Chronic venous disease, varicose veins and venous ulcers

• Chronic venous disease is a slowly progressive disorder in which veins in the lower limb stop working efficiently, usually because their valves leak and the calf muscle pump fails. The pressure in the leg veins rises, fluid leaks, and over years this produces varicose veins, swelling, skin staining, hardening of the skin and, in the end, venous ulcers.
• Varicose veins are not only a cosmetic problem. They are the common outward sign of a valve problem deeper in the system, and they can progress to complications even when they look mild.
• Duplex ultrasound is the key investigation: it shows whether the valves at the groin and knee leak, which veins are involved, and it guides treatment.
• Compression therapy controls symptoms and heals most venous ulcers, but it does not remove the underlying reflux.
• Early treatment of the leaking vein itself with endovenous ablation (or surgery where ablation is not possible) relieves symptoms and reduces the chance that a venous ulcer comes back.

By the end of this page you should be able to:

1. Explain the full chain from valve failure to varicose veins, skin damage and venous ulcer.
2. Use the CEAP classification to stage chronic venous disease and name the categories that mark high risk.
3. Describe what a duplex ultrasound can and cannot prove, including the standard definition of venous reflux.
4. Plan conservative, interventional and surgical management for varicose veins, including pregnancy and recurrence.
5. Describe the assessment and care of a venous leg ulcer, including compression pressures and arterial screening.
6. Compare the treatment ladder in the NICE CG168 guidance with the structure of the ESVS 2022 guideline.

Two tools are used alongside CEAP. They are mentioned here so that you recognise them in the literature:

• Revised Venous Clinical Severity Score (r-VCSS): an evaluative score that records 10 clinical features (pain, varicose veins, oedema, skin pigmentation, inflammation, induration, ulcer number, ulcer size, ulcer duration and use of compression) so that improvement after treatment can be measured.
• CEAP (below): a classification, not a score; it describes what is present rather than how much it matters.

The most widely used classification for chronic venous disease is CEAP: Clinical, Etiological, Anatomical, Pathophysiological. It was first published in 1995 and revised in 2004 and again in 2020. The 2020 version is the one most current articles use. It has four parts:

• C (Clinical): what can be seen or felt, from no signs to an active ulcer.
• E (Etiological): whether the disease is primary (valve or wall degeneration), secondary (post-thrombotic, obstruction, extravenous compression) or congenital.
• A (Anatomical): which level is involved (superficial, deep or perforator veins).
• P (Pathophysiological): whether there is reflux, obstruction, both, or none.

The full classification is in the table.

The clinical point of CEAP is that C4, C5 and C6 are the "advanced" classes: they carry strong pressure in the tissues and they mark the patients who are at real risk of developing a first or recurrent venous ulcer. A first-time patient with a C2 varicose vein and minimal symptoms is at a very different point in the disease. ^[3]

Venous disease is common and becomes more common with age. Exact figures depend on which definition is used, but the overall pattern is consistent across large studies:

• Superficial venous incompetence (leaking valves in the superficial system) affects 30 to 40% of the population. ^[4]
• Varicose veins of clinical significance (CEAP C2) make up roughly 18.8% of people with venous reflux disease on examination or duplex ultrasound. ^[2]
• Venous ulcers are the end stage: one review gives a prevalence of 1.69% in the elderly population, with a long, recurrent course and a reduced quality of life for those affected. ^[3]
• The annual cost of venous leg ulcers in the United States has been estimated at 14.9 billion US dollars. ^[3]
• Female sex, multiple pregnancies, age, prolonged standing, trauma and obesity all increase the chance of developing the disease. ^[3]
• Many people with reflux never develop symptoms. The Edinburgh Vein Study and the Bonn Vein Study, classical population studies quoted in the duplex review, showed that reflux in both the superficial and deep systems is far more common than symptoms. ^[4]

There is no single cure: the condition is chronic and recurring, and prevention of progression is the realistic goal.

Chronic venous disease is not one disease. It is the end result of three different problems, sometimes in combination:

1. Primary valvular incompetence. The valves in the superficial or deep veins degenerate or fail, so that blood flows backwards (reflux) instead of towards the heart. This is the commonest cause of varicose veins in otherwise healthy adults. ^[3]
2. Post-thrombotic change. After a deep vein thrombosis the valves are destroyed and the vein wall remodels. The resulting post-thrombotic syndrome gives very high venous pressure and is the commonest cause of severe skin change and ulcer.
3. Obstruction or extravenous compression. A blocked deep vein, a pelvic mass or, in pregnancy, uterine compression, and iliac venous outflow obstruction raise the venous pressure without any valve problem.

Risk factors that cannot be changed: age, female sex, a family history, and the leg-vein anatomy a person is born with. Risk factors that can be modified: obesity, lack of physical activity, prolonged standing or sitting, and smoking. Pregnancy is a distinct, reversible risk factor (discussed with management).

The medical student should be able to walk the whole chain in either direction. It runs like this.

• Veins are thin-walled, low-pressure vessels with one-way valves. In the leg they lie in three systems: superficial (the great and small saphenous veins and their tributaries, just below the skin), deep (the tibial, popliteal and femoral veins, enclosed in the deep fascia), and perforators (the small veins that pass through the fascia and connect the two).
• The deep system returns blood against gravity because of the calf muscle pump. When the calf contracts it squeezes the deep veins; when it relaxes they refill from the superficial system through the perforators. This is the "muscle pump"; walking is the single best venous drainage the leg has.
• Valves make the pump one-directional. They stop blood falling back down. In a normal leg the pressure in the foot vein is high when standing still, and falls when walking as the calf pump empties the deep veins.

1. Valve failure (from age, stretch, high pressure, a previous clot or a wall defect) makes one vein leak. Blood falls backwards during diastole and between steps.
2. Reflux raises the hydrostatic column. The pressure in the veins above the leak no longer falls with walking. The ambulatory venous pressure (the pressure when walking) rises.
3. The superficial system distends. Veins that were never meant to carry arterial-level pressure stretch, become tortuous, lose their elastic recoil and become true varicose veins. Perforator valves fail next, which is why varicose veins and perforators are usually studied together.
4. Microcirculation suffers. Chronic venous hypertension opens the capillaries. Red cells leak out and break down, staining the skin with haemosiderin (brown staining), and fibrin cuffs form around capillaries that impair diffusion of oxygen and nutrients.
5. Inflammation follows. Leucocytes adhere and migrate, releasing proteases and inflammatory signals; the skin becomes inflamed (stasis dermatitis), then fibrotic and hard (lipodermatosclerosis), then fragile. Atrophie blanche is the pale, scarred end stage.
6. Tissue death. When the skin and subcutaneous tissue can no longer repair themselves, the skin breaks and an ulcer forms, usually on the medial gaiter (just above the ankle), where the pressure transmission is greatest.

Each symptom and sign of chronic venous disease can be read off from the chain above.

• Aching and heaviness after standing or in the evening come from venous distension and the high hydrostatic column; they worsen with gravity and ease with leg elevation.
• Swelling (oedema) of the ankle and lower leg comes from raised capillary pressure and increased permeability.
• Varicose veins are the visible distension of superficial veins that have lost their valves.
• Itching, eczema and brown staining are capillary leakage and haemosiderin deposition.
• Hardened, fibrotic skin (lipodermatosclerosis) is the chronic fibrotic end point of long-standing inflammation.
• Atrophie blanche is the pale, sclerotic, scar-like change left when the microcirculation has failed; it is a warning that an ulcer is likely.
• Venous ulcers form where the skin and subcutaneous tissue finally fail, usually in the gaiter area above the medial malleolus.

• Heaviness, aching and discomfort in the leg, usually worse after standing or sitting for long periods, worse in warm weather, and worse at the end of the day; relieved by leg elevation and by walking.
• Swelling of the ankle and lower leg, often worse in the evening and gone by morning.
• Itching and burning over varicose veins or over the gaiter skin.
• Night cramps and restless legs in some patients.
• Visible bulging veins that the patient is concerned about cosmetically; often the first thing noticed.
• Pain from a thrombosed varicose vein (superficial vein thrombosis): a sudden, hard, red, tender lump along a varix.

A common and important trap is that many people with venous reflux have no symptoms at all, so the mere presence of a varicose vein does not prove that it is causing the patient's symptoms. The symptoms must be attributed only after other causes (arterial, neuropathic, musculoskeletal) have been excluded.

Examine standing first, then lying.

Standing:

• Distribution and size of varicose veins: great and small saphenous territories, anterior accessory saphenous vein, lateral thigh perforator veins.
• Look for the saphenous junctions at the groin (sapheno-femoral junction) and behind the knee (sapheno-popliteal junction). A cough impulse at the groin suggests reflux across the sapheno-femoral junction.
• Oedema: pitting oedema of the ankle. In advanced lipodermatosclerosis the limb takes on an "upside-down champagne bottle" shape.
• Skin changes: pigmentation (haemosiderin), eczema, lipodermatosclerosis, atrophie blanche, corona phlebectatica.
• Venous ulcers: most often in the gaiter region just above the medial malleolus; the ulcer is usually shallow, with sloping edges and a granulating or sloughy base.

Lying:

• Trendelenburg test (manual tourniquet): a teaching manoeuvre to show whether reflux is above a tourniquet at the thigh or below it. It has been largely replaced by duplex ultrasound, but the reasoning behind it is still exam material.
• Power (calf) pump: calf muscle bulk and strength.

Always check the arterial supply as well (pulses, ankle-brachial pressure index). Arterial disease is common in the same age group and is easily missed when an ulcer is present.

Two different questions arise, and they need different answers.

Question 1: the patient has leg symptoms; is it venous disease? The common mimics are: arterial claudication or critical limb ischaemia (pain on walking, relieved by rest, cold foot, absent pulses), neuropathy and radicular pain, musculoskeletal pain, knee or ankle arthritis, lymphoedema (non-pitting, squared toes, Stemmer sign), and heart failure or renal disease (bilateral, symmetrical pitting oedema).

Question 2: a leg ulcer is present; is it venous? The differential of a lower-limb ulcer is broad and only a venous ulcer can be treated with high compression. Use the appearance, site, surrounding skin and, above all, the arterial check.

The most important number in venous ulcer care is the arterial check: a low ankle-brachial pressure index (under 0.8) is a reason to treat the arterial disease first and to avoid high compression. ^[5]

Which veins leak, and how much of the limb is affected, are decided before any test is requested. The history should establish: family history, pregnancies, previous thrombosis, previous varicose surgery, symptom pattern (standing, walking, night), trauma, and duration of skin change.

Duplex ultrasound (B-mode imaging with colour and spectral Doppler) is the single investigation that confirms the diagnosis, maps the disease and plans treatment. NICE CG168 recommends that duplex ultrasound is used to confirm the diagnosis of varicose veins and the extent of truncal reflux, and to plan treatment. ^[1]

A complete examination of the lower limb venous system includes:

• Junctions: the sapheno-femoral junction and the sapheno-popliteal junction.
• Trunks: the great saphenous vein, the small saphenous vein and the anterior accessory saphenous vein.
• Perforators: especially in the medial calf.
• Deep system: common femoral, femoral, popliteal and calf veins, looking for thrombosis and recanalisation.
• Pelvic veins if there are atypical (perineal or posterior thigh) varices.

The scan is done standing or tilted upright, so that gravity provokes reflux. To produce reflux, antegrade flow is first generated by a quick manual or cuff compression below the measurement site; the compression is released suddenly and the vein is watched for reversed flow.

The practical definition of venous reflux: on standing, reversed flow lasting 0.5 seconds or more after release of compression (or after a Valsalva manoeuvre) is pathological in the superficial veins. This threshold is the most commonly used cut-off and is recommended in guidelines, although the review of quantitative ultrasound notes that reflux time is actually a qualitative measure of presence or absence, and that it correlates only weakly with symptoms. ^[4]

The whole examination is anatomical as much as haemodynamic: the surgeon needs to know exactly which segment is leaking so that treatment can be targeted to it.

• Ankle-brachial pressure index (ABPI): screening test for arterial disease before compression or surgery. In the compression study reviewed, patients with ABPI under 0.8 were excluded, so ABPI under 0.8 marks the practical point at which high compression is unsafe. ^[5]
• Air plethysmography or strain-gauge plethysmography: useful in research and in specialised centres; the venous filling index is the most established global parameter, but these are not routine.
• CT or MR venography: reserved for suspected deep obstruction, a pelvic source (May-Thurner, pelvic venous reflux) or a complex post-thrombotic picture.
• Intravascular ultrasound: used in specialised centres for deep or iliac obstruction; not routine for varicose veins.

A patient with an aching, standing-dependent varicose vein at the medial calf is most often found to have a great saphenous vein that is incompetent from the sapheno-femoral junction down to the upper calf, with one or two leaking calf perforators. Treatment of the junction and trunk first (ablation) leaves only the tributaries to deal with. A patient with isolated lateral thigh varices often has an incompetent anterior accessory saphenous vein or a lateral thigh perforator, and may need targeted treatment to that vein.

There are no blood tests that diagnose venous disease. The diagnosis is clinical plus duplex. Three staging and severity tools run alongside:

• CEAP (above): describes what is present.
• Revised Venous Clinical Severity Score (r-VCSS): the ten-attribute score (pain, varicose veins, oedema, skin pigmentation, inflammation, induration, ulcer number, ulcer size, ulcer duration and compression therapy), used to measure change after treatment.
• Patient-reported outcomes: Aberdeen Varicose Vein Questionnaire (AVVQ) and VEINES-QOL/Sym; these are used in trials and audits to check that the treatment helped the patient, not just the vein. ^[4]

1. Compression treats the pressure, ablation or surgery treats the reflux. Compression controls symptoms and heals ulcers; it does not close the leaking vein. Very few patients who need treatment of symptoms will be satisfied for long with compression alone.
2. Treat the refluxing trunk and junction first. Once the great saphenous vein and its junction are closed, most tributary veins shrink.
3. Offer interventional treatment early in symptomatic veins, rather than waiting for complications.
4. Treat venous ulcers as active disease. Treating the ulcer with dressings without treating the reflux guarantees recurrence.
5. Work as a team. Chronic venous disease involves primary care, vascular surgery, wound care and (for ulcers) a multidisciplinary wound team.

Conservative measures are the background for every patient, whether or not they have an intervention.

• Graduated compression: hosiery or bandages that are tightest at the ankle and loosest at the calf. For varicose veins with symptoms this is the fall-back when interventional treatment is unsuitable. ^[1]
• Weight management: advice on weight loss when the patient is overweight. ^[1]
• Movement: regular light to moderate activity, walking and calf exercises; avoid standing or sitting still for long periods.
• Elevation: leg elevation above the heart when resting, especially at night.
• Skin care: emollients, treatment of eczema (topical steroid for short courses under supervision), protection from trauma and scratches.
• Treatment of superficial thrombophlebitis: anti-inflammatory drugs, compression, and sometimes anticoagulation; the patient should be reassessed because thrombus can extend into the deep system.

NICE guideline CG168 (published 2013, last reviewed 2016, with a surveillance decision in 2016 that no change was needed) sets out a clear ladder for the vascular service. ^[1]

Key points of the NICE pathway: ^[1]

• After interventional treatment, compression is used for no more than 7 days if it is used at all. Prolonged compression after ablation is not recommended. ^[1]
• Compression hosiery is not offered to treat varicose veins on its own, unless interventional treatment is unsuitable for the person. ^[1]
• Information (explanation of the condition, treatment options, expected benefits and risks, the chance of new varicose veins, the number of sessions that may be needed) is part of the treatment, not a preamble.
• Refer people with bleeding varicose veins immediately to a vascular service. ^[1]
• Refer people with symptomatic primary or recurrent varicose veins, with lower-limb skin changes thought to be due to chronic venous insufficiency, with superficial vein thrombosis and suspected venous incompetence, with a venous leg ulcer, or with a healed venous leg ulcer.

• Radiofrequency (RF) ablation and endovenous laser ablation (EVLA) close the leaking trunk from inside by delivering heat that coagulates the vein wall. They are the usual first-line interventional treatment. Under local tumescent anaesthesia, a sheath is inserted at the lowest point of reflux; the catheter is pulled back while energy is delivered, and the vein closes. ^[1]
• Outcomes: the review of the two major modern guidelines rates anatomic closure of the saphenous vein at five years and the need for reintervention as the measurable end points, with quality of life rated highest. ^[2]
• Safety: endovenous heat-induced thrombosis (clot extending into the deep vein) is the complication to watch for; routine scanning after treatment in the first week is standard in many services.

• Ultrasound-guided foam sclerotherapy mixes a sclerosant with gas to create a foam that displaces blood and injures the vein lining, producing fibrosis and closure. It is particularly useful for tortuous veins and for veins that are unsuitable for ablation.
• Saphenous surgery (high ligation and stripping plus phlebectomy) is the fallback where ablation and foam are unsuitable; it is still effective, and lower recurrence rates than foam have been quoted for the great saphenous vein. Recovery is longer.

The task specifically asks for NICE CG168 and the ESVS 2022 guideline, so both are named here.

• NICE CG168 is a relatively short UK guideline published in 2013 (last reviewed 2016, when no new evidence was found to change the recommendations). It is focused on diagnosis and interventional treatment of varicose veins, the referral pathway into a "vascular service", and management during pregnancy. ^[1]
• ESVS 2022 is the European equivalent but is structured very differently: it is an 83-page guideline on the management of chronic venous disease of the lower limbs, of which the management of C2 varicose veins is one part. It was produced by the European Society for Vascular Surgery and rates recommendations by the European Society of Cardiology system (four classes of recommendation, three levels of evidence). ^{[2] [6]}
• The 2025 comparison of the two major guidelines (ESVS and the SVS/AVF/AVLS) concluded that the overall recommendations agreed, although they disagreed on the strength of several recommendations because of different methodology: the US multi-society guideline uses the GRADE system, while ESVS uses the ESC system. Both were rated high quality by AGREE II appraisal. ^[2]
• The ESVS 2022 guideline lists 21 new recommendations for C2 disease over the 2015 edition (7 class 1, 8 class 2A, 4 class 2B, 2 class 3). ^[2]
• In short, the two guidelines do not contradict each other; they differ in emphasis. NICE is a service pathway document; ESVS is a broader chronic venous disease document that includes the same treatment ladder. ^[6]

A venous ulcer is an open wound on the lower leg, usually in the gaiter, that has failed to heal. It is the most disabling end of chronic venous disease and has a high rate of recurrence. Managing it well is more about organisation than about dressings.

Assessment on first contact

• History: duration of ulcer, number of previous ulcers, history of deep vein thrombosis, previous varicose surgery, mobility, comorbidity (diabetes, heart failure, rheumatoid arthritis).
• Examination: appearance of the wound, surrounding skin, oedema, ankle movement, lipodermatosclerosis.
• Arterial check: ankle-brachial pressure index before any compression is applied; treat arterial disease first where present.
• Duplex ultrasound: to map reflux in the superficial and perforator veins and to plan later treatment.

Local wound care

• Debride necrotic or sloughy tissue (sharp, enzymatic, autolytic according to local strategy).
• Absorbent, non-adherent dressings changed according to exudate, keeping the wound bed moist and the skin free of maceration.
• Treat infection: only when there is evidence of bacterial invasion (erythema, oedema, odour, increased pain, fever); antibiotics for a limited course, with escalation criteria.
• Control oedema and lymph: compression, elevation, movement, skin protection.
• Nutrition: adequate protein intake, correction of anaemia.
• Skin care around the ulcer: emollients, protection from trauma.

Compression Compression is the cornerstone of venous ulcer care: used correctly it heals 40% to 95% of venous ulcers. ^[5]

The standard clinical teaching, consistent with the trial evidence, is:

• High compression (moderate pressure 35 to 40 mmHg, or a higher pressure above 45 mmHg at the ankle) is used when the arterial supply is adequate (ABPI at least 0.8), giving the best healing. ^[5]
• A trial that compared moderate pressure (35 to 40 mmHg) with high pressure (greater than 45 mmHg) in 116 patients with venous leg ulcers found a significantly higher 24-week healing rate with high pressure (55.0% versus 32.1%, p = 0.022), and greater improvement in quality of life. ^[5]
• Patients with mixed (arterial plus venous) disease need reduced or no compression and specialist assessment of the arterial component. ^[5]
• After the ulcer heals, maintenance compression must continue, because the recurrence rate is high without it.

Venous intervention in ulcer disease

• Ultrasound-guided foam sclerotherapy of incompetent superficial and perforator veins can be used early; even around an active ulcer, closing the reflux shortens healing time.
• Surgery and endovenous ablation have been shown to reduce recurrence after healing: a randomised trial of 500 patients found that surgery to correct superficial venous reflux combined with compression reduced ulcer recurrence compared with compression alone. ^[3]
• Deep venous reconstruction is reserved for severe disease with deep outflow obstruction or deep incompetence after failure of conservative and superficial treatment.

Prevention of recurrence

• After healing, keep the patient in maintenance compression (usually a class 2 to class 3 stocking) and review at intervals.
• Advise on: weight, exercise and calf pump, elevation, skin moisturising, and prompt presentation with any new breakdown.
• Many recurrences are prevented by addressing the patient's problem (immobility, obesity, depression, ill-fitting shoes) rather than adding more dressing.

Pregnancy is a special case because of venous compression by the uterus, a rise in circulating volume, hormonal vascular laxity, and progesterone effects on the vein wall.

• Give pregnant women with varicose veins information on the effect of pregnancy on varicose veins. ^[1]
• Do not carry out interventional treatment during pregnancy other than in exceptional circumstances. ^[1]
• Consider compression hosiery for symptom relief of leg swelling associated with varicose veins. ^[1]
• Reassess after delivery, because many varices regress and others can be treated definitively once the postpartum period is past.
• Rule out a deep vein thrombosis (unilateral swelling, pain, warmth) in a pregnant woman with a new leg problem: this is an emergency, not a varicose-vein problem.

• Older adults: venous disease and arterial disease commonly coexist; check the feet, the pulses and the ABPI. Skin is fragile; avoid adhesive dressings and shear.
• Children with varicose veins: uncommon; think of congenital venous malformation or Klippel-Trenaunay syndrome if a child presents with varices.
• Patients with limited mobility: depend on pumps; compression applied by a trained practitioner is essential.
• Dark skin: early venous skin change is harder to see on dark skin; rely on tenderness, thickening, temperature and careful photography.

• Duplex ultrasound is often not available. Clinical examination, a hand-held Doppler and careful history take you a long way: hand-held Doppler gives a sound over the sapheno-femoral junction during a cough or with compression that is good enough to decide on referral.
• Compression: graduated compression bandages, tubular compression (size by ankle circumference) or elastic hosiery are cheap and effective; the skill is in application and in teaching the patient and family.
• Where ablation is unavailable, high ligation and stripping and phlebectomy under local or spinal anaesthesia are well established.
• Where wound care resources are limited, the priorities are: debridement, offloading from the ankle, moist dressings (saline-soaked gauze is acceptable), maintenance of the skin around the ulcer, and referral for any arterial suspicion.
• Family and community nurses are usually the people who apply compression daily; support them.

Complications of varicose veins and chronic venous disease:

• Superficial vein thrombosis (thrombophlebitis): painful red vein; can extend into the deep system.
• Haemorrhage from a varicose vein after accidental damage or (rarely) spontaneously from thin skin over a vein.
• Venous eczema and lipodermatosclerosis (skin complications of long-standing hypertension).
• Venous leg ulcer (C6): the most serious chronic complication.
• Deep vein thrombosis as a separate event that worsens the outcome.
• After interventional treatment: endovenous heat-induced thrombosis, paraesthesia (especially where the great saphenous vein lies close to the saphenous nerve), skin burns with laser (rare), recurrence of reflux.
• After surgery: wound infection, numbness (saphenous nerve injury), recurrence, scarring.

• Varicose veins tend to progress if the underlying reflux is not treated, but progression is not inevitable: many people with C1 or C2 disease remain stable for decades.
• A first venous ulcer, once healed, recurs in a large proportion of patients unless maintenance compression and, where appropriate, treatment of reflux are in place.
• Patient-reported quality of life improves after successful treatment, and the improvement is greatest when the treatment addresses the cause (the refluxing vein) rather than the appearance alone.

There is no primary prevention programme for varicose veins, but several habits slow progression:

• Maintain a healthy body weight.
• Regular walking and calf-pump exercise (calf raises, ankle circles).
• Avoid prolonged standing or sitting; take movement breaks.
• Leg elevation when resting.
• Avoid constipation (straining raises intra-abdominal pressure).
• Properly fitted compression hosiery during pregnancy, long haul travel, or when standing for work.

There is no population screening programme for varicose veins. Patients with skin changes (C4 and above) should, however, be identified early in primary care and referred for assessment, because intercepting the disease at the stage of skin change is far cheaper than treating an ulcer.

• Chronic venous disease is a spectrum from asymptomatic spider veins to a venous leg ulcer, driven by raised venous pressure.
• The three mechanisms are primary valvular reflux, post-thrombotic change, and venous obstruction.
• The pathophysiological chain is valve failure, reflux, raised ambulatory venous pressure, microvascular inflammation, skin damage, ulcer.
• CEAP stages the disease: C4, C5 and C6 mark the patients at real risk of ulceration.
• Duplex ultrasound is the diagnostic and treatment-planning investigation; reflux of 0.5 seconds or more in a superficial vein after compression is abnormal.
• Compression therapy controls symptoms, heals ulcers (40% to 95% if applied correctly) and reduces recurrence; it does not close the leaking vein. ^[5]
• NICE CG168 recommends a ladder: endothermal ablation first, then foam sclerotherapy, then surgery, with compression used for no more than 7 days after intervention.
• ESVS 2022 covers chronic venous disease as an 83-page guideline of which C2 varicose veins are one part; it agrees with the NICE ladder in practice.
• Venous ulcer care has three pillars: local wound care, adequate compression after arterial screening (ABPI 0.8 or more), and treatment of reflux to prevent recurrence.
• Pregnancy: information and compression for symptoms during pregnancy, and no interventional treatment unless exceptional.
• Bleeding varicose veins are an emergency referral; a new unilateral leg swelling in pregnancy is a thrombosis until proven otherwise.

Related topics and prerequisites are listed as empty in the front matter because this is a standalone curriculum topic. Natural follow-ups are deep vein thrombosis and post-thrombotic syndrome, peripheral arterial disease, leg ulcer care, and the use of duplex ultrasound.