pigmentation changes of the skin overlying the SVT are often observed. The cord may remain palpable for several weeks to months after an initial episode of SVT. In a patient with varicose veins, there may be a history of local trauma. Other known risk factors of SVT should be elicited. Strong risk factors include a history of varicose veins, thrombophilic disorders, autoimmune diseases, sclerotherapy, intravenous catheterisation, and a previous history of SVT.
Examination
On physical examination, in a patient with pre-existing varicose veins, there is a tender 'worm-like' mass deep to the skin. The overlying skin is warm and erythematous, and there is often oedema of the surrounding area, without generalised swelling of the whole limb. In a patient without varicose veins, there is often a palpable cord, sometimes nodular, associated with warmth, tenderness, and erythema along the course of a non-varicose superficial vein. Erythema and oedema may extend for some distance into the surrounding tissue, making distinction from cellulitis difficult.
Notably, it is notoriously difficult to predict the proximal extent of the thrombus during the physical examination, especially as the axial superficial veins become less superficial as they approach the inguinal region.
Concomitant deep vein thrombosis or pulmonary embolism
It is important to examine for the presence of underlying DVT, because risk of thrombus propagation extends beyond the period when local signs and symptoms of SVT predominate.[39] The prevalence of concomitant DVT varies widely in the literature from 2.6% to 65.0%; one meta-analysis of 4358 patients with SVT reported concomitant DVT in 18.1% of cases.[40] Where present, DVT is thought to be contiguous with SVT in 50% to 75% of cases. The thrombus extends by contiguity to the deep venous system through the saphenofemoral or saphenopopliteal junctions, or, less commonly, through the perforating veins.[41]
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 also 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.
Infected SVT
Signs of infected SVT may be present, usually when the SVT is the result of vein instrumentation or cannulation, and can include high fever, frank pus at the site of injection or cannulation, and lymphangitis.
Suspected arterial insufficiency
In patients with suspected arterial insufficiency by history and/or physical examination, an assessment of the ankle-brachial pressure index should be performed prior to the prescription of compression stockings.
Doppler ultrasound investigation
Although the diagnosis of SVT is primarily clinical, duplex ultrasound is recommended for all patients to exclude concurrent ipsilateral DVT, to confirm the clinical diagnosis of SVT, and to show thrombus extension and proximal thrombus location in reference to the saphenofemoral and saphenopopliteal junctions.[1] Ultrasound of the contralateral limb at the time of diagnosis is reserved for patients with symptoms or those at high risk for thrombosis, such as in patients with hypercoagulable state.[44]
Clinical examination does not always reveal the true extent of the SVT; surgical exploration often shows extension of the thrombotic process 5-10 cm higher than the level that was clinically suspected.[45]
Systematic Doppler ultrasonography reveals a large number of DVTs concomitant with SVT (between 5.6% to 36.0%).[14][46][47][48][49][50] Variability can be explained by differences between studies with regard to the definition of DVT (i.e., proximal or distal, with or without muscular vein involvement). Doppler ultrasonography has been shown to be highly sensitive (>95%) and specific (>95%) to diagnose symptomatic and asymptomatic proximal vein DVT.[51][52] The sensitivity and specificity for SVT is not known.
Several studies have shown that the risk of progression to DVT is higher when the SVT is present in the proximal greater saphenous vein or the saphenofemoral junction.[53][54][55] Factors proposed to predict underlying DVT include: male sex, history of DVT, short interval between onset of symptoms and diagnosis, and severe chronic venous insufficiency.[56]
Greater saphenous vein SVT, bilateral SVT, age >60 years, and bed rest have been suggested as high-risk factors for underlying DVT but not confirmed.
Further investigations
A biopsy should be ordered in SVT cases that are recurrent and/or migratory, and when inflammatory diseases such as polyarteritis nodosa are being considered. This is best accomplished by an elliptical incision transverse to the long axis of the vessel rather than a punch biopsy. Small vessels in the superficial dermis are characteristically spared.[57]
Further evaluation for underlying venous thromboembolism risk factors
Includes thrombophilia screening and assessment for underlying malignancy. This is indicated in patients with the following:
SVT not associated with varicose veins
Extensive saphenous vein thrombosis on Doppler ultrasonography with or without concomitant DVT or PE
Recurrent SVT
Idiopathic SVT
It can also be considered for patients with an above-knee SVT, but this may not be necessary for patients with large varicose veins/superficial venous incompetence and a first-time above-knee SVT.
It should be noted, however, that the utility and cost-effectiveness of screening for thrombophilic states in patients with SVT has not been well studied. Thrombophilia screening includes testing for the presence of factor V Leiden and prothrombin G20210A genetic variants; deficiencies of protein S, C, and antithrombin III; positive lupus anticoagulant and anticardiolipin antibodies; and hyperhomocysteinaemia.
Suspected pulmonary embolism
In patients with suspected SVT with concomitant respiratory symptoms or signs of PE (chest pain, dyspnoea, syncope), pulmonary CT angiography or a ventilation perfusion scan to look for concomitant PE should be performed. If both tests are non-conclusive and PE is still suspected, then a conventional pulmonary angiogram is indicated. One study of patients with SVT in the thigh found that asymptomatic PE was common, detected in 20% to 33% by perfusion lung scan.[58]
Clinical and Doppler ultrasonography follow-up
Patients with SVT involving varicose veins and patients with a clear reason for the SVT (e.g., intravenous cannulation, sclerotherapy, oral contraceptive pill use) likely need no further diagnostic workup, but follow-up is recommended for all patients until the SVT resolves and for at least 3 months following treatment. See Monitoring.
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