The varicose veins are not inherently dangerous, but they can progress and be accompanied by occasionally significant complications. The following situations correspond to the main identified risks.
1. Deep vein thrombosis (DVT) and venous thromboembolism (VTE).
Deep vein thrombosis (DVT), venous thromboembolism (VTE) and peripheral arterial disease (PAD) are serious vascular disorders that can lead to potentially fatal complications. DVT occurs when a blood clot forms in a deep vein, most commonly in the legs. The varicose veins can predispose to the development of DVT, as weakened venous valves lead to venous stasis, slowing blood flow. This stagnation renders the blood more susceptible to coagulation. In addition, chronic venous disease is accompanied by low-grade inflammation of the vein wall, which also favours clot formation. The combination of impaired blood flow and an inflammatory state thus contributes to the development of DVT. If a portion of the clot detaches, it can travel through the circulation and reach the lungs, causing a pulmonary embolism.
A large cohort study involving 212,984 patients with varicose veins, compared with an equally sized matched control group, demonstrated a clear association between varicose veins and the occurrence of serious vascular events. Over a median follow-up of 7 to 8 years, individuals with varicose veins had a fivefold increased risk of deep vein thrombosis (incidence of 6.55 versus 1.23 per 1,000 person-years). The risks of pulmonary embolism (0.48 vs 0.28 per 1,000 person-years) and peripheral arterial disease (10.73 vs 6.22 per 1,000 person-years) were also higher, although these associations may be partially influenced by shared comorbidities. While this study does not establish direct causality, it shows that adults with varicose veins bear a significantly greater burden of thrombotic and vascular events.
Clinically, the sudden onset or rapid worsening of leg swelling, combined with redness, localised warmth or the presence of a firm, tender cord in a patient with varicose veins should prompt urgent evaluation by venous Doppler ultrasound. This examination allows for the exclusion of deep vein thrombosis and the prompt guidance of patient management.
2. Venous ulcers of the lower limbs and chronic skin lesions.
Venous leg ulcers represent the most advanced and severe complication of chronic venous disease. They develop when prolonged venous hypertension leads to progressive lesions of the skin and microcirculation. Before an ulcer appears, patients typically present a series of skin changes, such as hyperpigmentation, dry, pruritic and inflammatory skin, similar to eczema. Over time, the subcutaneous tissues harden and retract (lipodermatosclerosis), and small whitish areas reminiscent of scars may appear (white atrophy).
These changes result from a decrease in oxygen supply linked to elevated venous pressure and inefficient circulation, combined with persistent inflammation. The skin, particularly around the medial ankle, becomes thinner and more fragile. It may eventually crack and develop into a slow-healing, painful wound: the venous leg ulcer. These lesions are often recurrent, markedly impair mobility and quality of life, and carry a significant risk of secondary infection.
Data from recent reviews identify lower limb venous ulcers as the most burdensome consequence of chronic venous disease, due to their high recurrence rates and significant long-term impact on healthcare.
3. Superficial thrombophlebitis and inflammation.
Superficial thrombophlebitis is a common inflammatory complication of varicose veins. It occurs when the slowing and turbulence of blood flow in a dilated superficial vein favour the formation of a clot. Varicose veins associated with longstanding venous reflux create an environment of stasis and endothelial irritation, making the superficial venous network particularly vulnerable. When a clot forms, the affected segment becomes painful, warm, red and firm on palpation. Although this condition often appears localised, the underlying biological process reflects a more global inflammatory and procoagulant activation. This is evidenced by an elevation of biomarkers such as D-dimer, thrombin–antithrombin complexes and C-reactive protein. D-dimer is a fragment resulting from clot breakdown, thrombin–antithrombin complexes attest to active coagulation, and elevated C-reactive protein indicates an underlying inflammatory state.
Clinical data show that superficial thrombophlebitis should not be regarded as a benign condition. In a large cohort of patients with varicose veins, approximately 7.2% developed superficial thrombophlebitis. The risk of extension is particularly high when the thrombus involves the main trunks of the great or small saphenous vein, owing to their communication with the deep venous system. Although less frequent, pulmonary embolism has also been reported in this context. These findings emphasise that superficial thrombophlebitis is both a complication of venous disease and a potential warning sign of deeper thrombotic involvement, warranting prompt assessment and Doppler ultrasound examination.
These findings emphasise that superficial thrombophlebitis is both a complication of venous disease and a potential warning sign of deeper thrombotic involvement, warranting prompt assessment and Doppler ultrasonography.
4. Variceal bleeding.
Bleeding from varicose veins occurs when increased venous pressure, coupled with thinning of the overlying skin, leads to the spontaneous — or minimal-trauma — rupture of a dilated superficial vein. Although relatively rare, this complication is well documented. Initially, the bleeding may appear moderate, but the high pressure in these veins can result in significant haemorrhage. A significant blood loss may lead to dizziness, syncope, or even haemorrhagic shock in the most severe cases. In the absence of treatment of the underlying vein, recurrences are possible, and progressive weakening of the surrounding skin increases the risk of further episodes.