Chronic venous insufficiency and varicose veins

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Superficial or deep venous reflux and outflow obstruction raise ambulatory venous pressure. The clinical spectrum runs from telangiectasia and varicose veins through oedema, eczema/pigmentation, lipodermatosclerosis and healed or active ulceration.

Symptoms include aching, heaviness, itching, throbbing and swelling that worsen with standing. Severity of visible veins does not reliably predict symptoms or complications, so referral is based on bleeding, symptoms and skin/ulcer consequences rather than appearance alone.

Intervention treats the reflux source. Adjuncts—walking/calf-pump exercise, weight management, elevation, skin care and compression when appropriate—support symptom control but do not replace a NICE-indicated vascular assessment.

Key points

Varicose veins are dilated tortuous superficial veins caused by venous reflux; chronic venous insufficiency describes the oedema, skin change and ulceration produced by sustained venous hypertension.
Refer immediately for bleeding varicose veins.
Refer symptomatic primary or recurrent varicose veins, venous skin changes, superficial vein thrombosis with suspected incompetence, a venous ulcer unhealed after 2 weeks or a healed venous ulcer.
A vascular service uses duplex ultrasound to confirm truncal reflux, map anatomy and plan treatment.
For confirmed truncal reflux, NICE treatment order is endothermal ablation, then ultrasound-guided foam sclerotherapy if unsuitable, then surgery if foam is unsuitable.
Do not offer compression hosiery as definitive treatment for varicose veins unless intervention is unsuitable; hosiery may still relieve symptoms or manage oedema/ulcer risk in selected patients.
During pregnancy, do not perform interventional treatment except in exceptional circumstances; compression hosiery may be used for symptom relief.
Unilateral sudden swelling or pain requires DVT assessment rather than being attributed automatically to chronic venous disease.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Primary superficial venous reflux

Vein-wall dilatation and valve incompetence permit retrograde flow, producing tortuous superficial veins. Age, family tendency, pregnancy and prolonged standing commonly increase susceptibility or symptoms.

Post-thrombotic deep venous disease

Previous DVT may leave valve destruction and residual outflow obstruction. The resulting deep venous hypertension can drive oedema, skin change and secondary superficial reflux.

Raised pressure and impaired calf pump

Obesity, pregnancy, immobility and reduced ankle movement increase hydrostatic load or weaken calf-muscle emptying. These factors aggravate venous hypertension even when they are not the sole cause.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Reflux or outflow obstruction
Incompetent valves allow blood to fall back during standing, while deep obstruction impedes return. Either mechanism raises the volume and pressure carried by lower-limb veins.
2
Ambulatory venous hypertension
The calf pump no longer lowers venous pressure effectively during walking. Sustained pressure dilates superficial tributaries and transfers stress to capillaries and surrounding tissue.
3
Oedema and inflammation
Increased capillary hydrostatic pressure drives fluid and red-cell products into the interstitium. Persistent leucocyte activation and inflammation cause itching, eczema and haemosiderin pigmentation.
4
Fibrosis and ulceration
Chronic inflammation remodels skin and subcutaneous fat, producing induration and lipodermatosclerosis. Fragile, poorly nourished gaiter skin can then break down into a recurrent venous ulcer.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Symptomatic varicose veins

Aching, heaviness, swelling, itching or throbbing attributed to visible primary or recurrent varices; meets NICE vascular-referral criteria.

Venous oedema

Dependent pitting ankle/lower-leg swelling, often worse later in the day and improved by elevation; bilateral causes and cardiac/renal disease remain alternatives.

Venous skin change

Gaiter hyperpigmentation, stasis eczema, induration and lipodermatosclerosis indicate chronic venous hypertension and warrant vascular referral.

Venous ulcer history

An active ulcer below the knee that has not healed within 2 weeks, or a healed venous ulcer, meets referral criteria.

Bleeding varicosityRed flag

External bleeding can be brisk from a small skin breach, especially with dependency; elevate, apply firm direct pressure and refer immediately.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Lower-limb venous duplex ultrasoundFirst step
Why
Confirm diagnosis, define truncal reflux and plan intervention.
Interpretation and limitations
Map great/small saphenous and tributary reflux, deep patency and prior-treatment anatomy; duplex findings must match the symptomatic territory.
02
ABPI before therapeutic compression
Why
Exclude clinically important arterial insufficiency when compression is considered, especially with skin breakdown/ulceration.
Interpretation and limitations
ABPI 0.8–1.3 usually supports full venous compression; lower, high or unreliable values need modified/specialist assessment.
03
Clinical CEAP description
Why
Record visible class and complications consistently.
Interpretation and limitations
C2 varicose veins, C3 oedema, C4 skin change, C5 healed ulcer and C6 active ulcer; CEAP supports communication but does not replace symptom/history assessment.
04
DVT Wells pathway when acute features occur
Why
Distinguish chronic venous disease from acute thrombosis.
Interpretation and limitations
Use NICE D-dimer/ultrasound timing; chronic varicosities do not protect against DVT.
05
Targeted systemic oedema assessment
Why
Identify heart, kidney, liver, drug or lymphatic causes when swelling is bilateral/atypical.
Interpretation and limitations
JVP, cardiac/respiratory findings, urinalysis, renal/liver tests and medication review are driven by clinical context.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Deep-vein thrombosis

Sudden unilateral swelling, deep pain and tenderness require acute DVT assessment. Chronic venous disease more often causes longstanding dependent symptoms, pigmentation and visible varices, although both can coexist.

Lymphoedema

Lymphatic swelling often involves the dorsum of the foot and becomes firm or non-pitting, with skin thickening. Varicosities, gaiter pigmentation and reflux on duplex favour venous disease.

Cardiac, renal or hepatic oedema

Systemic fluid retention is commonly bilateral and accompanied by jugular venous, urinary or hepatic abnormalities. Isolated gaiter changes and mapped reflux support a predominantly local venous cause.

Cellulitis

Fever, pain and rapidly spreading unilateral warmth favour infection. Chronic bilateral itch, scale, pigmentation and oedema are more consistent with stasis eczema than recurrent cellulitis.

Peripheral arterial disease

Arterial ulcers are often distal, painful and punched out with a cool foot and reduced pulses. Venous ulcers favour the gaiter region with oedema and preserved warmth.

Additional chapter-specific clues

Acute thrombotic mimic/complicationRed flag

A tender cord suggests SVT; sudden diffuse unilateral swelling, deep pain or PE symptoms require urgent DVT/PE assessment.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01bleedingBleeding varicose veinFirst stepActive or recent spontaneous bleeding from a varicosity.

1First: lie the patient down, elevate the limb above heart level and apply firm direct pressure with a pad until bleeding stops.
2Next: assess haemodynamics, haemoglobin and anticoagulant use; resuscitate and transfer urgently if bleeding is ongoing or significant.
3Next: refer immediately to a vascular service even after haemostasis because rebleeding risk persists.
4DefinitiveEscalationEscalation: urgent duplex and definitive ablation/sclerotherapy of the reflux source according to the vascular team.

02referralSymptomatic or complicated diseaseSymptoms, venous skin change, qualifying ulcer history, recurrent SVT or recurrent varicose veins.

1First: examine pulses, oedema and skin; rule out acute DVT/infection and protect any ulcer.
2Next: refer to a vascular service under NICE CG168 and arrange ABPI if compression/wound treatment is planned.
3Next: vascular duplex confirms truncal reflux and maps treatment.
4EscalationEscalation: immediate referral for bleeding; expedite severe skin breakdown, ulceration or rapidly progressive symptoms.

03interventionConfirmed truncal refluxDuplex-confirmed reflux associated with symptoms or complications.

1First: offer endothermal ablation when anatomically/clinically suitable.
2Next: if endothermal treatment is unsuitable, offer ultrasound-guided foam sclerotherapy.
3Next: if foam is also unsuitable, offer surgery; treat tributaries at the same session when appropriate.
4EscalationEscalation: if intervention is unsuitable or declined, use appropriately assessed compression and supportive care with review of complications.

04pregnancyVaricose veins in pregnancyNew or worsening varices during pregnancy.

1First: assess for DVT or bleeding red flags rather than assuming all symptoms are physiological.
2Next: offer advice, elevation/activity and compression hosiery for symptom relief when fitted appropriately.
3Next: do not offer interventional treatment during pregnancy except exceptional specialist circumstances.
4EscalationEscalation: reassess after pregnancy if symptoms or reflux persist and then apply the standard duplex/intervention pathway.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Venous ulceration

Sustained microvascular pressure and inflammation cause gaiter skin breakdown. Ulcers can be painful, exudative and recurrent, impairing mobility and quality of life.

Stasis dermatitis and lipodermatosclerosis

Chronic oedema and red-cell extravasation produce eczema, pigmentation and subcutaneous fibrosis. Skin becomes inflamed and fragile, increasing ulcer risk and sometimes mimicking cellulitis.

Superficial vein thrombosis

Thrombosis within a varicose tributary causes a tender, erythematous cord. Extension towards the deep system or accompanying diffuse swelling requires assessment for venous thromboembolism.

Variceal bleeding

Thin skin over a pressurised superficial vein can rupture after trivial trauma or spontaneously. Bleeding may be brisk while the limb is dependent and needs elevation, firm direct pressure, immediate medical assessment and vascular referral.

Secondary skin infection

Excoriated eczema or an open ulcer can permit bacterial infection. New pain, warmth, rapid erythematous spread or systemic illness distinguishes infection from stable inflammatory skin change.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Track pain, heaviness, pruritus, oedema, bleeding and impact on activity rather than vein appearance alone.
Inspect gaiter skin for eczema, pigmentation, induration and ulceration at follow-up.
Check compression fit, skin tolerance and arterial status; reassess if pain, pallor, numbness or coldness develops.
After intervention, review treated-vein closure/complications according to the vascular protocol and assess residual symptoms.
After any ulcer heals, maintain recurrence prevention and prompt re-referral for skin breakdown.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Referral is not cosmetic

Pain, swelling, skin change, SVT and ulcer history are clinical indications even when the visible veins seem modest.

Bleeding can be deceptively dramatic

Venous pressure falls rapidly with elevation and direct pressure, but definitive reflux treatment is still needed.

Treatment order is examinable

Endothermal ablation precedes foam, which precedes surgery when each earlier option is unsuitable.

Compression has two roles

It is core treatment for venous ulceration after arterial assessment, but NICE does not use it as definitive varicose-vein treatment when intervention is suitable.

Venous eczema is often mistaken for cellulitis

Chronic bilateral itch, scale and pigmentation favour stasis dermatitis; fever, pain and rapid unilateral spread favour infection.

11Common pitfallsFrequent interpretation and management errors.

01
Applying a tourniquet proximal to a bleeding varicosity instead of elevation and direct pressure.
02
Offering lifelong hosiery without vascular referral to an otherwise suitable patient with symptomatic truncal reflux.
03
Treating stasis eczema repeatedly with antibiotics as cellulitis.
04
Starting strong compression without assessing arterial perfusion in a patient with ulceration or weak pulses.
05
Performing routine varicose-vein intervention during pregnancy.