What causes chronic venous insufficiency?

The most common cause is failure of the one-way valves in the superficial leg veins — particularly the great saphenous vein — allowing blood to pool under pressure (venous reflux). Prior deep vein thrombosis is another major cause (post-thrombotic syndrome). Risk factors include age over 50, female sex, multiple pregnancies, prolonged standing occupations such as nursing or retail, obesity, and a family history of varicose veins. The resulting venous hypertension drives microcirculatory inflammation that produces the characteristic skin changes and, eventually, ulceration.

Do compression stockings need to be worn permanently?

Compression stockings manage symptoms and slow disease progression but do not reverse the underlying valve damage. For people with significant reflux, a vascular surgeon can offer endovenous ablation to close the incompetent vein — after which compression requirements often reduce. In the meantime, class II (20–30 mmHg) knee-high stockings worn during waking hours are the single most effective daily step to control oedema and discomfort. They work best when applied on rising before oedema accumulates, and should be replaced every 4–6 months as elasticity wanes.

When do varicose veins need a specialist opinion?

Not all varicose veins require procedural treatment. Referral to vascular surgery is appropriate when varicose veins cause significant symptoms affecting daily life, when CEAP stage C3 or above is present (oedema, skin changes, or ulceration), after recurrent superficial thrombophlebitis, or when a varicosity has bled. Modern endovenous thermal ablation — laser or radiofrequency — is performed as a day procedure under local anaesthesia and has replaced surgical stripping as first-line treatment for great or small saphenous vein reflux per the ESVS 2022 guideline.

How is a venous leg ulcer treated?

A venous leg ulcer requires multilayer compression bandaging as the primary treatment — without sustained compression, wound dressings alone achieve little. An ABI must confirm no significant arterial disease before bandaging is applied. Wound care addresses moisture balance and infection control; antibiotics are used only when clinical cellulitis is present, not routinely. Oral pentoxifylline 400 mg three times daily has modest Cochrane-level evidence as an adjunct. Healing typically takes weeks to months, and recurrence is high without addressing the underlying venous reflux through vascular intervention.

What is the difference between a venous and an arterial leg ulcer?

Venous ulcers sit around the medial malleolus (inner ankle), are shallow with irregular edges, and are surrounded by brown pigmentation (haemosiderin) and skin changes typical of CVI. Arterial ulcers from peripheral arterial disease typically occur on the toes or foot dorsum, are deep and 'punched out', and are associated with absent pulses, claudication, and pain at rest. A bedside ABI distinguishes the two: ABI above 0.8 supports compression; below 0.5 warrants urgent vascular review and rules out compression. Mixed-aetiology ulcers require specialist input.

Chronic venous insufficiency

Chronic venous insufficiency and varicose veins: the AU GP approach

By Dr HB Lo, FACRRM Reviewed 3 July 2026 8 min read

Chronic venous insufficiency (CVI) occurs when leg vein valves fail to return blood efficiently, causing pooling that progresses from varicose veins and leg oedema through skin changes to venous ulceration.

Management centres on graduated compression stockings (class II, 20–30 mmHg). Confirm ankle-brachial index (ABI) before prescribing — compression can worsen limb ischaemia in significant arterial disease.

Refer to vascular surgery for symptomatic varicose veins, skin changes (CEAP C3+), or active venous leg ulcers. Endovenous thermal ablation (EVLA/RFA) has largely replaced surgical stripping.

Chronic venous insufficiency (CVI) encompasses a spectrum from cosmetic thread veins through troublesome varicose veins to debilitating venous leg ulcers. It is among the most common chronic conditions presenting to Australian general practice, affecting an estimated 25–40% of adults to some degree. Despite its prevalence, CVI is frequently undertreated — partly because patients normalise their symptoms and partly because the management pathway is not always clearly understood.

The underlying problem is impaired venous return from the lower limbs. In most cases this results from valvular incompetence — valve leaflets in the superficial venous system fail to close completely, allowing retrograde blood flow (reflux) during standing and walking. The consequence is sustained venous hypertension that drives progressive damage: expanding varicosities, fluid transudation into the interstitium (oedema), inflammatory skin changes, and ultimately mucosal breakdown into a venous ulcer.

Understanding the CEAP classification helps structure both assessment and management. Stages range from C0 (no visible signs) through C1 (thread veins), C2 (varicose veins ≥3 mm), C3 (oedema), C4a/b (pigmentation, lipodermatosclerosis), C5 (healed ulcer), and C6 (active ulcer). The suffix S (symptomatic) or A (asymptomatic) qualifies each stage. In Australian general practice, most referrals are appropriate from C3 upward or for symptomatic C2 disease affecting quality of life.

A. Core clinical — the AU general-practice framework

Risk factors

CVI risk is highest in: age over 50, female sex, multiple pregnancies, prolonged standing occupations (nursing, retail, hospitality, manufacturing), obesity (BMI ≥30), family history of varicose veins, and prior deep vein thrombosis (DVT). Post-thrombotic syndrome — CVI following DVT — is often more severe and involves the deep venous system, making it less amenable to superficial endovenous treatment.

Symptoms

Patients describe aching, heaviness, or throbbing in the legs that worsens through the day and with prolonged standing, and improves with leg elevation or walking. Itching over varicosities, restless legs at night, and end-of-day ankle swelling are common. In advanced disease, the perimalleolar skin becomes brown (haemosiderin deposition from red cell extravasation), indurated and fibrous (lipodermatosclerosis), or develops white scarring (atrophie blanche). Acute complications include superficial thrombophlebitis — a red, hot, tender cord along a varicosity — and, rarely, acute haemorrhage from a varicosity.

Examination

eTG Cardiovascular and ANZSVS recommend a structured lower-limb examination:

Inspect the full leg for varicosities, skin pigmentation, lipodermatosclerosis, and active ulceration.
Palpate varicosities (tenderness suggests thrombophlebitis) and assess oedema.
Assess the arterial supply: palpate femoral, popliteal, and pedal pulses. Perform a bedside ankle-brachial index (ABI) — this is the safety check before any compression prescription.
- ABI > 0.8: compression is safe.
- ABI 0.5–0.8: compression with caution; reduced pressure.
- ABI < 0.5: compression is contraindicated; urgent vascular review.
Exclude systemic causes of bilateral oedema before attributing it to CVI: cardiac failure, hypoalbuminaemia, nephrotic syndrome, cirrhosis, and drug-induced oedema (amlodipine, pioglitazone, NSAIDs are common offenders).

Investigations

Duplex venous ultrasound is the gold standard. It maps the venous anatomy, identifies reflux in the great and small saphenous veins and perforators, quantifies obstruction in post-thrombotic limbs, and plans endovenous intervention. It is Medicare-rebatable (item 55244 range) and should be requested before any planned vascular procedure.

ABI is a bedside test that every GP can perform. It is the essential safety step before prescribing compression.

Bloods in selected patients: FBC (anaemia from chronic blood loss in long-standing ulcers), albumin (nutritional support needed for wound healing), HbA1c (diabetes complicates healing), ferritin.

B. Compression therapy — evidence and prescribing

Compression is the cornerstone of management for all symptomatic CVI, supported by Cochrane systematic reviews and endorsed by both ANZSVS and Wounds Australia.

How compression works

Graduated compression applies highest pressure at the ankle and progressively less towards the knee, reducing venous diameter, improving valve coaptation, accelerating venous return, and reducing the interstitial fluid transudation that drives oedema and skin damage.

Classes and selection

Per eTG and AMH:

Class I (15–20 mmHg): mild symptoms or prophylaxis in pregnancy.
Class II (20–30 mmHg): symptomatic CVI, oedema, C3–C4 skin changes — the standard for most GP prescriptions.
Class III (30–40 mmHg): severe disease, post-DVT, active or healed venous ulcers.

Knee-high stockings are appropriate for most patients; thigh-high for proximal or pelvic venous involvement.

Prescribing well

Apply on rising before oedema accumulates; remove at bedtime. Replace every 4–6 months. Adherence is approximately 50% — counsel patients on donning aids (rubber gloves, stocking-donners), the rationale for daily use, and signs of skin breakdown. ABI must be documented before prescribing class II or higher.

Multilayer compression bandaging (4-layer or short-stretch) is first-line for active venous leg ulcers. District nursing services or wound clinics provide ongoing application.

Lifestyle adjuncts

Exercise: walking, swimming, or cycling activates the calf-muscle pump — the most effective physiological mechanism for venous return. This is as important as stockings.
Weight management: reduces mechanical venous load.
Leg elevation above hip level for 20–30 minutes, two to three times daily.
Avoid prolonged static positions: regular walking breaks for standing-occupation patients.

Pharmacological adjuncts

Pentoxifylline 400 mg three times daily (PBS general schedule) has modest Cochrane-level evidence as an adjunct for venous leg ulcer healing and can be considered alongside compression bandaging per AMH. Micronised purified flavonoid fraction (Daflon) has Cochrane evidence for symptom relief but is not PBS-subsidised. Systemic diuretics have no demonstrated role in CVI-related oedema.

C. Managing complications: thrombophlebitis and venous ulcers

Superficial thrombophlebitis

A thrombosed varicose vein segment presents as a red, hot, tender cord along a varicosity with local induration. Management per eTG: NSAIDs for analgesia, compression, and continued ambulation. A duplex ultrasound is warranted to exclude extension into the deep venous system — particularly when the affected segment is within 5 cm of the saphenofemoral or saphenopopliteal junction. Extended prophylactic anticoagulation (fondaparinux or low-molecular-weight heparin) is recommended for proximal extension or high-risk patients.

Recurrent superficial thrombophlebitis in the same varicosity segment warrants vascular referral for definitive treatment, and raises suspicion for an underlying malignancy (Trousseau’s phenomenon) if atypical features are present.

Active venous leg ulcer

Wounds Australia Best Practice guidelines are the primary AU reference. Key principles:

Confirm venous aetiology: ABI to exclude arterial disease; duplex to map reflux.
Multilayer compression bandaging drives healing: without sustained compression, dressings alone are insufficient.
Wound care: moisture-balance dressing selection (foam for moderate exudate, alginate for heavy, hydrocolloid for dry); non-adherent contact layer.
Antibiotic selection: treat clinical cellulitis only (surrounding erythema, warmth, fever, spreading) with flucloxacillin; do not use antibiotics routinely for wound colonisation.
Nutrition: ensure adequate protein, vitamin C, and zinc — deficiencies impair wound healing.
Pentoxifylline as adjunct.
Refer to vascular surgery for reflux treatment once the ulcer is healing — without addressing underlying reflux, recurrence rates exceed 70% within five years.

D. Australian operations

Referral to vascular surgery

Per ANZSVS, referral is appropriate for:

Symptomatic varicose veins affecting quality of life (C2S).
CEAP C3 or above (oedema, skin changes, ulceration).
Recurrent superficial thrombophlebitis.
Bleeding varicosity.
Healed or active venous ulcer — reflux treatment reduces recurrence.
Suspected May-Thurner syndrome (iliac vein compression causing left-leg-predominant CVI in younger women).

The referral should include: ABI result, duplex ultrasound report, CEAP stage, symptom duration and impact, and current medications (anticoagulants, vasodilators).

Modern procedural options per ESVS 2022:

Endovenous laser ablation (EVLA) or radiofrequency ablation (RFA): outpatient, local anaesthesia, comparable efficacy to surgical stripping with fewer complications and faster recovery — now the first-line procedural treatment.
Foam sclerotherapy: for residual accessory veins and reticular veins.
Cyanoacrylate glue (VenaSeal) or mechanochemical ablation (ClariVein): non-thermal alternatives.
Iliac vein stenting: for May-Thurner or post-thrombotic iliac obstruction.

MBS and funding

Standard GP consultations use MBS items 23/36/44. The GP Chronic Condition Management Plan (GPCCMP, items 965/967 from 1 July 2025) funds allied health for patients with chronic venous leg ulcers — district nursing for wound care, dietitian for nutritional support, and physiotherapy for calf-muscle rehabilitation. The 75+ Health Assessment (item 707) and ATSI Health Assessment (item 715) are structured opportunities to identify and stage CVI. Duplex venous ultrasound is Medicare-rebatable (item 55244 range). Endovenous ablation procedures attract specific Medicare item numbers (32523 range) but are primarily performed in the private sector.

E. Special populations

Pregnancy. Varicose veins worsen with each pregnancy due to progesterone-mediated venous wall relaxation and mechanical uterine compression of pelvic veins. Class I–II compression stockings (thigh-high if extensive) are safe from early pregnancy. Vascular intervention should be deferred until at least three months postpartum — most varicosities improve after delivery, though many persist.

Older adults. Venous leg ulcers are most prevalent in people over 65. Comorbidities including peripheral arterial disease, diabetes, cardiac failure, and malnutrition complicate healing. A multidisciplinary approach — GP, district nursing, wound clinic, dietitian, and podiatry — typically improves outcomes. The GPCCMP (items 965/967) funds this coordination. Falls risk is relevant: oedematous, painful legs and bulky dressings increase fall risk; physiotherapy input on balance and strength supports safe mobilisation.

People with limited mobility. Wheelchair-users, those with hemiplegia, and post-stroke patients have impaired calf-muscle pump function. Intermittent pneumatic compression (IPC) devices, limb elevation, and passive calf compression can partially compensate. Weight management and seated leg exercises (ankle pumps, heel-toe raises) are encouraged where possible.

Aboriginal and Torres Strait Islander people. Skin conditions, venous ulcers, and their secondary infection are more prevalent in ATSI communities, compounded by higher rates of diabetes and chronic kidney disease. Culturally safe wound management and close liaison with Aboriginal Community Controlled Health Organisations (ACCHOs) and visiting allied health services supports effective care. The ATSI Health Assessment (item 715) is a formal opportunity to identify CVI and venous ulcer risk.

When to escalate

Consider emergency presentation or urgent same-day review when:

A varicosity bleeds acutely — direct pressure and leg elevation immediately; emergency assessment to secure the bleeding point.
Cellulitis extends above the knee or is accompanied by systemic features (fever, rigors, hypotension, confusion).
DVT is suspected clinically — duplex ultrasound urgently, or via the emergency department if access is delayed.
ABI falls below 0.5 on a limb with a venous ulcer — this indicates significant arterial disease and warrants urgent vascular review before any compression is applied.

Semi-urgent referral to vascular surgery within four weeks is appropriate for C4 skin changes, healed ulcers (C5), active ulcers (C6), or recurrent superficial thrombophlebitis at the saphenofemoral junction.

What this article is and is not

This is general health information drawn from Australian clinical guidelines — Therapeutic Guidelines (eTG), Wounds Australia, ANZSVS, AMH — and the ESVS 2022 international guideline. It is not personal medical advice and does not create a doctor–patient relationship. Decisions about compression class, wound dressing selection, or referral timing are made with your own GP and treating clinicians.

For consumer resources: HealthDirect — Varicose veins, Better Health Channel, and Wounds Australia.

Sources cited

Frequently asked questions

What causes chronic venous insufficiency?

The most common cause is failure of the one-way valves in the superficial leg veins — particularly the great saphenous vein — allowing blood to pool under pressure (venous reflux). Prior deep vein thrombosis is another major cause (post-thrombotic syndrome). Risk factors include age over 50, female sex, multiple pregnancies, prolonged standing occupations such as nursing or retail, obesity, and a family history of varicose veins. The resulting venous hypertension drives microcirculatory inflammation that produces the characteristic skin changes and, eventually, ulceration.
Do compression stockings need to be worn permanently?

Compression stockings manage symptoms and slow disease progression but do not reverse the underlying valve damage. For people with significant reflux, a vascular surgeon can offer endovenous ablation to close the incompetent vein — after which compression requirements often reduce. In the meantime, class II (20–30 mmHg) knee-high stockings worn during waking hours are the single most effective daily step to control oedema and discomfort. They work best when applied on rising before oedema accumulates, and should be replaced every 4–6 months as elasticity wanes.
When do varicose veins need a specialist opinion?

Not all varicose veins require procedural treatment. Referral to vascular surgery is appropriate when varicose veins cause significant symptoms affecting daily life, when CEAP stage C3 or above is present (oedema, skin changes, or ulceration), after recurrent superficial thrombophlebitis, or when a varicosity has bled. Modern endovenous thermal ablation — laser or radiofrequency — is performed as a day procedure under local anaesthesia and has replaced surgical stripping as first-line treatment for great or small saphenous vein reflux per the ESVS 2022 guideline.
How is a venous leg ulcer treated?

A venous leg ulcer requires multilayer compression bandaging as the primary treatment — without sustained compression, wound dressings alone achieve little. An ABI must confirm no significant arterial disease before bandaging is applied. Wound care addresses moisture balance and infection control; antibiotics are used only when clinical cellulitis is present, not routinely. Oral pentoxifylline 400 mg three times daily has modest Cochrane-level evidence as an adjunct. Healing typically takes weeks to months, and recurrence is high without addressing the underlying venous reflux through vascular intervention.
What is the difference between a venous and an arterial leg ulcer?

Venous ulcers sit around the medial malleolus (inner ankle), are shallow with irregular edges, and are surrounded by brown pigmentation (haemosiderin) and skin changes typical of CVI. Arterial ulcers from peripheral arterial disease typically occur on the toes or foot dorsum, are deep and 'punched out', and are associated with absent pulses, claudication, and pain at rest. A bedside ABI distinguishes the two: ABI above 0.8 supports compression; below 0.5 warrants urgent vascular review and rules out compression. Mixed-aetiology ulcers require specialist input.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.