Chronic Venous Insufficiency

General Mechanisms

• CVI results from structural or functional abnormalities of the venous system of the lower extremities, most commonly due to venous reflux.
• Other mechanisms include chronic venous obstruction or a mixed pattern of reflux and obstruction.
• Valvular reflux is the principal abnormality, often developing after deep vein thrombosis (DVT) through valve damage and recanalisation. Up to 50% of patients may develop CVI within 5–10 years following a DVT episode.
• Less common causes include congenital absence of venous valves, calf muscle pump dysfunction, or venous outflow obstruction.

Role of Venous Reflux

• Reflux occurs when venous valves fail to prevent retrograde flow, resulting in persistent venous hypertension.
• The great saphenous vein (GSV) is most frequently implicated, especially near its termination at the saphenofemoral junction.
• Valve failure may arise spontaneously in congenitally weak valves or be acquired due to trauma, thrombosis, hormonal influences (e.g., pregnancy), or environmental factors such as prolonged standing.

Superficial Venous Insufficiency

• In this subtype, deep veins remain structurally normal while incompetent superficial valves allow blood to flow backward into dilated superficial veins.
• More than 80% of leg varicosities are linked to incompetence of the GSV.
• Reflux is usually confined to the superficial venous system, and although it frequently causes varicosities and skin changes, it rarely progresses to severe CVI unless extensive.

Deep Venous Insufficiency

• Most often arises from damage to the deep venous valves following DVT, leading to loss of competency and unopposed retrograde flow.
• Congenital valve malformations or vessel abnormalities can also be responsible.
• Hydrostatic pressures in the lower limb rise significantly without effective valve function, promoting chronic venous hypertension and sequelae such as oedema and ulceration.

Congenital and Genetic Syndromes

• Klippel-Trénaunay-Weber (KTW) syndrome represents a less common but important cause. It is characterised by port-wine stains, varicosities, and hypertrophy of bone or soft tissue.
• In the Parkes Weber variant, arteriovenous malformations coexist with venous abnormalities.
• Persistence of embryonic venous structures such as the sciatic vein creates additional reflux pathways.
• These anomalies often overwhelm normal lymphatic drainage, producing secondary lymphoedema.
• Surgical intervention in KTW syndrome is challenging due to the risk of worsening venous abnormalities postoperatively.

Contribution of Virchow’s Triad

• Venous incompetence may also follow thrombus formation influenced by stasis, hypercoagulability, and endothelial injury.
• This mechanism further underscores the link between DVT and progression to chronic venous disease.

Risk Factors

Age

• Incidence increases markedly after age 55.

Sex

• More common in women, particularly those who are obese.

Genetics

• Family history of varicose veins or venous pathology increases susceptibility.

Lifestyle and Occupation

• Prolonged standing or sitting, sedentary behaviour, and smoking contribute to venous hypertension.
  
  

Hormonal and Reproductive Factors

• Pregnancy and oral contraceptive use predispose to CVI by increasing venous pressures and altering vessel wall tone.

Previous Medical History

• Prior DVT, thrombophlebitis, leg trauma, and hypertension increase risk.

Other Factors

• Low dietary fibre intake has been associated with higher incidence in some studies.

Normal Venous Function

• Efficient venous return from the lower extremities requires:
  • Functional calf and foot muscle pumps.
  • Patency of deep and superficial veins.
  • Competent bicuspid valves to prevent retrograde flow.
• In health, venous pressures in the leg remain relatively low during ambulation (<20 mmHg), as the calf muscle pump and venous valves reduce pressure with each contraction.

Mechanisms of Venous Hypertension

• CVI develops when venous reflux, obstruction, or a combination of both disrupts normal haemodynamics, leading to sustained ambulatory venous hypertension.
• In deep venous incompetence, pressures may double during walking, causing venous congestion.
• Ambulatory venous hypertension drives a cycle of oedema, inflammation, and tissue hypoxia, resulting in characteristic skin and soft tissue changes.

Structural and Cellular Changes

Lipodermatosclerosis

• Results from capillary proliferation, fat necrosis, and fibrosis of the dermis and subcutaneous tissue.

Hyperpigmentation

• Brawny oedema due to red blood cell extravasation and haemosiderin deposition in the skin.
• Chronic inflammation and hypoxia eventually cause ulcer formation, usually around the medial malleolus.

Theories of Ulcer Development

Fibrin cuff hypothesis (Burnand)

• Elevated venous pressure causes leakage of plasma proteins, especially fibrinogen, into pericapillary tissue, forming a “fibrin cuff” that impedes oxygen diffusion.

White cell trapping hypothesis (Coleridge-Smith)

• Venous hypertension slows capillary flow, trapping leukocytes. These cells release proteolytic enzymes and free radicals, damaging the endothelium, increasing permeability, and worsening tissue hypoxia.

Primary vs. Secondary CVI

Primary CVI

• Occurs without preceding DVT, often linked to congenital valve defects, altered venous wall biochemistry, or elastin deficiency.
• Studies indicate ~70% of patients with CVI have primary disease.

Secondary CVI

• Develops after DVT, where inflammatory injury and scarring damage valves and narrow the lumen, perpetuating reflux and obstruction.

Valve and Vein Dysfunction

Superficial Venous Incompetence

• Usually due to widened venous diameters or malformed valves, preventing normal cusp closure.
• Often localised at the saphenofemoral junction.

Deep Venous Incompetence

• Frequently follows DVT, which leads to adhesion, scarring, and destruction of valve leaflets.

Perforator Valve Failure

• Allows high-pressure flow from deep to superficial veins, causing dilation of superficial vessels and progressive valve failure.

Progression of Disease

Junctional valve failure

• Commonly occurs at the saphenofemoral or saphenopopliteal junction, leading to progressive reflux down the leg.

Perforator valve failure

• Seen at sites such as the Hunterian or Boyd perforators, introducing high pressures into the superficial system.
• These mechanisms result in varicosities, venous dilation, and recirculation loops that prolong venous clearance time.
• Experimental data show that reflux volumes exceeding 15 mL/s in the GSV, SSV, and popliteal vein strongly correlate with venous ulceration, whereas reflux <10 mL/s rarely results in ulceration.

Microcirculatory Dysfunction

• Impaired clearance of metabolic by-products such as lactate and carbon dioxide further contributes to tissue injury.
• Chronic venous stasis is not always true stagnation; recirculation of blood between refluxing superficial veins and competent deep veins prolongs transit time, worsening tissue hypoxia.
• These microvascular changes explain why some patients with venous hypertension remain ulcer-free, while others develop chronic ulceration.

Molecular and Inflammatory Factors

• Studies have demonstrated increased expression of adhesion molecules and endothelial activation in CVI.
• Elevated circulating P-selectin has been correlated with disease severity, suggesting platelet and endothelial dysfunction play a role in pathogenesis.

United States Statistics

• CVI is recognised as a major public health issue. More than 11 million men and 22 million women over the age of 40 are affected by varicose veins, and over 2 million adults present with advanced disease.
• It is estimated that 2–5% of the American population demonstrate clinical signs of CVI.
• Prevalence of varicosities is widely reported to range from 7% to 60%, with most studies suggesting around 40% have demonstrable venous reflux.
• Venous stasis ulcers affect about 500,000 individuals in the US, while the mean incidence of hospitalisation for CVI is 92 per 100,000 admissions.
• Epidemiological surveys suggest 10–35% of adults may be affected, with 4% of those aged ≥65 years developing venous ulcers.
• Venous ulcer prevalence in the US ranges from 1% to 3%, with ulcer care accounting for nearly 2% of overall healthcare expenditure.

International Statistics

• CVI prevalence is higher in industrialised nations such as Western Europe and the United States, largely attributed to sedentary lifestyles and reduced physical activity.
• Approximately 1–2% of adults globally develop lower-limb ulceration, with 70–90% of these ulcers caused by CVI.
• International pooled data suggest:
  • 8% prevalence for CEAP class C3 (oedema).
  • 4% prevalence for C4 (skin changes due to CVI).
  • 1% prevalence for C5 (healed venous ulcer).
  • 0.42% prevalence for C6 (active ulcer).

Age-Related Demographics

Age

• Prevalence rises with age, with peak incidence observed in women aged 40–49 years and men aged 70–79 years.
• Reticular veins typically appear first in adolescence or early adulthood, progressing over time to perforator incompetence and truncal varicosities.
• Findings from the Bochum study in children aged 10–12 years demonstrated that symptoms and abnormal venous tests often precede visible varicosities.
• Active venous ulceration affects <1% of the population overall, but increases to 3% in those older than 65 years.

Sex-Related Demographics

Sex

• At all ages, CVI is more common in women than men.
• In younger adults, incidence is <10% in men compared with ~30% in women.
• After the age of 50, prevalence increases to 20% in men and ~50% in women.

Risk Factors

Age

• Advancing years are one of the strongest predictors of CVI.

Sex

• Female sex is strongly associated with higher prevalence.

Obesity

• Increases venous pressures and risk of valve failure.

Family History

• Genetic predisposition to varicosities and venous reflux.

Occupation

• Prolonged standing or sitting contributes to venous hypertension.

Other Factors

• Pregnancy and sedentary lifestyle further heighten risk.

Key Diagnostic Factors

Presence of Risk Factors

• Increasing age, family history of venous disease, prolonged standing (orthostatic occupation), smoking (especially in men), history of DVT, female sex, and multiparity are commonly reported antecedents.

Corona Phlebectatica (Ankle Flare)

• Fan-shaped pattern of small intradermal veins around the ankle or foot, often considered an early sign of advanced venous disease.

Ankle Swelling

• Typically begins as unilateral pitting oedema but may become bilateral.
• Oedema is initially confined to the ankle region and later extends to the leg and foot.

Hyperpigmentation (Brawny Oedema)

• Reddish-brown discoloration of the ankle and lower leg.
• Caused by extravasation of red blood cells and deposition of haemosiderin under the skin due to prolonged venous hypertension.

Lipodermatosclerosis

• Chronic inflammatory and fibrotic changes in the supramalleolar skin and subcutaneous tissue.
• May cause tightening of the skin and, in severe cases, contracture of the Achilles tendon.

Atrophie Blanche

• Well-defined, round or irregular white, shiny patches of atrophic skin, often surrounded by dilated capillaries and pigmented areas.

Leg Ulcers

• Usually occur in the “gaiter area” of the lower leg, particularly above the medial malleolus but can also occur near the lateral malleolus.
• May present as healed scars or active ulcers.

Other Diagnostic Factors

Leg Fatigue, Aching, and Discomfort

• Symptoms worsen throughout the day and after prolonged standing.
• Relief is typically achieved with leg elevation.

Heavy Legs

• A common complaint, particularly towards the evening.

Leg Cramps

• Associated with venous stasis and often accompanied by stasis eczema.

Telangiectasias

• Dilated intradermal venules (<1 mm), representing one of the earliest visible signs.

Reticular Veins

• Dilated, non-palpable subdermal veins (<3 mm), often a precursor to varicosities.

Dilated Tortuous Veins

• Classic varicose veins, defined as palpable, subcutaneous dilated veins.

Dry and Scaly Skin

• Commonly represents venous stasis dermatitis with associated eczematous changes.

Less Common Factors

Skin Burning and Itching

• Often reported with venous eczema and stasis dermatitis.

Unilateral Leg Swelling

• May indicate underlying iliac vein obstruction, more frequently on the left side, and can be the predominant symptom in some patients.

Symptom Behaviour

Pain and Discomfort

• Characteristically worse with prolonged standing and relieved by walking or leg elevation.
• Heat tends to aggravate symptoms, while cold offers relief.
• Compression stockings often improve venous pain but worsen arterial pain, aiding differentiation.

Subjective Symptoms

• Patients may describe throbbing, cramping, aching, heaviness, burning, swelling, and restless legs.
• Symptoms can fluctuate with hormonal changes; e.g., many pregnant women with varicose veins report significant discomfort.
• In deep venous insufficiency, aching and heaviness are almost universal.

Venous Ulcer Symptoms

• Non-healing ulcers are typically located around the medial malleolus, an area of high venous pressure due to perforators.

Risk Factors Reported in History

Age

• Prevalence of CVI rises steadily with advancing age.

Family History

• Strongly associated with both varicose veins and advanced venous disease.

Smoking

• Particularly linked to severe CVI in men.

Deep Vein Thrombosis

• Up to half of patients develop CVI within 5–10 years of a DVT due to post-thrombotic valvular reflux.

Orthostatic Occupation

• Jobs requiring long periods of standing, such as construction work, predispose to CVI.

Female Sex

• Associated with higher incidence of venous disease, influenced by hormonal and reproductive factors.

Obesity (Waist Circumference)

• Elevated BMI and central obesity increase venous pressures, worsening reflux.

Ligamentous Laxity

• Suggested by associated features such as flat feet and prior hernia repairs, reflecting connective tissue weakness predisposing to venous failure.

Hallmark Cutaneous and Soft-Tissue Signs

Oedema

• Pitting oedema beginning at the ankle (often unilateral early, bilateral with progression); may extend to the leg and foot.
• May reflect venous reflux/obstruction; consider alternative/systemic causes (hepatic, renal, cardiac failure, infection, trauma, drugs) when findings are disproportionate or atypical.

Hyperpigmentation (Brawny Oedema)

• Reddish-brown discolouration of the ankle and lower leg caused by red cell extravasation and haemosiderin deposition due to long-standing ambulatory venous hypertension.

Venous (Stasis) Dermatitis

• Dry, scaly, eczematous changes over the gaiter area; often pruritic and may coexist with weeping or secondary infection.

Chronic Cellulitis

• Recurrent inflammatory episodes over chronically oedematous skin; distinguish from acute bacterial cellulitis by bilaterality and absence of systemic features.

Atrophie Blanche

• Porcelain-white, atrophic plaques with surrounding telangiectasia and hyperpigmentation; frequent in advanced disease and often adjacent to ulcers.

Ulceration

• Typically in the gaiter region (proximal/posterior to the medial malleolus; occasionally lateral).
• May be healed (C5) or active (C6); assess size, depth, exudate, edge, surrounding dermatitis, and signs of infection or malignant change (rare Marjolin transformation).

Early and Supportive Surface Venous Signs

Corona Phlebectatica (Ankle/ Malleolar Flare)

• Fan-shaped mat of small intradermal veins at the ankle or foot; an early marker of advanced venous disease.

Telangiectasias

• Dilated intradermal venules <1 mm; often symptomatic and may predate visible varicosities.

Reticular Veins

• Dilated, non-palpable subdermal veins <3 mm; frequently a precursor to truncal varices.

Dilated Tortuous Veins (Varicosities)

• Palpable, subcutaneous, tortuous veins; look for distribution along the great/small saphenous territories and clusters over perforator sites.

Pattern Recognition and Distribution Clues

Medial vs Lateral Ankle Changes

• Medial ankle hyperpigmentation, eczema, and ulceration strongly suggest venous stasis (dependent on competence/patency of the GSV and perforators).
• Lateral-sided isolated lesions more often imply prior trauma or arterial insufficiency rather than pure venous disease.

Visible Venous Distension

• Normal superficial veins can be visible at the foot/ankle and sometimes the popliteal fossa; dilatation above the ankle usually implies pathology.
• Bulging over known perforator sites (e.g., mid-thigh, proximal calf) suggests perforator incompetence.

Lymphatic Overlap and Mimics

Venolymphatic Oedema

• Secondary lymphoedema from lymph overproduction in severe venous hypertension; may produce non-pitting elements with skin thickening.
• Primary lymphatic obstruction should be considered when swelling is non-pitting, involves the dorsum of the foot (“squared toes”), or lacks classic venous skin changes.

Bedside Manoeuvres

Trendelenburg Test

• Purpose: Differentiate superficial-system reflux from deep-system valve incompetence and localise high-pressure entry points.
• Method: Elevate the limb to empty superficial veins → occlude the suspected junction (commonly the saphenofemoral junction) → have the patient stand → observe venous filling.
• Interpretation:
  • Slow filling with occlusion followed by rapid filling when occlusion is released indicates a junctional reflux point into the superficial system.
  • Immediate rapid filling despite occlusion suggests additional reflux pathways or deep-system valve incompetence between the groin and escape point.
• Implication: Deep-system incompetence limits interventional options; compression remains central.

Examination Caveats and Scope

Limits of Inspection and Palpation

• Visual patterns guide suspicion but are not definitive; similar findings occur in arterial disease, neuropathic ulcers, vasculitic/rheumatologic dermatoses, malignant lesions, and infectious ulcers.
• Physical examination should be complemented by objective testing (e.g., duplex ultrasound) to map reflux/obstruction, define perforator involvement, and plan treatment.

First-Line Test

Duplex Ultrasound

• Role: Initial and most important diagnostic study; maps sites of reflux and obstruction across superficial, perforator, and deep systems.
• Protocol essentials: Perform a reflux study (not just DVT exclusion) with the patient upright if safely able. Systematically assess: common femoral, femoral, popliteal, great saphenous (saphenofemoral junction, upper/mid/distal thigh, calf), small saphenous, and anterior accessory saphenous (if present).
• Diagnostic thresholds for reflux:
  • Superficial veins: valve closure time >0.5 seconds.
  • Deep veins (e.g., femoral, popliteal): >1.0 second.
• Technique notes: Use distal calf compression or Valsalva to provoke reflux; colour flow/Doppler waveforms to characterise direction and duration. Operator dependent; document reflux pathways and CEAP class to guide therapy.

Imaging to Consider (Problem-Solving / Complex Disease)

Ascending (Contrast) Phlebography

• Current place: Largely supplanted by duplex; reserved by specialists for complex CVI (e.g., mapping in iliac obstruction or uncertain patterns).
• Output: Defines obstruction level and collateral pathways; can target intervention planning.

CT Venography

• Use case: Congenital, advanced, or anatomically complex CVI; excellent anatomical detail of pelvic/abdominal venous structures.

MR Venography

• Use case: High-quality mapping of deep and pelvic venous systems; useful where non-vascular mimics are suspected or when radiation/iodinated contrast is undesirable.

CT Abdomen & Pelvis / Abdominal–Pelvic Ultrasound

• Indication: Suspected extrinsic compression (e.g., mass effect) in iliac vein disease; may reveal pelvic or abdominal causes of venous outflow impairment.

Intravascular Ultrasound (IVUS)

• Use case: Specialist, secondary test to confirm significance of iliac/iliofemoral lesions, size stents, and guide therapy; delineates endoluminal stenosis/obstruction not fully appreciated on external imaging.

Physiological / Functional Testing

Air Plethysmography (APG)

• Role: Non-invasive quantification of global venous function (reflux, obstruction, calf pump failure).
• Indices: Venous filling index and refilling time correlate with CVI severity; useful when duplex findings are equivocal or for pre/post-intervention assessment (primarily in specialist/research settings).

Ambulatory Venous Pressure (AVP) Monitoring

• Role: Criterion standard for haemodynamic assessment (research/specialist contexts).
• Method: Needle cannulation of the dorsal foot vein with pressure transduction during ambulation.
• Note: Valuable prognostically but rarely used due to invasiveness and availability of robust non-invasive alternatives.

Classification to Standardise Assessment

CEAP Classification (Clinical–Aetiology–Anatomy–Pathophysiology)

• Purpose: Uniform reporting, diagnosis, and longitudinal tracking of CVI burden and outcomes.
• Clinical (C): C0 no signs → C1 telangiectasia/reticular, C2 varicose, C3 oedema, C4a pigmentation/eczema, C4b lipodermatosclerosis/atrophie blanche, C4c corona phlebectatica, C5 healed ulcer, C6 active ulcer (with “r” for recurrent).
• Aetiology (E): Ep primary; Es secondary (intravenous/extraveneous subcategories where used); Ec congenital; En none identified.
• Anatomy (A): As superficial (e.g., GSV/SSV/AASV/telangiectasia/reticular), Ad deep (e.g., CFV/FV/POPV/tibial/peroneal/pelvic/IVC), Ap perforator (thigh/calf), An none identified.
• Pathophysiology (P): Pr reflux, Po obstruction, Pr,o both, Pn none.
• Pair CEAP with a reflux map from duplex to direct management (compression, ablation, stenting, surgery).

Laboratory and Ancillary Points

Laboratory Studies

• D-dimer: Frequently elevated in chronic/recurrent superficial/deep thrombosis; limited utility for acute VTE exclusion in established CVI.
• Syndromic CVI (e.g., Klippel–Trénaunay): Consider targeted tests (e.g., platelet count for consumptive thrombocytopenia) when clinically indicated.

Ultrasonographic Refinements

• Reflux mapping is essential and both sensitive and specific for patterns of venous insufficiency; pulsatile flow in the GSV may signal severe superficial insufficiency in selected cohorts.

Venous and Related Conditions

Varicose Veins

• Dilated, tortuous superficial veins often coexist with CVI but may occur independently.
• Important to differentiate uncomplicated cosmetic varicosities from those associated with venous hypertension and tissue damage.

Stasis Dermatitis

• Chronic eczematous inflammation in the gaiter region.
• Can mimic cellulitis; presence of bilateral involvement, itching, and scaling helps distinguish.

Acute Deep Vein Thrombosis (DVT)

• Presents with sudden unilateral swelling, tenderness, warmth, and erythema.
• Must be excluded in all cases of new or rapidly worsening oedema using duplex ultrasound.

Lymphoedema

• Typically unilateral; characterised by “buffalo hump” of the dorsum of the foot and positive Stemmer’s sign (inability to pinch skin at the base of the toes).
• Duplex ultrasound is usually normal or minimally abnormal, helping distinguish from venous insufficiency.

Lipedema

• Symmetrical enlargement of legs sparing the feet, associated with tenderness and easy bruising.
• Unlike CVI, oedema does not improve with leg elevation.

Ulcerative and Cutaneous Mimics

Diabetic Foot Ulcer

• Found over plantar pressure points or dorsum of toes.
• Associated with neuropathy and repetitive trauma.
• Diagnosis supported by elevated fasting glucose (≥7 mmol/L) and history of diabetes.

Arterial Ulcer

• Typically distal (toe tips, lateral malleolus), punched out, and painful.
• Frequently gangrenous.
• Exclude with ankle–brachial index (ABI): values <0.9 suggest arterial disease; <0.8 strongly abnormal.

Squamous Cell Carcinoma (Marjolin Ulcer)

• Arises in long-standing non-healing ulcers.
• Features irregular, indurated edges.
• Confirmed by skin biopsy.

Pyoderma Gangrenosum

• Rapidly enlarging painful ulcers with undermined edges.
• May worsen after debridement due to pathergy.
• Biopsy helps confirm diagnosis and rule out infection or malignancy.

Kaposi’s Sarcoma

• Seen in immunosuppressed patients (HIV, post-transplant).
• Presents as raised, violaceous skin lesions that may be mistaken for venous disease.
• Biopsy confirms diagnosis.

Systemic Causes of Oedema

Congestive Heart Failure

• Bilateral pitting oedema with dependent blebs or bullae in advanced cases.
• Rarely associated with ulceration.
• Investigations: chest X-ray (cardiomegaly, pulmonary congestion, pleural effusion); echocardiography (systolic/diastolic dysfunction).

Renal Disease

• Oedema usually bilateral; ulceration uncommon.
• Investigations: elevated urea, creatinine, potassium; urinalysis may show haematuria or proteinuria.

Hepatic Disease

• Oedema occurs in decompensated cirrhosis or severe liver dysfunction.
• Investigations: abnormal liver function tests, evidence of portal hypertension.

Musculoskeletal and Other Mimics

Ruptured Popliteal (Baker’s) Cyst

• Presents with sudden calf swelling and pain, often mistaken for DVT.
• Ultrasound or MRI can confirm.

Soft Tissue Haematoma or Mass

• May present as a painful, swollen limb; history of trauma or anticoagulant therapy important.

Exertional Compartment Syndrome

• Exercise-induced calf pain and swelling.
• Diagnosed with compartment pressure testing.

Gastrocnemius Tear (“Tennis Leg”)

• Acute calf pain following sudden exertion; palpable gap or bruising present.
• Confirmed by ultrasound or MRI.

Core Principles

• Alleviate venous hypertension, heal or prevent ulcers, reduce symptoms, and correct reflux/obstruction where feasible.
• Combine compression, skin care, risk modification, and targeted interventions based on duplex-mapped pathology.

Compression Therapy

Prescription and Technique

• Cornerstone for oedema, stasis dermatitis, and venous leg ulcers.
• Wear first thing in the morning, remove when recumbent at night; ensure correct size and donning aids.
• Classes:
  • Class 1 (low): mild oedema/control.
  • Class 2–3 (medium/high): usually required for established CVI; prior ulcers often need ≥30–40 mmHg.

Adherence

• Non-adherence (≈30–65%) is the main cause of failure; recurrence is roughly halved in adherent patients.
• TED/anti-embolic stockings (<20 mmHg) are inadequate for CVI.

Evidence Signals

• Compression heals ulcers faster than no compression; multilayer outperform single-layer systems.
• Progressive calf-maximising compression may improve pain/symptoms versus traditional degressive designs.
• Intermittent pneumatic compression: option for post-thrombotic syndrome or refractory oedema when stockings are insufficient.

Pharmacotherapy

Skin Care and Topicals

• Regular emollients for xerosis/eczema.
• Avoid long-term topical antibiotics and non-specific ointments (sensitisation, barrier damage); growth factors lack consistent benefit.

Systemic Agents

• Pentoxifylline (adjunct to compression): modest improvement in ulcer healing in RCTs/meta-analyses.
• Micronised purified flavonoid fraction (MPFF/diosmin–hesperidin): meta-analytic signal for faster healing when added to standard care (availability varies by country).
• Not effective for healing: aspirin, ifetroban, stanozolol, routine antibiotics, hydroxyrutosides.
• Venoactive agents (where available) can reduce leg pain/heaviness in CVI.

Invasive and Endovascular Options (Duplex-Directed)

Superficial Venous Reflux (Great/Small Saphenous, Tributaries)

• Endovenous ablation (laser or radiofrequency): minimally invasive, outpatient; now first-line in most centres.
  • Post-procedure: compression 24 h/day for 1–3 days, then daytime 1–2 weeks; avoid strenuous leg exercise for ~1 week.
• Foam sclerotherapy: ultrasound-guided; useful for trunks/tributaries and recurrent disease. Be aware of transient visual disturbance/migraine; very rare stroke reported.
• Saphenous surgery (stripping/ligation): still effective; reduces ulcer recurrence when added to compression in reflux-positive patients (e.g., ESCHAR).
• Comparative effectiveness (duplex-defined success) over ≈2–3 years in large meta-analyses: laser ≈94%, RFA ≈84%, surgery ≈78%, foam ≈77%; major DVT complications ≈1–3% overall.
• Early ablation in patients with active ulcers accelerates healing and increases ulcer-free time versus deferred ablation.

Perforator Incompetence

• Endovenous perforator ablation (laser/RFA) or targeted ligation when perforators are key reflux sources.

Iliac/Iliofemoral Outflow Obstruction

• Consider intravascular ultrasound (IVUS) to confirm lesion significance.
• Balloon angioplasty and stenting in selected cases (often left-sided) can significantly improve pain/oedema and ulcer healing when obstruction is dominant.

Deep Venous Reflux (Selected Centres)

• Valve repair/valvuloplasty, axillary/brachial valve transplantation, or segment transposition: niche options after failure of conservative therapy, with better results in primary than post-thrombotic disease.

Physical Modalities and Wound Care

Elevation and Exercise

• Frequent leg elevation (above heart when supine; above thighs when seated) decreases venous pressure.
• Walking, cycling, swimming benefit patients with an intact calf pump; tailor activity if outflow obstruction limits tolerance.

Ulcer Care

• Multilayer compression systems and appropriate dressings (exudate control, peri-wound protection).
• Unna boot (zinc oxide paste bandage) is a time-honoured option in ambulant patients.
• Assess and treat infection, contact dermatitis, and pain; consider adjunct agents (pentoxifylline/MPFF) with compression in large or long-standing ulcers.

Post-Procedure Care and Surveillance

After Ablation/Surgery

• Continue daytime compression if residual deep reflux or persistent oedema.
• Duplex ultrasound for suspected DVT or persistent symptoms.
• Individualise thromboprophylaxis based on risk.

Prevention and Long-Term Measures

Lifestyle and Risk Factor Modification

• Avoid prolonged standing/sitting; encourage regular ambulation and calf-pump activation.
• Weight management, smoking cessation, and optimised control of comorbidities.
• Early, sustained compression can prevent progression to dermatitis/ulceration in at-risk patients.

Disease Course and Progression

• CVI is not a benign condition; without correction of the underlying reflux or obstruction it is progressive, with symptoms that typically worsen over time.
• Early symptoms of aching, heaviness, and swelling often progress to cutaneous changes, including hyperpigmentation, lipodermatosclerosis, and eventually non-healing ulcers.
• Ulceration is the most debilitating long-term complication. Ulcers may recur repeatedly, particularly if venous hypertension persists.

Ulcer-Related Outcomes

• Chronic venous ulcers are painful, disabling, and difficult to treat.
• Abbade et al demonstrated that longstanding, large ulcers and recurrent ulcers were the major complications in venous ulcer patients. Risk factors include severe lipodermatosclerosis, a history of prior ulcers, and disease duration beyond two years.
• Approximately 1 million Americans are affected by venous ulcers, with around 100,000 disabled due to their condition.
• Even partial reduction of reflux volume and pressure below a threshold can allow ulcers to heal, though skin atrophy and pigmentation changes are generally irreversible.
• Recurrence of venous ulcers is 50% lower among patients adherent to compression stockings compared with those non-adherent.

Thromboembolic Risk

• Patients with CVI have a significantly increased lifetime risk of DVT and pulmonary embolism (PE).
• In an analysis of hospitalised patients, DVT occurred in 1.3%, amputation in 1.2%, and mortality reached 1.6%.
• Up to 50% of patients with untreated varicose veins will develop superficial thrombophlebitis, and DVT is present in nearly 45% of patients who appear to have isolated superficial disease.
• Risk of DVT is threefold higher in patients with superficial varicosities than in the general population.
• Among hospitalised patients with visible venous insufficiency, 60% develop phlebitis, and in half of these cases it progresses to DVT.
• Roughly half of DVT patients have detectable PE, with mortality exceeding 30% in that group.

Haemorrhagic Complications

• Fatal bleeding can occur from varicose veins; 23 deaths were documented in England and Wales in 1973.
• Such haemorrhage, although uncommon, is often mismanaged; it should be considered a serious complication of advanced venous disease.

Surgical and Interventional Outcomes

• Superficial venous interventions (stripping, ablation, or sclerotherapy) improve ulcer healing and reduce recurrence when reflux is corrected.
• Deep venous procedures remain challenging:
  • Valvuloplasty combined with perforator ligation yields superior outcomes in up to 80% at five years for congenital valve absence.
  • Vein valve transplantation and allograft/cadaveric vein reconstructions are under evaluation with long-term results still uncertain.
  • Procedures such as saphenous vein crossover grafts or Husni bypass for iliofemoral and femoral vein occlusion show high failure rates (20–40%) and are used infrequently.

Prognostic Reassurance

• CVI, even when severe, is not typically limb-threatening, unlike peripheral arterial occlusive disease or diabetic vascular disease.
• Long-term adherence to compression therapy remains the single most effective strategy in reducing recurrence and complications.
• Patients with CEAP C4–C6 disease or a history of ulcers generally require lifelong stockings (30–40 mmHg).

Chronic Venous Ulceration

• One of the most disabling outcomes of CVI, usually in the gaiter region, most often around the medial malleolus.
• Results from sustained venous hypertension, oedema, lipodermatosclerosis, and skin breakdown.
• Ulcers are slow to heal, recurrent, and significantly impair quality of life.

Deep Vein Thrombosis (DVT)

• Patients with CVI have a predisposition to thrombus formation due to venous stasis and endothelial injury.
• May occur spontaneously or as a complication of interventions such as saphenectomy or endovenous ablation, where the risk is around 1–3%.
• Prophylaxis should be considered in higher-risk patients.

Superficial Thrombophlebitis

• Often complicates varicosities in CVI.
• Clinically important because of its frequent association with concurrent or subsequent DVT.

Lipodermatosclerosis

• Caused by chronic microvascular injury with capillary elongation, fibrosis, and leakage.
• Characterised by induration, pigmentation, and tightening of the skin, with potential contracture around the ankle joint.

Atrophie Blanche

• Small, white, scar-like patches of atrophic skin with surrounding telangiectasia and pigmentation.
• Often seen in advanced disease and commonly associated with ulcer recurrence.

Secondary Lymphoedema

• Long-standing venous hypertension overwhelms lymphatic drainage.
• Leads to chronic swelling with non-pitting features, which increases ulcer risk.

Stasis Dermatitis

• Presents as venous eczema with erythema, dryness, scaling, and itching in the gaiter region.
• May progress to lichenification or weeping dermatitis and can become secondarily infected.

Recurrent Cellulitis

• Occurs in patients with oedema, dermatitis, or ulceration.
• Risk is lower with adherence to compression and good hygiene, but infection when present can be severe and requires urgent treatment.

Secondary Haemorrhage

• Varicose veins under high pressure can erode through the skin, leading to bleeding.
• Bleeding may be severe and occasionally fatal if not promptly managed.

Haemosiderin Deposition

• Results from chronic venous hypertension and red cell extravasation.
• Causes characteristic reddish-brown pigmentation (“brawny oedema”) around the ankle and lower leg.
• Usually permanent and part of the chronic skin changes in CVI.

Chronic Pain and Disability

• Persistent leg pain, heaviness, and swelling are common.
• Ulcers, infection, and skin changes further limit mobility and can cause long-term disability and reduced quality of life.

1. Abbade LP, Lastoria S, Rollo HA. Venous ulcer: clinical characteristics and risk factors. Int J Dermatol. 2011;50(4):405-411.
2. Azar J, Rao A, Oropallo A. Chronic venous insufficiency: a comprehensive review of management. J Wound Care. 2022;31(6):510-519.
3. Beebe-Dimmer JL, Pfeifer JR, Engle JS, Schottenfeld D. The epidemiology of chronic venous insufficiency and varicose veins. Ann Epidemiol. 2005;15(3):175-184.
4. Blann AD, Lip GY, McCollum CN. Circulating endothelial cell/leucocyte adhesion molecules in peripheral artery disease. Thromb Haemost. 2002;87(2):301-307.
5. Bonkemeyer Millan S, Gan R, Townsend PE. Venous Ulcers: Diagnosis and Treatment. Am Fam Physician. 2019;100(5):298-305.
6. Browse NL, Burnand KG, Lea Thomas M. Varicose Veins: Pathology and Treatment. London: Chapman & Hall; 1988.
7. Burnand KG, Whimster I, Naidoo A, Browse NL. Pericapillary fibrin in the ulcer-bearing skin of the leg: the cause of lipodermatosclerosis and venous ulceration. BMJ. 1982;285(6348):1071-1072.
8. Callam MJ. Epidemiology of varicose veins. Br J Surg. 1994;81(2):167-173.
9. Christopoulos D, Nicolaides AN, Szendro G. Venous reflux: quantification and correlation with the clinical severity of chronic venous disease. Br J Surg. 1988;75(4):352-356.
10. Coleridge Smith PD, Thomas P, Scurr JH, Dormandy JA. Causes of venous ulceration: a new hypothesis. BMJ. 1988;296(6638):1726-1727.
11. Eberhardt RT, Raffetto JD. Chronic venous insufficiency. Circulation. 2014;130(4):333-346.
12. Evans CJ, Fowkes FG, Ruckley CV, Lee AJ. Prevalence of varicose veins and chronic venous insufficiency in men and women in the general population: Edinburgh Vein Study. J Epidemiol Community Health. 1999;53(3):149-153.
13. Fowkes FG, Evans CJ, Lee AJ. Prevalence and risk factors of chronic venous insufficiency. Angiology. 2001;52(1 Suppl):S5-S15.
14. Gillespie DL, Cordts PR, Hartono C, Woodson J, Obi-Tabot E, LaMorte WW, Menzoian JO. The role of air plethysmography in monitoring results of venous surgery. J Vasc Surg. 1992;16(5):674-678.
15. Gohel MS, Barwell JR, Taylor M, et al. Long-term results of compression versus surgery in chronic venous ulceration (ESCHAR). BMJ. 2007;335:83.
16. Gohel MS, Heatley F, Liu X, et al. A randomized trial of early endovenous ablation in venous ulceration (EVRA). N Engl J Med. 2018;378:2105-2114.
17. Jia X, Mowatt G, Burr JM, Cassar K, Cook J, Fraser C. Systematic review of foam sclerotherapy for varicose veins. Eur J Vasc Endovasc Surg. 2007;34(6):741-750.
18. Jull AB, Arroll B, Parag V, Waters J. Pentoxifylline for treating venous leg ulcers. Cochrane Database Syst Rev. 2012;(12):CD001733.
19. Jull AB, Wadham A, Bullen C, Parag V, Waters J. Aspirin as adjuvant therapy for venous leg ulcers: randomized clinical trial. Br J Surg. 2008;95(9):1142-1148.
20. Kistner RL, Ferris EB. Primary deep venous valve incompetence: correction by valvuloplasty. Surgery. 1984;95(6):703-708.
21. Lurie F, Passman M, Meisner M, et al. The 2020 update of the CEAP classification for chronic venous disorders. J Vasc Surg Venous Lymphat Disord. 2020;8(3):342-352.
22. Mosti G, Iabichella ML, Partsch H. Compression stockings with a pressure profile decreasing from distal to proximal are more effective than degressive stockings in chronic venous insufficiency. Phlebology. 2012;27(3):107-113.
23. Mutlak O, Aslam M, Standfield NJ. Chronic venous insufficiency: a new concept to understand pathophysiology at the microvascular level – a pilot study. Perfusion. 2019;34(1):84-89.
24. Neglén P, Raju S. Intravascular ultrasound scan evaluation of the obstructed vein. J Vasc Surg. 2002;35(4):694-700.
25. Nelzén O, Bergqvist D, Lindhagen A. Venous and non-venous leg ulcers: clinical history and appearance in a population study. Br J Surg. 1994;81(2):182-187.
26. Nicolaides AN, Allegra C, Bergan J, Bradbury A, Cairols M, Carpentier P, et al. Management of chronic venous disorders of the lower limbs. Int Angiol. 2008;27(1):1-59.
27. Nicolaides AN, Zukowski AJ. The value of dynamic venous pressure measurements. World J Surg. 1986;10(6):919-924.
28. O’Meara S, Cullum N, Nelson EA, Dumville JC. Compression for venous leg ulcers. Cochrane Database Syst Rev. 2012;(11):CD000265.
29. O’Meara S, Martyn-St James M, Adderley UJ. Alginate dressings for venous leg ulcers. Cochrane Database Syst Rev. 2015;(8):CD010182.
30. Orhurhu V, Chu R, Xie K, Kamanyi GN, Salisu B, Salisu-Orhurhu M, et al. Management of Lower Extremity Pain from Chronic Venous Insufficiency: A Comprehensive Review. Cardiol Ther. 2021;10(1):111-140.
31. Owens LV, Farber MA, Young ML, Carlin RE, Criado-Pallares E, Passman MA, Keagy BA, Marston WA. Value of air plethysmography in predicting outcome after surgery for CVI. J Vasc Surg. 2000;32(5):961-968.
32. Porter JM, Moneta GL. Reporting standards in venous disease: an update. J Vasc Surg. 1995;21(4):635-645.
33. Rabe E, Pannier F, Koelemay M, Vestergaard A, Mounsey AL, Shepherd AC, et al. Epidemiology of chronic venous disorders in geographically diverse populations: results from the Vein Consult Program. Int Angiol. 2012;31(2):105-115.
34. Stucker M, Debus ES, Hoffmann J, Mumme A, Gabriel M, Thiede A, et al. Bochum study: epidemiology of varicose veins in children. Phlebology. 2001;16(2):53-57.
35. Tsai S, Dubovoy A, Wainess RM, Upchurch GR Jr, Wakefield TW. Trends of inpatient venous thromboembolism in the United States: 1988-2000. J Vasc Surg. 2004;40(6):1232-1238.
36. van den Bos RR, Arends L, Kockaert M, Neumann M, Nijsten T. Endovenous therapies of lower extremity varicosities: a meta-analysis. J Vasc Surg. 2009;49(1):230-239.