Varicose Veins — Causes, CEAP Classification, Endovenous Ablation & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Varicose veins are permanently dilated, elongated, and tortuous superficial veins — most commonly affecting the great saphenous vein (GSV) and its tributaries in the medial thigh and calf, or the small saphenous vein (SSV) in the posterior calf. They result from incompetent venous valves that fail to prevent retrograde blood flow (venous reflux) during standing or ambulation, causing venous hypertension in the superficial venous system and progressive vein wall dilatation. Varicose veins are extremely common — affecting approximately 30% of women and 15% of men in developed countries, making chronic venous disease the most prevalent vascular condition. They are classified using the CEAP (Clinical, Aetiological, Anatomical, Pathophysiological) classification: C0 (no visible venous disease) to C6 (active venous ulcer). Beyond cosmesis, symptomatic varicose veins cause aching leg pain (particularly after prolonged standing), heaviness, swelling, night cramps, pruritus, and in advanced disease (CEAP C4-C6), chronic venous insufficiency with skin changes (lipodermatosclerosis, haemosiderin deposition, atrophie blanche) and venous leg ulceration — the most severe complication, affecting 1-2% of adults over 60 with a prevalence of 1 per 100,000 population. NICE Technology Appraisal 232 (2013, updated 2023) recommends endovenous thermal ablation (laser or radiofrequency) as the first-line treatment for eligible patients with symptomatic varicose veins — a significant advance over the historical gold standard of surgical high tie and strip under general anaesthesia.

The primary pathophysiological mechanism is incompetence of the venous valves — the bicuspid valves within the superficial and deep venous system that normally permit only unidirectional (antegrade, upward) blood flow toward the heart. When these valves become incompetent, retrograde venous reflux occurs during standing, causing blood to pool in the dependent superficial veins. Elevated venous pressure over time leads to structural changes in the vein wall — smooth muscle hypertrophy, collagen remodelling, and wall weakening — causing progressive dilatation. The great saphenous vein (GSV) is most commonly affected — incompetence typically begins at the sapheno-femoral junction (SFJ) at the groin where the GSV joins the femoral vein, then propagates distally. Reflux can also occur in the small saphenous vein (SSV) at the sapheno-popliteal junction (SPJ) behind the knee. Risk factors: female sex (2:1 ratio — oestrogen and progesterone promote venous smooth muscle relaxation and valvular incompetence); pregnancy (the most important precipitating factor — increased circulating blood volume, inferior vena cava compression by the gravid uterus raising venous pressure, and hormonal effects; varicose veins worsen with each pregnancy; venous reflux may partially improve postpartum but valvular damage is often permanent); positive family history — first-degree relatives of affected individuals have 3-4-fold higher risk (autosomal dominant inheritance with variable penetrance; mutations in FOXC2 gene in hereditary lymphoedema-distichiasis also cause varicose veins); obesity (BMI above 30 — increases intra-abdominal pressure and venous back-pressure); prolonged standing occupation (nurses, teachers, chefs, shop assistants — gravitational venous hypertension accelerates valve damage); increasing age (progressive loss of venous wall elasticity and valve competence); deep venous thrombosis (DVT) — post-thrombotic syndrome causes valvular destruction and secondary varicose veins; constipation and raised intra-abdominal pressure (Valsalva manoeuvres repeatedly transmitted to femoral veins).

Symptoms of varicose veins are related to venous hypertension in the superficial venous system. Visible signs: dilated, tortuous, dark blue or purple veins visible beneath the skin surface — typically along the medial thigh and calf (GSV distribution) or posterior calf (SSV); may be palpable as thick, ropey, or knobbly cords. Thread or spider veins (telangiectasia and reticular veins — CEAP C1) are smaller, intradermal, and not true varicose veins. Symptoms: aching, throbbing, or heavy leg pain — typically worse after prolonged standing or sitting with legs dependent, improved by elevation; ankle swelling and pitting oedema — most pronounced at the end of the day; night cramps (particularly in the calf — nocturnal muscle cramps from venous congestion); pruritus (itching) over the varicosities or the gaiter area (lower leg) from venous eczema and haemosiderin deposition; restless legs; and skin changes in advanced chronic venous insufficiency: lipodermatosclerosis (firm, woody induration of the lower leg skin — from panniculitis and fibrin deposition around dermal capillaries); haemosiderin hyperpigmentation (brown-bronze staining of the gaiter area skin from red blood cell extravasation and haemoglobin degradation); atrophie blanche (white, atrophic, scar-like areas surrounded by hyperpigmentation — indicates severe chronic venous hypertension); and venous eczema (varicose or stasis eczema — inflamed, scaly, weeping skin overlying varicose veins or the gaiter area). Complications (CEAP C5-C6): superficial thrombophlebitis (thrombosis in a varicose vein — local pain, erythema, induration along the vein, low-grade fever); bleeding from a varicose vein (from trauma or spontaneous rupture — capillary pressure can cause significant bleeding in elderly patients on anticoagulation); venous leg ulcer (CEAP C6 — persistent, non-healing ulcer in the gaiter area, typically above the medial malleolus — a chronic wound requiring specialist management).

Clinical assessment: careful history of symptom duration, severity, impact on quality of life (AVVQ — Aberdeen Varicose Vein Questionnaire — validated patient-reported outcome measure for assessing varicose vein impact), risk factors, previous treatments, and family history. Venous clinical examination: inspect both legs in standing position — identify varicosities, their distribution (GSV vs. SSV territory), CEAP classification, and associated skin changes. Tap (percussion) test and cough impulse test to assess saphenous vein incompetence (historical — superseded by duplex ultrasound). Handheld Doppler: bedside assessment of retrograde flow at the sapheno-femoral junction (SFJ) and sapheno-popliteal junction (SPJ) with the patient standing — augmentation and subsequent reflux sounds on release of manual compression confirm valvular incompetence. Duplex ultrasound (colour Doppler ultrasound): the definitive diagnostic investigation — provides anatomical mapping of the great and small saphenous veins, identifies sites of valvular incompetence (SFJ, SPJ, perforator incompetence), measures reflux duration (pathological reflux defined as above 0.5 seconds in superficial veins), assesses deep venous system patency and competence (important before treating superficial reflux — if deep venous system is occluded and superficial system is the primary outflow, ablating superficial veins may worsen venous outflow). Required before all interventional treatments. CEAP classification based on clinical and haemodynamic assessment: C0 — no visible disease; C1 — spider/thread veins; C2 — varicose veins; C3 — oedema; C4a — skin changes (pigmentation, eczema); C4b — lipodermatosclerosis, atrophie blanche; C5 — healed ulcer; C6 — active ulcer. ABPI (ankle-brachial pressure index): essential before applying compression therapy — ABPI below 0.8 is a contraindication to high-grade compression (risk of limb ischaemia).

Conservative management: lifestyle measures and compression hosiery are appropriate for mild varicose veins or patients not eligible or not wishing for intervention. Compression stockings (class 2 — 18-24 mmHg; class 3 — 25-35 mmHg) reduce venous hypertension, improve symptoms, reduce oedema, and slow skin deterioration — they do not treat the underlying reflux. Regular leg elevation; weight loss; exercise (walking promotes calf muscle pump action, improving venous return). Interventional treatment — NICE TA232 (2013, updated 2023) recommends: endovenous thermal ablation as first-line treatment for symptomatic varicose veins due to GSV or SSV reflux. Endovenous laser ablation (EVLA): a laser fibre is introduced into the GSV or SSV under ultrasound guidance and local tumescent anaesthesia; laser energy (810-1470 nm) is delivered as the fibre is slowly withdrawn — heating the vein wall causing collagen denaturation and permanent vein occlusion; day-case procedure (30-60 minutes); return to normal activity within 1-3 days; treated vein absorbed within weeks; 90-95% anatomical closure at 1 year; comparable outcomes to surgical stripping with faster recovery and fewer complications. Radiofrequency ablation (RFA — ClosureFAST system): uses radiofrequency energy (120 degrees Celsius) delivered in 20-second treatment cycles along the vein — similar efficacy to EVLA; slightly less post-procedure bruising. Mechanochemical ablation (MOCA — ClariVein): combines a rotating wire (mechanical damage to the vein wall) with sclerosant injection (polidocanol) — requires no tumescent anaesthesia; suitable for patients unable to tolerate infiltration. Foam sclerotherapy: ultrasound-guided injection of foam sclerosant (sodium tetradecyl sulfate or polidocanol foam — mixture of sclerosant and air or CO2 at 1:4 ratio) into the target vein causing endothelial damage, thrombosis, and fibrosis; suitable for smaller veins, residual veins after ablation, and as an alternative first-line for patients not suitable for thermal ablation; 80-85% initial closure rates, somewhat lower long-term than thermal ablation. Surgical high tie, ligation, and stripping: historically the gold standard — high tie of the SFJ or SPJ under general or spinal anaesthesia followed by stripping of the GSV using a stripper device; now reserved for patients unsuitable for endovenous techniques or complex recurrent disease. Avulsions/phlebectomy: ambulatory phlebectomy (multiple stab avulsions under local anaesthesia) for large tributary veins not amenable to ablation — typically combined with or following truncal vein ablation. Venous leg ulcer treatment: high-compression bandaging (4-layer or equivalent — reduces ambulatory venous pressure); wound debridement; moist wound dressings; treatment of associated infection; early vascular surgical referral for EVLA to reduce ulcer healing time and recurrence (NICE-endorsed following EVRA trial evidence — venous ablation within 2 weeks of ulcer presentation significantly reduces healing time).

Superficial thrombophlebitis: thrombosis within a varicose vein segment — causes painful, firm, erythematous cord along the course of the affected vein; most cases are managed with NSAIDs and compression; ultrasound is important to exclude DVT propagation and assess proximity to the sapheno-femoral junction (within 3-4 cm — increased DVT risk; requires fondaparinux or low molecular weight heparin anticoagulation). DVT extension from superficial thrombophlebitis occurs in approximately 20% of cases. Variceal haemorrhage: spontaneous or traumatic bleeding from a thinned varicosity — can be surprisingly profific; immediate management: lie the patient down, elevate the leg, apply firm local pressure. Venous leg ulceration (CEAP C6): the most severe complication — affects 1-2% of the adult population; venous ulcers are the most common cause of chronic leg ulceration (70% of all leg ulcers); they are chronic, recurrent, and significantly impair quality of life; healing requires sustained high-grade compression bandaging and definitive treatment of the underlying venous reflux. Treatment complications after EVLA or RFA: bruising and discomfort along the treated vein (expected — resolves 1-4 weeks); thermal skin burns (rare with adequate tumescent anaesthesia); nerve injury (paraesthesia in the saphenous nerve distribution after GSV ablation — affects up to 10%, typically temporary); DVT (1-5% — prophylactic LMWH and early mobilisation reduce risk); endovenous heat-induced thrombosis (EHIT) in the femoral vein (rare, 0.3% — requires anticoagulation). Recurrence: 20-30% of treated patients develop symptomatic recurrence of varicose veins within 5-10 years — from new valve incompetence, recanalisation, or neovascularisation at the treated junction site.

Regular physical activity — particularly walking, cycling, and swimming — activates the calf muscle pump (the gastrocnemius and soleus muscles propel venous blood from the deep calf veins toward the heart during contraction), significantly reducing ambulatory venous hypertension and the rate of varicose vein progression; 30 minutes of daily walking is the most cost-effective preventive measure. Maintain a healthy body weight: obesity (BMI above 30) substantially increases intra-abdominal pressure, venous back-pressure, and the rate of valvular degeneration — weight loss in obese patients with varicose veins reduces symptom severity and venous hypertension. Avoid prolonged uninterrupted standing: take regular movement breaks (calf raises, short walks every 30-60 minutes) if occupation requires prolonged standing; calf raises (rising onto the toes repeatedly — 20-30 repetitions) are particularly effective for activating the calf muscle pump during long periods of standing. Elevate the legs when resting: raising the legs above the level of the heart (lying with legs propped on pillows or using a recliner) promotes venous drainage and reduces oedema — beneficial for symptomatic relief and in preventing progression. Compression hosiery: graduated compression stockings (class 2 — 18-24 mmHg minimum) worn during waking hours provide sustained reduction in venous hypertension and are recommended for all patients with symptomatic varicose veins awaiting intervention, and for long-distance travel (economy class syndrome prevention). During pregnancy: early use of prescription-grade maternity compression hosiery reduces varicose vein progression and associated symptoms. Avoid tight-fitting garments that constrict at the thigh (tourniquets to venous return). After varicose vein treatment: continued compression hosiery for 2-6 weeks following thermal ablation improves vein closure rates; long-term maintenance of a healthy weight and regular exercise minimises recurrence risk.

Go to A&E immediately for: uncontrolled bleeding from a ruptured varicose vein — lie down, elevate the leg above the level of the heart, and apply firm pressure; most variceal haemorrhage stops with local pressure and elevation; if bleeding is profuse or uncontrolled, emergency care is required; and leg swelling, pain, and redness with warmth and tenderness — possible deep venous thrombosis (DVT) requiring same-day D-dimer test and venous duplex ultrasound. See a GP for: symptomatic varicose veins causing aching, swelling, or skin changes that affect quality of life or daily activities; any skin changes over the lower leg (pigmentation, thickening, eczema, or an open wound) — these indicate advanced chronic venous disease (CEAP C4-C6) that requires prompt vascular assessment to prevent venous ulceration; and superficial thrombophlebitis (red, tender, firm cord along a varicose vein) — requires assessment with ultrasound to exclude DVT and determine if anticoagulation is needed. NICE NG168 (2020) provides criteria for NHS referral for treatment of varicose veins: any patient with symptomatic varicose veins (aching, swelling, skin changes, or previous superficial thrombophlebitis) should be referred to a vascular service for consideration of endovenous treatment. Cosmetic varicose vein treatment without symptoms is not funded by the NHS. For pregnancy-related varicose veins: most improve after delivery — defer referral until 3 months postpartum to allow assessment of spontaneous improvement before deciding on intervention.