Superficial vein thrombosis

Superficial vein thrombosis (SVT) is most often associated with prothrombotic conditions characterised by one or more of the components of the Virchow triad: vessel wall damage (catheterisation, intravenous drugs, sclerotherapy, inflammatory vascular diseases); stasis (varicose veins, immobilisation); and hypercoagulability (oral contraceptive medicines, inherited or acquired thrombophilia).

The aetiological diagnosis depends partly on the location of the SVT. For SVT of the lower limbs, the main cause remains varicose veins.[1][8] Varicose vein SVT is typically a mild condition, provided it is not saphenous, caused primarily by the slowing of blood flow in a dilated varicose vein in patients with venous disease.[3] Local trauma to a varicose vein is often a precipitating factor.

Non-varicose vein SVT is a heterogeneous group with a variety of possible underlying causes.[3] Autoimmune diseases (especially Behcet's and Buerger's disease), malignancy, and thrombophilia need to be identified or ruled out as causes in idiopathic, migrant, or recurrent SVT, and in the absence of varicose veins.[9]

For SVT of the upper limbs and the neck, the main cause consists of iatrogenic interventions such as intravenous catheters or infusion of drugs (chemotherapy, drug addiction).[10] Mondor's disease, which primarily affects superficial veins of the chest wall and breast in women, is idiopathic in most cases but can sometimes be associated with high-intensity exercise or trauma, and, on rare occasions, with breast cancer or thrombophilia.[11]

Thrombus formation in the vein is likely to be the result of interplay between the damaged vessel, the coagulation cascade, the fibrinolytic system, platelet activation, and activation of the inflammatory process.[12] However, the specific relation between these processes, particularly the coagulation and inflammatory cascades, remains unclear.

Vessel wall damage, whether due to cannulation of a vein or direct trauma to a varicose vein, may trigger a prostaglandin-mediated activation of the inflammatory cascade as well as platelet activation and accumulation.[12] At sites where the endothelium is severely inflamed (e.g., as a result of vessel wall damage or underlying autoimmune disorders), clotting intermediates are activated and accumulate; combined with stasis, this can initiate thrombosis. Histopathological studies of veins with SVT demonstrate swelling of endothelial cells, leukocyte infiltration of the vein wall, and other changes consistent with inflammation, along with fibrin deposition and thrombus formation.[12]

Association with varicose veins[2][3]

Varicose vein (VV)-SVT: primary SVT in a patient with venous disease, which is followed by sterile inflammation of the vein wall. It is typically a mild condition provided it is not saphenous. Slowing of blood flow in a dilated varicose vein is thought to be the most important causative factor.
Non-varicose vein (NV)-SVT: SVT in patients without venous disease. NV-SVT is a heterogenous group where either inflammation or thrombosis may dominate depending on the underlying cause. It can occur on any superficial vein.

Pathophysiology

Classification

Association with varicose veins[2][3]