Varicose Veins

Meet the patient

A 56-year-old nurse stands through every shift and comes home with heavy, aching calves and ankles that swell by evening and are normal by morning. Behind her left medial malleolus is a shallow, moist ulcer she has dressed herself for six months; the skin above it is brown and hard. She has never had the veins looked at.^[1][2]

The valve, the reflux, the gaiter

Varicose veins are permanently dilated, tortuous, elongated superficial veins of the leg measuring greater than or equal to 3 mm in diameter, distinct from reticular veins (1 to 3 mm) and telangiectases (less than 1 mm, "spider veins").^[4] They are the visible end-point of chronic venous disease, a continuum that runs from symptomless trunk veins through oedema, skin change and finally venous leg ulceration. The Edinburgh Vein Study, a cross-sectional survey of 1,566 adults aged 18 to 64, found that more than half of those with trunk varices reported at least one lower-limb symptom, refuting the once-common idea that varicose veins are merely a cosmetic problem.^[2]

The underlying lesion is almost always valvular incompetence. The single commonest site is the saphenofemoral junction (SFJ), where the great saphenous vein joins the common femoral vein in the groin; when its valve fails, high-pressure venous blood refluxes down the GSV. Less often the lesion is at the saphenopopliteal junction (SPJ), the perforator veins (Cockett, Boyd, Dodd), or — in secondary disease — at the deep vein valves themselves after a DVT.^[6][33]

A second distinction examiners reward: primary varicose veins (idiopathic valve and wall degeneration, the great majority) versus secondary varicose veins (post-thrombotic, post-traumatic, or congenital — Klippel–Trenaunay). The distinction changes management: a post-thrombotic limb with deep vein obstruction must never be stripped.^[27]

Classification

Varicose veins are classified three ways — by which vein is affected, by aetiology (primary versus secondary), and by the CEAP system, which encodes Clinical class, Etiology, Anatomy and Pathophysiology into a single descriptor. CEAP is the international language of venous disease and the single most examined fact on this topic.^[4][5]

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Epidemiology & Risk Factors

Varicose veins are among the commonest chronic diseases in adults. The Edinburgh Vein Study is the definitive population estimate: in 1,566 adults aged 18 to 64, the prevalence of trunk varices was 32 percent in women and 40 percent in men when measured by examination.^[1] Reviews report prevalence estimates from 2 to 56 percent in men and 1 to 60 percent in women, the spread reflecting differing definitions and measurement methods.^[3]

Risk factors fall into three groups — pressure load, wall weakness, and secondary damage:^[3]

• Age. Prevalence rises with each decade; valves degenerate and the vein wall loses elastic recoil. The Edinburgh study showed prevalence rising from under 20 percent in the twenties to over 50 percent in the sixties.
• Family history. A twin study found concordance of 67 percent in monozygotic versus 45 percent in dizygotic pairs, with heritability of liability estimated at 86 percent, and linkage to the FOXC2 region of chromosome 16.^[33] Age, family history and constipation were the factors most closely associated with chronic venous insufficiency in a 40,095-person Polish survey.^[3]
• Female sex and parity. The female excess is largely driven by pregnancy (progesterone relaxes venous smooth muscle; the gravid uterus obstructs pelvic venous return). Risk rises with each pregnancy. More than two pregnancies distinguished women with and without chronic venous insufficiency in the Polish survey.^[3]
• Obesity. Raises intra-abdominal pressure and reduces mobility of the calf pump. Obesity was strongly associated with chronic venous insufficiency in women in the Polish survey.^[3]
• Height and constipation. Taller stature and chronic constipation modestly increase risk; constipation was among the factors most closely associated with chronic venous insufficiency whatever the sex.^[3]
• Prior deep vein thrombosis. The cause of secondary (post-thrombotic) varicose veins; damaged deep vein valves allow reflux to be transmitted to the superficial system.^[35]
• Congenital. Klippel–Trenaunay syndrome, Parkes Weber syndrome, congenital valve agenesis.^[15]

^[27]

Pathophysiology

The unifying mechanism is ambulatory venous hypertension. In health, the superficial veins carry about 10 percent of lower-limb venous return at low pressure; the deep veins, surrounded by muscle, carry the rest. One-way bicuspid valves and the calf pump (the soleus and gastrocnemius squeezing the deep veins on each step) keep venous pressure at the ankle between 20 and 30 mmHg while walking. When valves fail, the system breaks down in a predictable cascade.^[1][4]

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The cascade, step by step:^[34]

1. Valve incompetence, usually at the SFJ. The valve leaflets no longer meet, so the column of blood between the heart and the ankle is continuous.
2. Reflux and venous pooling. On standing, blood flows retrograde down the GSV. The vein fills under hydrostatic pressure — at the ankle this can reach 80 to 90 mmHg.
3. Progressive dilation. The vein wall stretches, which separates the next valve's leaflets, which worsens reflux. This positive-feedback loop is why varicose veins progress rather than regress.
4. Perforator incompetence. High-pressure deep venous blood is forced outward through incompetent perforator veins (Cockett's below, Boyd's at the calf, Dodd's at the thigh) into the low-pressure superficial system. The superficial veins become "blown out" at these points.
5. Capillary leak and the fibrin cuff. Sustained venous hypertension opens endothelial gaps; plasma and red cells extravasate into the dermis. Fibrin precipitates as a pericapillary "cuff" that is thought to obstruct oxygen diffusion.
6. Haemosiderin deposition. Extravasated red cells lyse; haemoglobin breaks down to haemosiderin, which stains the skin the characteristic brown ("brawny") colour of chronic venous insufficiency. Biopsy studies show haemosiderin is always present in lipodermatosclerotic skin and ulcers, and no severe skin change occurs until iron overload develops.^[30]
7. Lipodermatosclerosis. Chronic inflammation and fibrin deposition fibrose the skin and subcutaneous fat into a hard, indurated, tender "inverted champagne-bottle" leg.
8. Atrophie blanche. Localised white scarred atrophy at sites of healed micro-infarcts.
9. Ulceration. Tissue hypoxia, inflammation and minor trauma finally break the skin — typically at the medial gaiter (above the medial malleolus) for GSV disease, or near the lateral malleolus for SSV disease.^[34]

Two specific syndromes follow from this anatomy. Primary varicose veins arise when healthy valves fail idiopathically — the picture above. Post-thrombotic syndrome arises after a DVT damages the deep vein valves; reflux and obstruction combine, the deep system fails, and the superficial veins dilate as a compensatory collateral pathway. Stripping them removes the patient's only escape route — the basis of the absolute rule never strip a post-thrombotic limb.^[35]

Worse on standing, relieved by walking

The Edinburgh Vein Study showed that the symptoms of varicose veins correlate poorly with the visible size of the vein: even small varices can ache, and large ones can be silent. The classical triad is visible tortuous veins, heaviness-aching that is worse on standing and at the end of the day, and skin change.^[2]

^{[2] [34]}

Atypical presentations that examiners test deliberately: the elderly patient with a non-healing "leg sore" that is in fact a venous ulcer with malignant change (Marjolin); the young pregnant woman with rapidly enlarging varicosities that largely regress post-partum; the post-DVT patient whose new varicosities are collaterals — not to be stripped; the patient with a Klippel–Trenaunay triad of varicose veins, limb hypertrophy and a port-wine stain (congenital). Each demands a different management decision.^[15][23]

Differential Diagnosis

Not every dilated leg vein is a primary varicose vein, and not every leg ulcer is venous. A short structured differential distinguishes the treatable from the dangerous.^[16]

^[16]

Less common but exam-worthy mimics include arthrogenic stasis (post-fracture or post-knee-replacement calf pump failure), heart failure and renal failure (bilateral pitting oedema without varices), lymphoedema (non-pitting, dorsum-of-foot involvement, Stemmer's sign positive) and vasculitic ulcer (small, painful, "punched-out", in autoimmune disease). Bilateral leg swelling without skin change is not primary varicose veins — look for a systemic cause.^[16]

Clinical & Bedside Assessment

The focused venous examination is performed with the patient standing (varices empty on lying and are missed). Bedside tourniquet tests are now largely historical — replaced by duplex ultrasound — but examiners still ask about them as a test of anatomical reasoning.^[27]

Inspection (standing): distribution of varicosities (medial equals GSV, posterior equals SSV, lateral equals non-saphenous or Klippel–Trenaunay), skin change (haemosiderin staining, eczema, lipodermatosclerosis, atrophie blanche), ulcer (site, size, base, edges), corona phlebectatica (fan of intradermal veins on the medial ankle — an early sign), saphena varix (soft, reducible, cough impulse-positive lump at the SFJ).^[34]

Palpation: tenderness along a varicose vein (thrombophlebitis), induration (lipodermatosclerosis), pitting oedema, temperature (cellulitis, arterial disease). Percussion/tap test (Cruveilhier–Baumgarten): tap the GSV at the SFJ — a palpable impulse transmitted distally through incompetent valves.^[34]

Bedside tourniquet tests (historical, superseded by duplex):^[27]

• Trendelenburg test. With the patient supine, elevate the leg to empty the veins. Apply a tourniquet at the SFJ level. Have the patient stand. If varices remain controlled, the SFJ is the point of reflux; release the tourniquet — rapid top-down filling confirms SFJ incompetence. If varices fill while the tourniquet is in place, the reflux is below the tourniquet (perforator disease).
• Perthe's test. Apply a tourniquet at mid-thigh and have the patient walk. If varices enlarge and the leg aches, the deep veins are obstructed and the superficial veins are functioning as collaterals — do not strip. If varices shrink, the deep veins are patent and the perforators are competent enough to allow safe ablation.
• Multiple tourniquet test (modified Trendelenburg). Three tourniquets (SFJ, mid-thigh, below-knee) localise the reflux level. ^[1]

Arterial check before any compression: palpate femoral, popliteal, posterior tibial and dorsalis pedis pulses; measure ABPI. Compression of a limb with undiagnosed arterial disease is a preventable cause of ischaemia and amputation.^[26]

Abdominal and pelvic examination: in any unusual or rapidly progressive presentation, exclude an iliac or pelvic mass (cancer causing secondary varicosities) and check for signs of portal hypertension (caput medusae is paraumbilical, not saphenous).^[27]

The full CEAP descriptor adds E (Ec congenital, Ep primary, Es secondary, En none), A (As superficial, Ap perforator, Ad deep, An none) and P (Pr reflux, Po obstruction, Pr,o both, Pn none). A complete CEAP for a typical primary GSV varicose vein with an active ulcer is therefore C6, Ep, As, Pr.^[4][5]

Duplex ultrasound — four questions decide management

Duplex ultrasound has replaced every historical bedside test and is the gold standard investigation for chronic venous disease.^[6][27]

Duplex ultrasound (venous colour-flow Doppler). Performed standing or with the leg dependent, the patient asked to perform a Valsalva or calf-squeeze. It answers the four questions that decide management:

• Where is the reflux? SFJ, SPJ, GSV, SSV, perforator, or non-saphenous.
• How far does it extend? Length of refluxing segment, diameter of the vein (predicts suitability for ablation; a GSV diameter above 5 to 6 mm ablates well).
• Are the deep veins patent and competent? Critical. Deep vein obstruction from DVT is an absolute contraindication to stripping or ablation of the superficial system in post-thrombotic limbs.
• Are there incompetent perforators? Pathological perforator: outward flow duration of 500 ms or more and diameter 3.5 mm or more underneath a healed or active ulcer.^[6]

Bloods. Routine bloods are not needed for primary varicose veins. Request a full blood count, glucose and lipids in a patient with an arterial risk factor or a non-healing ulcer; check a coagulation screen and D-dimer if DVT is suspected on duplex.^[34]

Other imaging — selective. MR or CT venography for complex pelvic reflux, congenital malformation, or suspected deep obstruction (May–Thurner syndrome, iliac compression). Ascending venography is now rarely diagnostic — it is reserved for planning deep venous stenting. Air plethysmography quantifies reflux and calf-pump function in research or difficult cases.^[34]

Always check the ABPI before any compression. A reading below 0.8 means arterial disease; refer for vascular assessment and avoid high-pressure compression.^[26]

Management — Resuscitation

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Most varicose veins are chronic, elective problems. Two presentations are time-critical.^[37]

Bleeding varix. A trivial skin breach over a high-pressure varix can cause catastrophic venous haemorrhage. The emergency management is simple but must not be omitted: lie the patient flat, elevate the leg above the heart, and apply direct, firm, prolonged pressure (a pad and bandage). Do not apply a tourniquet. Most bleeding stops with elevation and pressure. Once controlled, the varix is suture-ligated locally and the patient referred for definitive ablation; the bleeding will recur if the underlying reflux is left untreated.^[37][27]

Acute superficial thrombophlebitis. Superficial venous thrombosis is not benign: in the prospective POST study of 844 patients, just under a quarter had deep vein thrombosis or symptomatic pulmonary embolism at presentation, and 10 percent of those without developed a thromboembolic complication within three months.^[12] Image every case with duplex ultrasound to exclude concurrent DVT and define the upper extent of thrombus.^[13] Thrombus approaching or reaching the saphenofemoral junction is treated with therapeutic anticoagulation; the SURPRISE trial showed oral rivaroxaban 10 mg once daily for 45 days non-inferior to subcutaneous fondaparinux 2.5 mg once daily for 45 days in preventing thromboembolic complications, with no major bleeds in either group.^[14] Localised distal phlebitis causing pain can take an NSAID alongside compression and ambulation.^[13]

Active venous ulcer. The resuscitation phase is wound preparation: clean and debride the ulcer, swab for infection, exclude arterial disease by ABPI, and start multilayer high-compression bandaging (see below). Do not delay compression for "complete healing" — compression is the treatment that heals the ulcer.^[10]

Ablate, foam, strip — the CLASS-equivalent ladder

Definitive treatment follows a ladder: conservative measures for symptoms alone, endovenous ablation as the first-line definitive option for C2 to C6 disease with saphenous reflux, and open surgery reserved for those unsuitable for endovenous techniques. The CLASS trial found similar disease-specific quality of life after laser, foam and surgery, with fewer complications after laser; at five years, disease-specific quality of life was better after laser or surgery than foam.^[7][8]

^{[6] [17] [28] [20] [21] [31] [32] [10] [11]}

Conservative management

Conservative measures do not abolish reflux and do not prevent progression, but they reduce symptoms and are first-line when intervention is contraindicated (pregnancy, unfit patient, patient preference).^[32]

Other conservative measures: leg elevation above the heart for 30 minutes, two to three times a day; weight loss; regular walking, swimming or cycling to drive the calf pump; avoidance of prolonged standing and of constricting garments; heel raises to encourage calf activity. Phlebotonics (diosmin, hesperidin, rutosides — micronised purified flavonoid fraction) are popular in continental Europe and India for short-term symptom relief; the SVS guidelines regard the evidence as low-quality and do not recommend them routinely.^[6] Other conservative measures: leg elevation above the heart for 30 minutes, two to three times a day; weight loss; regular walking, swimming or cycling to drive the calf pump; avoidance of prolonged standing and of constricting garments; heel raises to encourage calf activity. Phlebotonics (diosmin, hesperidin — micronised purified flavonoid fraction) improved leg pain (RR 0.53), heaviness (RR 0.35) and swelling (RR 0.39) versus placebo in a meta-analysis of seven randomised double-blind trials.^[6]

Endovenous thermal ablation (EVLA, RFA) — first-line definitive

Thermal ablation delivers heat to the vein endothelium through a catheter positioned under ultrasound, causing irreversible thermal injury, fibrosis and permanent closure. The vein is accessed at the knee (retrograde) or ankle (antegrade) under local anaesthesia; tumescent anaesthesia (large-volume dilute lignocaine with adrenaline and bicarbonate) is infiltrated around the vein to compress it against the catheter, provide analgesia, and protect surrounding tissue (especially the saphenous and sural nerves) from thermal injury.^[7]

• Endovenous laser ablation (EVLA). A laser fibre delivers energy to the vein wall; higher wavelengths target water rather than haemoglobin. In a meta-analysis of 29 comparative studies, one-month GSV occlusion rates were about 98 percent for both EVLA and RFA.
• Radiofrequency ablation (RFA). Segmental heating of the vein in cycles; equivalent outcomes to EVLA overall, with less postprocedural pain, bruising and ecchymosis in meta-analysis.
• Outcomes. At five years in randomised-trial meta-analysis, pooled anatomical success was 88 percent for EVLA versus 83 percent for high ligation plus stripping and 34 percent for foam sclerotherapy. Complications after thermal ablation are mostly minor: bruising, transient pigmentation, phlebitis; venous thrombotic events occur in under 1 percent.^[28][38]

^{[7] [8]}

Ultrasound-guided foam sclerotherapy

Foam is second-line to thermal ablation in NICE CG168 but is used for recurrent varicosities after surgery, for non-saphenous varicosities, and for patients unfit for thermal ablation. In a systematic review of 69 studies, median complete occlusion was 87 percent; serious adverse events (pulmonary embolism, deep vein thrombosis) were under 1 percent, visual disturbance 1.4 percent, headache 4.2 percent, and matting or skin staining about 18 percent.^[18] Neurological complications are rare but documented: in a review of 10,819 sclerotherapy patients there were 97 neurological events (0.9 percent), most transient, and eleven patients with TIA or stroke had a right-to-left shunt, usually a patent foramen ovale — a known right-to-left shunt is a contraindication.^[19]

Mechanochemical ablation (MOCA) and cyanoacrylate glue

MOCA (ClariVein) combines a rotating wire tip that mechanically injures the endothelium with simultaneous delivery of a liquid sclerosant — no heat, no tumescent anaesthesia. Cyanoacrylate glue (VenaSeal) polymerises on contact with blood, instantly sealing the vein. In the VeClose randomised trial, cyanoacrylate closed 97.2 percent of GSVs at twelve months versus 97.0 percent for RFA, with faster time to closure.^[20] MOCA pooled anatomical success is 87 to 92 percent across cohort studies with major complications of 0.2 percent or less; both techniques avoid thermal nerve injury and are useful when tumescent anaesthesia must be avoided.^[21]

Open surgery (high saphenous ligation, stripping, avulsions)

When endovenous treatment is unsuitable (extremely large or tortuous varicosity, recurrent disease after previous surgery, or where the technology is unavailable), open surgery remains a durable option.^[38]

High saphenous ligation plus stripping (the "Trendelenburg operation"). A groin crease incision over the SFJ; the GSV is identified and ligated and divided flush with the common femoral vein; all tributaries are individually ligated. The GSV is then stripped to just below the knee using an invagination stripper — stripping to the ankle is avoided because it adds saphenous nerve injury: in a prospective study of primary GSV surgery stripped to the knee, numbness or paraesthesia still occurred in 27 percent of limbs at six weeks, mostly resolving by twelve months. Visible varicosities are removed through stab incisions (avulsion phlebectomies).^[29][38]

Saphenopopliteal junction ligation for SSV. The SPJ shows considerable anatomical variation, and clinical localisation is inaccurate — preoperative duplex marking is required before popliteal fossa exploration.^[27]

CHIVA (Cure Conservatrice et Hémodynamique de l'Insuffisance Veineuse en Ambulatoire) is a French hemodynamic strategy that preserves the saphenous vein by ligating only the reflux points. A Cochrane review of four randomised trials found fewer recurrences and fewer side effects than stripping but judged the evidence low to moderate quality with high risk of bias; it is not recommended routinely by NICE or SVS.^[17]

Venous ulcer (C6) — healing then prevention

The two-phase strategy is heal the ulcer with compression, then ablate the reflux to prevent recurrence.^[9]

^{[25] [10] [40] [36] [41]}

Wound care. Cleanse; debride slough where indicated; dressings chosen by exudate level. Routine systemic antibiotics do not heal venous ulcers and are reserved for clinical infection (cellulitis, increasing pain, systemic sepsis).^[10]

Pentoxifylline. The Cochrane review found that pentoxifylline, with or without compression, increases the chance of complete ulcer healing (relative risk 1.70 versus placebo or no treatment; 1.56 when added to compression). It is used as an adjunct in slow-healing or large ulcers; main adverse effects are gastrointestinal.^[11]

Specific Subtypes & Scenarios

^[24]

Recurrent varicose veins after previous surgery. Recurrence is common after open surgery — long-term series report recurrence approaching 70 percent at ten years. Neovascularisation at the SFJ is the major cause of ultrasound-confirmed groin recurrence: in re-operation specimens, 94 percent showed multiple new vessels at the stump site connecting back to the common femoral vein. A full repeat duplex is mandatory before any re-operation; endovenous ablation is preferred for recurrence because it avoids the scarred groin.^[38][22]

Post-thrombotic syndrome. The deep vein valves are destroyed by a previous DVT; reflux and obstruction combine. The varicosities are collaterals providing venous return. Compression is the mainstay; superficial ablation or stripping is generally contraindicated unless duplex confirms deep vein patency and an independent superficial contribution to reflux.^[35]

Klippel–Trenaunay syndrome. A congenital mixed vascular malformation with the triad of (1) capillary malformation (port-wine stain), (2) soft-tissue and bone hypertrophy (occasionally hypotrophy) of usually one lower limb and (3) atypical, mostly lateral varicosities without significant arteriovenous shunting. Management is largely conservative, with compression as the hallmark; imaging must confirm deep venous drainage before any intervention, because a proportion have deep vein hypoplasia or agenesis. Surgery or embolisation is reserved for selected, well-imaged cases in specialist centres. Parkes Weber syndrome adds a high-flow arteriovenous component.^[15]

Pregnancy. Varicosities appear or worsen because of progesterone-mediated venous dilatation, rising blood volume and iliac compression by the gravid uterus. Age and pregnancy are the established risk factors for varicose veins. Definitive treatment is deferred until after delivery; during pregnancy, manage with graduated compression stockings, leg elevation and avoidance of prolonged standing. Vulval varicosities are managed with a supportive pad and usually resolve post-partum.^[3]

Pelvic congestion syndrome and ovarian vein reflux. Pelvic pain, dyspareunia, vulval and thigh varicosities in women may arise from ovarian or internal iliac vein reflux. Suspect when varicosities extend above the inguinal ligament or appear after pregnancy. Diagnosed by transvaginal ultrasound, MR or CT venography; treated by coil embolisation, plugs or transcatheter sclerotherapy (SVS/AVF GRADE 2B).^[6]

May–Thurner syndrome. Compression of the left common iliac vein by the overlying right common iliac artery causing left leg venous hypertension, varicosities and a high risk of left iliofemoral DVT. Diagnosed on CT/MR venography; treated by iliac vein stenting. Suspect in any patient with isolated left-leg varicosities and oedema.^[34]

Complications & Pitfalls

Disease-related complications:^[34][13]

• Bleeding. Trauma to a high-pressure varix can cause life-threatening haemorrhage. Elevation and direct pressure; suture-ligature once controlled; definitive ablation to prevent recurrence.
• Superficial thrombophlebitis. Tender, erythematous, palpable cord along a varicose vein. Duplex every case: in POST, 24.9 percent had concurrent DVT or PE at presentation.^[12] Therapeutic anticoagulation if thrombus approaches the SFJ; NSAIDs and compression for localised distal phlebitis.^[13]
• Venous eczema. Itchy, erythematous, scaly skin in the gaiter area. Treat with emollients, mild topical steroid (e.g. clobetasone 0.05 percent for up to 7 days), and compression. Avoid sensitising topical antibiotics (neomycin).
• Lipodermatosclerosis. Painful fibrosis of the lower leg skin and subcutaneous tissue producing the "inverted champagne bottle" or "piano-leg" contour. Treat with compression; potent topical steroid short-course for the acute inflammatory phase.
• Atrophie blanche. White, scarred, avascular patches at sites of healed micro-infarcts — painful and may ulcerate.
• Venous ulcer. Discussed above.
• Marjolin ulcer. Squamous cell carcinoma arising in a long-standing venous ulcer. In the German Marjolin registry the mean ulcer duration before SCC diagnosis was nearly 16 years; suspicious features were therapy resistance despite optimal care (27 of 30 cases), foul odour (12), pain (3) and atypical morphology such as nodular wound bed or hypergranulation (10). Atypical appearance or failure to heal after six to twelve weeks of optimal care demands biopsy — spindle-shaped, multiple and serial if needed.^[23]
• Chronic venous insufficiency. The end-stage of untreated reflux — irreversible skin and subcutaneous damage even after the reflux is corrected.^[30]

Procedure-related complications:^[7][38]

• Endovenous ablation: bruising, skin pigmentation, DVT (rare, less than 1 percent), nerve injury (saphenous nerve when the GSV is ablated below the knee; sural nerve for SSV), skin burn, endovenous heat-induced thrombosis (EHIT) extending to the SFJ.
• Open surgery: groin wound infection, haematoma, lymphorrhoea, lymphocoele, nerve injury (saphenous below the knee, common peroneal near the fibular neck for SPJ surgery), DVT/PE, recurrence.^[38]

Prognosis & Disposition

Varicose veins are chronic and progressive; untreated, the CEAP class advances over years. Outcomes are best with definitive treatment of the refluxing trunk:^[28]

• Endovenous ablation. At five years in randomised-trial meta-analysis, pooled anatomical success was 88 percent for EVLA, with recurrent reflux at the SFJ in 22 percent. VCSS improvement is similar to surgery.^[28]
• Foam sclerotherapy. Pooled anatomical success at five years was 34 percent, significantly lower than EVLA or surgery; often used as a complement for residual tributaries.^[28]
• Open surgery. Pooled anatomical success 83 percent and SFJ recurrent reflux 12 percent at five years; recurrence after open surgery approaches 70 percent at ten years, mainly through neovascularisation.^[28][38]
• Venous ulcer. In ESCHAR, 24-week healing was 65 percent with compression alone and with added surgery; 12-month recurrence fell from 28 percent to 12 percent when superficial reflux was corrected. In EVRA, adding early endovenous ablation raised 24-week healing to 85.6 versus 76.3 percent and extended median ulcer-free time to 306 days.^[9][24]

Disposition: most patients are managed as day cases (endovenous) or outpatients (conservative, foam). An ulcer patient is managed in a community leg-ulcer clinic with weekly compression renewal and wound review, escalating to a vascular service if healing stalls at 12 weeks. A bleeding varix or suspected DVT/PE is an emergency.^[27]

Special Populations

Pregnancy. Defer definitive treatment until after delivery; manage with graduated compression, elevation and reassurance. Vulval varicosities nearly always resolve post-partum. Foam, EVLA, RFA and surgery are avoided during pregnancy.^[3]

Post-DVT / post-thrombotic. Compression is the mainstay. Avoid superficial ablation unless duplex confirms deep vein patency and an independent superficial contribution to reflux.^[35]

Elderly and frail. Conservative management if comorbidity makes intervention hazardous.^[27]

Diabetic and arterial disease. Always check ABPI; modify compression if below 0.8. A mixed arterial-venous ulcer with ABPI 0.5 to 0.8 heals poorly without revascularisation before compression.^[36]

Children. Varicose veins in children suggest a congenital cause (Klippel–Trenaunay, valve agenesis, Parkes Weber). Refer to a specialist vascular or vascular anomalies unit; routine adult ablation is rarely appropriate.^[15]

Patients on anticoagulation. Endovenous ablation can be performed with DOACs continued periprocedurally: DOAC use did not increase bleeding, DVT or EHIT and did not reduce closure durability to nine months in a retrospective comparative cohort.^[39]

Evidence, Guidelines & Regional Differences

The modern management of varicose veins rests on a few landmark trials and two practice-defining guidelines.^[6][17]

^{[17] [27]}

Where the evidence is weak. The place of routine perforator ablation in uncomplicated varicose veins is contested; the SVS recommends against selective perforator treatment in C2 disease. CHIVA shows fewer recurrences than stripping in a small, biased trial base but is not recommended routinely by NICE or SVS. The long-term benefit of non-thermal non-tumescent techniques (MOCA, cyanoacrylate) beyond three to five years is still maturing. Phlebotonics have inconsistent trial quality.^[17][21]

Exam Pearls

• SFJ incompetence is the commonest single cause of primary GSV varicose veins.^[1]
• Venous ulcer lies in the MEDIAL gaiter area (above the medial malleolus) for GSV disease; arterial ulcer is on the toes, foot, lateral malleolus or pressure points, is painful, and lies in a cold, pulseless, hairless limb.^[1]
• CEAP C6 is an active ulcer; C5 is a healed ulcer. Add "s" for symptomatic (e.g. C2s). The full descriptor for a primary GSV ulcer is C6, Ep, As, Pr.^[4][5]
• Duplex ultrasound is the gold standard. Always document deep vein patency before any intervention.^[1]
• EVLA and RFA are first-line definitive treatment (NICE CG168, SVS GRADE 1B); surgery is third-line.^[1][6]
• Never strip a post-thrombotic limb with deep vein obstruction — superficial veins are the only venous return.^[1]
• Always measure ABPI before compression; below 0.8 means arterial disease and contraindicates high-pressure compression.^[1]
• Marjolin ulcer is squamous cell carcinoma arising in a chronic venous ulcer — any ulcer change demands biopsy.^[1]
• Four-layer compression bandaging (Charing Cross system, around 40 mmHg at the ankle) heals 65 to 70 percent of venous ulcers at 6 months; adding saphenous ablation halves recurrence (ESCHAR).^[9]
• Trendelenburg test (historical) detects SFJ incompetence; Perthe's test detects deep vein obstruction.^[1]
• Haemosiderin staining is the brown pigment of chronic venous hypertension; lipodermatosclerosis is the "inverted champagne bottle" leg.^[1]
• CLASS trial: laser, foam and surgery are clinically equivalent at one and five years; laser has fewer complications.^[7][8]
• Pentoxifylline 400 mg PO TDS is an adjunct to compression in slow-healing venous ulcers (Cochrane).^[11]
• Strip the GSV only to just below the knee — stripping to the ankle injures the saphenous nerve.^[1]
• Klippel–Trenaunay triad: varicose veins + limb hypertrophy + port-wine stain; manage conservatively.^[1]

Self-test — a 56-year-old woman with a 4 cm ulcer above the medial malleolus and an ABPI of 0.9. What is the first definitive step?ShowHide

Four-layer compression bandaging to heal the ulcer (ABPI permits high-pressure compression), with duplex ultrasound to map the reflux, and saphenous ablation (EVLA or RFA) once the ulcer is healing to prevent recurrence (ESCHAR). Pentoxifylline 400 mg PO TDS may be added as an adjunct. Never apply high-pressure compression without confirming ABPI; never biopsy a healing ulcer unless change suggests Marjolin.^[1][9]

Ward-round test

Three stems. Cover the answer, say it aloud, then reveal.^[1]

1. A 60-year-old woman has a 4 cm ulcer above the medial malleolus, brown haemosiderin-stained skin, and an ABPI of 0.9. What is the ulcer, and what is the first treatment step?^[1][9]
2. A year later the ulcer has finally healed and she wants her varicose veins "sorted". What single intervention most reduces the chance of the ulcer coming back?^[1][9]
3. A man with a previous iliofemoral DVT now has severe calf varicosities and lipodermatosclerosis, and asks for stripping. Why do you refuse unless duplex proves the deep veins are patent?^[1]

Ward-round answersShowHide

1. A venous (GSV-system) ulcer. An ABPI of 0.9 permits high-pressure compression, so start four-layer compression bandaging (Charing Cross system, about 40 mmHg at the ankle) and arrange duplex to map the reflux.^[1][9]
2. Ablation of the saphenous reflux (EVLA or RFA). The ESCHAR trial showed compression alone heals most ulcers, but adding correction of the superficial reflux halves recurrence at one year — from about 28 percent down to 12 percent.^[9]
3. Because they may be his only route of venous return. In a post-thrombotic limb with deep-vein obstruction the superficial varicosities are collaterals; stripping them can be limb-threatening. Compress, and ablate only if duplex confirms deep-vein patency and an independent superficial contribution.^[1]

References43ShowHide

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