The varicose veins are not inherently dangerous, but they can progress and lead to sometimes significant complications. The following situations represent the main identified risks.
1. Deep vein thrombosis (DVT) and venous thromboembolism (VTE).
Deep vein thrombosis (DVT), venous thromboembolism (VTE), and peripheral artery disease (PAD) are serious vascular disorders that can lead to potentially life-threatening complications. DVT occurs when a blood clot forms in a deep vein, most often in the legs. The varicose veins can promote the development of DVT, because the weakening of venous valves leads to venous stasis and slows blood flow. This stagnation makes blood more prone to clotting. Additionally, chronic venous disease is accompanied by low-grade inflammation of the vein wall, which also favors clot formation. The combination of disturbed blood flow and an inflammatory state thus contributes to DVT development. If part of the clot detaches, it can travel through the circulation and reach the lungs, causing a pulmonary embolism.
A large cohort study including 212,984 patients with varicose veins, compared to 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 common comorbidities. While this study does not establish a direct causal link, it shows that adults with varicose veins have a significantly greater burden of thrombotic and vascular events.
From a clinical perspective, the rapid onset or worsening of leg swelling, associated with redness, localized warmth, or the presence of a firm, tender cord in a patient with varicose veins, should prompt an urgent evaluation by venous Doppler ultrasound. This examination allows exclusion of deep vein thrombosis and quickly guides patient management.
2. Venous ulcers of the lower extremities 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 skin and microcirculatory damage. Before an ulcer appears, patients typically exhibit a sequence of skin changes, such as hyperpigmentation, dry, itchy, and inflamed skin similar to eczema. Over time, the subcutaneous tissues harden and contract (lipodermatosclerosis), and small white scar-like areas may appear (white atrophy).
These alterations result from a decrease in oxygen supply linked to elevated venous pressure and inefficient circulation, coupled with persistent inflammation. The skin, particularly around the medial ankle, then becomes thinner and more fragile. It can eventually crack and develop into a painful, slow-healing wound: the venous leg ulcer. These lesions often recur, severely impairing mobility and quality of life, and carry a significant risk of secondary infection.
Data from recent reviews have identified lower extremity venous ulcers as the most severe consequence of chronic venous disease, owing 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 slowed and turbulent blood flow in a dilated superficial vein promotes the formation of a clot. Varicose veins associated with longstanding venous reflux create an environment of stasis and endothelial irritation, rendering the superficial venous network particularly vulnerable. When a clot forms, the affected segment becomes painful, warm, red, and firm on palpation. Although this lesion often appears localized, the underlying biological process reflects a more systemic inflammatory and procoagulant activation. This is evidenced by elevated biomarkers such as D-dimer, thrombin–antithrombin complexes, and C-reactive protein. D-dimer is a fragment resulting from fibrin degradation, thrombin–antithrombin complexes indicate active coagulation, and elevated C-reactive protein signifies an underlying inflammatory state.
Clinical data show that superficial thrombophlebitis should not be considered 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 thrombosis involves the main trunks of the great or small saphenous vein, due to their communication with the deep venous system. Although less common, pulmonary embolism has also been reported in this context. These data underscore that superficial thrombophlebitis is both a complication of venous disease and a potential warning sign of deeper thrombotic involvement, warranting prompt evaluation and Doppler ultrasound.
These findings emphasize that superficial thrombophlebitis is both a complication of venous disease and a potential warning sign of deeper thrombotic involvement, warranting prompt evaluation with Doppler ultrasound.
4. Variceal bleeding.
Variceal bleeding occurs when increased venous pressure, combined with thinning of the overlying skin, leads to the spontaneous — or after minimal trauma — rupture of a dilated superficial vein. Although relatively rare, this complication is well documented. Initially, the bleeding may appear moderate, but the elevated pressure in these veins can lead to significant hemorrhage. Significant blood loss can cause dizziness, syncope, or even hemorrhagic shock in the most severe cases. Without treating the underlying vein, recurrences are possible, and the progressive weakening of the surrounding skin increases the risk of future episodes.