Chronic venous insufficiency

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

Chronic venous disease covers symptoms or signs related to abnormal lower-limb veins; chronic venous insufficiency (CVI) usually denotes the advanced clinical spectrum with oedema, trophic skin damage or ulceration. Superficial reflux is common, but deep reflux, post-thrombotic obstruction, non-thrombotic iliac obstruction, calf-muscle pump failure and restricted ankle movement may act alone or together. Persistent ambulatory venous hypertension drives capillary leakage and inflammation. The result progresses from dependent swelling to venous eczema, haemosiderin pigmentation, lipodermatosclerosis, atrophie blanche and ulceration. CEAP provides a descriptive clinical class, while symptom scores and serial measurements track change.

Treatment pairs conservative control of venous hypertension with correction of treatable reflux or obstruction. Walking, calf-pump exercise, ankle mobility, weight management and elevation can reduce dependency. Compression is an active treatment requiring an appropriate device, pressure, fit and arterial safety assessment. ESVS recommends 20–40 mmHg ankle pressure for C3 oedema and for C4b lipodermatosclerosis or atrophie blanche; the exact device must account for limb shape, dexterity, neuropathy and ability to apply it. NICE referral criteria include chronic venous pigmentation or eczema, SVT with suspected incompetence, and both active and healed venous ulcers. Duplex then maps treatment targets, while suspected iliac or caval obstruction may require abdominal duplex and cross-sectional imaging.

Key points

CVI is advanced chronic venous disease with oedema, skin change or ulceration caused by sustained venous hypertension from reflux, obstruction, calf-pump failure or combinations.
Examine the entire limb and abdomen and obtain full venous duplex for reflux or obstruction; identify acute DVT, arterial disease, infection, systemic oedema and proximal outflow clues before attributing symptoms to superficial veins.
Before sustained compression measure ankle pressure and ABPI, adding toe pressure when calcification may make ABPI unreliable; avoid sustained compression below ABPI 0.6 or ankle pressure 60 mmHg, and in active mixed ulceration also below toe pressure 30 mmHg. Modified compression requires close supervision.
Before sustained compression, measure ankle pressure and ABPI; in diabetes or suspected arterial calcification add toe pressure because a falsely high ABPI can conceal impaired perfusion.
For C3 venous oedema, ESVS recommends below-knee stockings, inelastic bandages or adjustable garments delivering 20–40 mmHg at the ankle, after arterial and neurological safety assessment.
Severe arterial disease with ABPI below 0.6 or ankle pressure below 60 mmHg is a contraindication to sustained compression; mixed disease needs modified compression under close supervision, not an unsupervised standard system.
Refer venous pigmentation, eczema, lipodermatosclerosis, atrophie blanche, active ulcer or healed ulcer to a vascular service; skin care alone does not address the venous cause.

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

Superficial venous reflux

Valve failure in saphenous trunks, tributaries or perforators permits retrograde flow and raises dependent pressure in the distal superficial and microvascular beds.

Deep post-thrombotic disease

Previous DVT can leave residual obstruction and valve destruction. Both increase ambulatory pressure, and proximal iliofemoral disease may generate venous claudication and collaterals.

Pump and outflow failure

Restricted ankle movement, calf weakness, immobility, obesity or iliac compression reduces venous emptying and can amplify reflux that would otherwise cause fewer symptoms.

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

1
Ambulatory venous hypertension
Failed valves, obstruction or poor calf ejection prevents pressure falling during walking, maintaining abnormally high distal venous and capillary pressures.
2
Capillary leakage
Elevated hydrostatic pressure drives fluid and proteins into tissue, initially causing dependent pitting oedema and later overloading lymphatic clearance.
3
Inflammation and fibrosis
Leukocyte activation, endothelial injury and iron deposition produce eczema, pigmentation and progressive dermal and subcutaneous fibrosis called lipodermatosclerosis.
4
Barrier breakdown
Poor microcirculatory exchange, inflammation, oedema and minor trauma impair repair, producing atrophie blanche and a recurrent ulcer-prone gaiter region.

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

Dependent venous symptoms

Aching, heaviness, cramps, itching and swelling often worsen after prolonged standing and later in the day, with relief from walking or elevation. Symptoms are nonspecific and must be matched to objective signs.

Oedema and corona

Early oedema is typically pitting around the ankle. Corona phlebectatica, visible varicosities and progressive lower-leg swelling support venous hypertension, while foot and toe involvement suggests a lymphatic component.

C4 skin injury

Brown haemosiderin pigmentation, stasis eczema, indurated inverted-bottle lower leg, lipodermatosclerosis and ivory atrophie blanche indicate inflammatory and fibrotic consequences of chronic pressure.

Ulcer phenotype

Venous ulcers are usually shallow, irregular and exudative in the gaiter region, often with oedema and skin change. Atypical site, punched-out edge, severe rest pain or absent pulses requires another cause.

Outflow obstruction

Whole-limb swelling, venous claudication, prior iliofemoral DVT and abdominal or suprapubic collaterals suggest proximal deep obstruction rather than isolated superficial reflux.

Red flags requiring action

Abrupt asymmetric swelling, deep pain or new chest symptoms is not routine chronic venous disease and requires urgent VTE assessment.
Rest pain, gangrene, a cold foot, rapidly worsening tissue loss or absent pulses suggests severe arterial insufficiency; stop plans for sustained compression and obtain urgent vascular review.
Rapidly spreading erythema, fever, hypotension, crepitus or pain out of proportion suggests serious infection and needs urgent reassessment.
Acute breathlessness, orthopnoea, pulmonary oedema or unstable decompensated heart failure makes routine compression unsafe until haemodynamic status is assessed.
Prominent abdominal or cross-pubic collaterals, venous claudication or whole-limb swelling suggests proximal outflow obstruction and needs specialist imaging strategy.

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
Full lower-limb venous duplex ultrasoundFirst step
Why
Map superficial and deep reflux, identify post-thrombotic change or obstruction, and determine whether an anatomical target matches the clinical territory.
Interpretation and limitations
Reflux below the inguinal ligament may support superficial treatment; abnormal common femoral flow, collaterals or discordant severe symptoms should prompt assessment for supra-inguinal obstruction.
02
Ankle systolic pressure and ABPI
Why
Identify clinically important arterial disease before sustained compression and provide an absolute perfusion measure as well as a pressure ratio.
Interpretation and limitations
ABPI below 0.6 or ankle pressure below 60 mmHg contraindicates sustained compression. Borderline results require vascular interpretation; calcified incompressible arteries may give a deceptively normal or high ratio.
03
Toe pressure or toe-brachial index
Why
Assess distal perfusion when diabetes, renal disease, neuropathy or an unexpectedly high ABPI raises concern for medial arterial calcification.
Interpretation and limitations
Toe vessels are less affected by medial calcification. A low toe pressure can expose arterial compromise hidden by ABPI and guides whether modified compression is possible under supervision.
04
Abdominal duplex and cross-sectional venous imaging
Why
Evaluate iliac or caval obstruction when symptoms, collaterals or lower-limb duplex findings suggest disease above the inguinal ligament.
Interpretation and limitations
CT or MR venography defines anatomy and alternative pelvic causes; intravascular ultrasound is reserved for selected specialist cases when intervention is being considered.
05
Serial limb and skin assessment
Why
Establish baseline circumference, pitting, CEAP class, eczema, induration and any wound dimensions for monitoring treatment response.
Interpretation and limitations
Reduced swelling and softer skin support effective pressure control, but worsening pain, colour, sensation or tissue integrity after compression suggests poor fit, neuropathic injury or arterial compromise.

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

Lymphoedema

Toe and dorsal-foot swelling, Stemmer sign and later non-pitting fibrosis favour lymphatic failure, although advanced venous disease can cause secondary lymphatic overload.

Systemic fluid retention

Bilateral oedema with orthopnoea, raised venous pressure, ascites or renal dysfunction suggests cardiac, hepatic or renal disease and changes compression safety.

Peripheral arterial disease

Claudication, rest pain, coolness, diminished pulses and distal tissue loss identify an arterial component requiring quantified perfusion before compression.

Acute deep vein thrombosis

Sudden asymmetry or pain superimposed on chronic swelling requires a formal DVT pathway; prior venous disease does not explain an abrupt change.

Inflammatory skin disease

Contact dermatitis, cellulitis, vasculitis and inflammatory ulceration may mimic venous eczema or complicate it; distribution, systemic features and wound morphology discriminate.

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

01Initial assessmentChronic oedema with skin changeFirst stepUse for persistent lower-leg swelling, pigmentation, eczema, induration or suspected venous ulceration.

1Take a venous and VTE history, define daily symptom pattern and mobility, and examine standing varicosities, oedema distribution, skin, ulcers, pulses and abdominal collaterals.
2Exclude acute DVT, infection, severe arterial ischaemia and decompensated systemic disease before assigning a chronic venous diagnosis or applying compression.
3Arrange venous duplex and arterial pressure assessment; add toe pressure when ABPI may be unreliable and proximal venous imaging when outflow obstruction is suspected.
4Start suitable exercise, elevation, emollient-based skin care and appropriately selected compression after safety checks, and refer qualifying skin change or ulcer history to a vascular service.

02Compression pathwaySafe pressure selectionUse before prescribing stockings, bandages or adjustable compression for venous oedema or C4 skin disease.

1Check pulses, ankle pressure and ABPI, neuropathy, skin integrity, heart failure status, limb shape, dexterity and the person’s capacity to apply or obtain help with the device.
2When arterial perfusion is adequate, select a below-knee system delivering 20–40 mmHg at the ankle for C3 oedema or C4b skin induration, fitted by trained staff.
3Do not use sustained compression at ABPI below 0.6 or ankle pressure below 60 mmHg; use modified compression in mixed disease only within a closely supervised specialist plan.
4Review early for pain, colour change, numbness, pressure injury, slippage and adherence, then remeasure after oedema changes because fit and delivered pressure can alter.

03Escalation pathwayPersistent severe CVIEscalationUse when symptoms, skin damage or swelling persists despite well-delivered conservative treatment.

1Confirm adherence, device fit, ankle mobility and that dermatitis, infection or systemic oedema is not driving apparent treatment failure.
2Revisit duplex anatomy and refer to a vascular service for superficial reflux treatment; if proximal obstruction is suspected, complete specialist venous imaging before intervention.
3Maintain compression and skin protection when safe after intervention, because deep disease, calf-pump failure and recurrence may continue to generate venous hypertension.

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

Venous ulceration

Progressive microvascular injury and fragile fibrotic skin culminate in an open gaiter wound with pain, exudate and high recurrence risk.

Secondary lymphatic failure

Longstanding high interstitial fluid load damages lymphatic clearance, making oedema harder, more extensive and less fully reversible with elevation.

Infection and dermatitis

Barrier disruption predisposes to eczema, contact allergy and cellulitis, while colonisation of an open wound alone does not establish clinical infection.

Mobility decline

Pain, limb heaviness, joint stiffness and fear of wounds reduce walking, further weakening the calf pump and reinforcing venous hypertension.

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

Measure ankle or calf circumference at consistent landmarks and review pitting, skin tension and daily fluctuation to judge oedema response.
Inspect under compression for new pain, pallor, cyanosis, coolness, numbness, pressure damage or blistering; remove the device and reassess perfusion if these occur.
Track eczema, pigmentation, induration and any ulcer dimensions; recurrent inflammation may reflect poor pressure control, contact dermatitis or infection rather than simple treatment failure.
Ask whether the patient can don and remove the device, tolerates it through the day and has practical support; a theoretically effective stocking fails if it cannot be worn.
Repeat arterial assessment when symptoms change, the wound deteriorates, pulses weaken or a prolonged interval and vascular risk make the original measurement unreliable.
After superficial or deep intervention, reassess symptoms and duplex when clinically indicated, while continuing prevention for residual venous hypertension.

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

CVI has several pumps and pipes

Superficial reflux, deep reflux, obstruction and calf-pump impairment often coexist. A single visible varicosity may be only one component of the haemodynamic problem.

Use absolute pressure too

An ABPI ratio can mislead when vessels are calcified or systemic pressure is low. ESVS therefore couples the ratio with ankle pressure and recommends toe assessment in diabetes.

Compression is a prescription

The modality, ankle pressure, stiffness, fit and monitoring plan matter. Stockings, inelastic bandages and adjustable wraps behave differently and require trained selection.

C5 remains advanced disease

A healed ulcer signals persistent recurrence risk. The skin has closed, but underlying reflux or obstruction and the need for preventive compression or intervention remain.

Look above the groin

Abdominal and cross-pubic collaterals or whole-limb symptoms are clues to iliac or caval obstruction; treating superficial collaterals without understanding outflow can be harmful.

11Common pitfallsFrequent interpretation and management errors.

01
Starting strong sustained compression because the limb looks venous without measuring arterial perfusion risks ischaemic injury in mixed disease.
02
Accepting a high ABPI as reassuring in diabetes can miss calcified incompressible arteries; toe pressure adds a safer distal assessment.
03
Treating venous eczema with repeated steroid courses while ignoring reflux, oedema and referral criteria addresses inflammation but not its driver.
04
Assuming all oedema is superficial reflux misses heart failure, renal disease, lymphoedema, medication effects and proximal venous obstruction.
05
Ablating visible collateral veins in severe outflow obstruction before specialist mapping can remove a compensatory drainage pathway.
06
Prescribing hosiery without checking dexterity, limb shape, fit and follow-up produces non-use, constriction or pressure damage rather than effective compression.

Find your next topic