Chronic Venous Insufficiency and Varicose Veins

Background

Chronic venous disease (CVD) is among the most prevalent vascular disorders worldwide.^[1]

• Epidemiology:
• Up to 30% of adults have varicose veins (CEAP C2).^[2]
• Advanced stages (CEAP C4–C6) affect ~3–5% of the population ^[2].
• Burden:
• Major socioeconomic impact (work loss, chronic ulcers).
• Venous ulcers account for ~70% of chronic leg ulcers.^[1]
• Definitions:
• Varicose veins (VV): dilated, tortuous subcutaneous veins ≥3 mm.^[3]
• 13CVI: advanced CVD with skin changes or ulceration (CEAP C3–C6).^[3]

Etiology and Risk Factors

• Primary venous insufficiency:
• Valve incompetence in superficial (GSV, SSV) or perforator veins.^[1]
• Familial/genetic predisposition (weakened vein wall, valve malformation).^[2]
• Secondary venous insufficiency:
• Post-thrombotic syndrome (PTS) after 12VTE.^[4]
• Obstruction (iliac vein compression/May–Thurner syndrome).^[5]
• Risk factors:
• Female sex, pregnancy, obesity, age, standing occupations, prior 12VTE, congenital anomalies.^[2]

Pathophysiology

Valve failure leads to retrograde flow and ambulatory venous hypertension. This sustained pressure triggers leukocyte trapping in capillaries, which activates inflammatory cascades and causes microangiopathy. The resulting capillary leakage and fibrin deposition create a pericapillary fibrin cuff that impairs oxygen diffusion. This chronic inflammation and tissue hypoxia cause progressive dermal changes including lipodermatosclerosis (fibrosis and induration of subcutaneous fat) and atrophie blanche (white atrophic skin with telangiectasias). Without intervention, these changes culminate in venous ulceration ^[1].

CEAP Classification

The complete CEAP classification includes four components:^[3]

• Clinical (C0–C6): as listed above
• Etiology (E):
• Ec: congenital
• Ep: primary
• Es: secondary (post-thrombotic)
• En: no venous cause identified
• Anatomy (A):
• As: superficial veins
• Ap: perforator veins
• Ad: deep veins
• An: no venous location identified
• Pathophysiology (P):
• Pr: reflux
• Po: obstruction
• Pr,o: both reflux and obstruction
• Pn: no venous pathophysiology identifiable

Each classification includes a symptomatic (S) or asymptomatic (A) suffix. For example, "C2, Ep, As, Pr, S" describes symptomatic varicose veins due to primary superficial venous reflux.

The Venous Clinical Severity Score (VCSS) is a complementary 10-item scale that quantifies venous disease severity. It scores pain, varicose veins, edema, pigmentation, inflammation, induration, active ulcers, ulcer duration, ulcer size, and compression therapy use (0–3 points each, maximum 30 points). VCSS provides a standardized method for tracking disease progression and treatment outcomes ^[3],[6].

Clinical Presentation

• Varicose veins: aching, heaviness, swelling, cosmetic concerns.^[1]
• 13CVI: edema, skin changes, recurrent cellulitis, ulcers.^[1]
• Post-thrombotic syndrome: pain, swelling, skin hyperpigmentation.^[4]
• Venous claudication: pain with walking relieved by rest/elevation (iliac vein obstruction).^[7]

Non-invasive

Reflux thresholds and technique:

Duplex ultrasound should be performed with the patient standing or in reverse Trendelenburg position to maximize venous filling.^[8] Reflux is provoked using distal compression and release (calf squeeze), augmentation, or Valsalva maneuver. Pathologic reflux is defined as retrograde flow lasting >0.5 seconds in superficial and perforator veins, or >1.0 seconds in deep veins.^[8]

Systematic mapping should include: *Junctional reflux:** saphenofemoral junction (SFJ) and saphenopopliteal junction (SPJ) *Truncal reflux:** great saphenous vein (GSV) and small saphenous vein (SSV) *Accessory saphenous veins:** anterior accessory GSV (AAGSV) and posterior accessory GSV (PAGSV) *Perforator veins:** particularly in the medial calf (Cockett perforators) and thigh (Hunterian, Dodd)

Documentation should specify location, diameter, and reflux duration at each level ^[8],[6].

Advanced imaging

• CT/MR venography: for iliocaval obstruction, stent planning.^[8]
• Intravascular ultrasound (IVUS): gold standard for iliac vein stenosis/May–Thurner.^[7]

Functional tests (rare in practice)

• Air plethysmography.
• Ambulatory venous pressure.^[1]

General/Conservative

Compression therapy dosing:

Compression stockings should be prescribed based on disease severity: *C2–C3 (symptomatic varicose veins/edema):** 20–30 mmHg *C4 (skin changes):** 30–40 mmHg *C5–C6 (ulcers):** 30–40 mmHg, with higher pressures (~40 mmHg at ankle) during active ulceration^[8]

Donning aids (stocking applicators, glides) significantly improve adherence, particularly in elderly patients or those with limited mobility.^[8]

Contraindications and precautions:

Arterial disease must be screened before prescribing compression. Check ABI^[9] (see 3Ch. 3 for technique) or 10Ch. 10 for interpretation: *ABI <0.5:** avoid compression or use very low pressure (<15 mmHg) *ABI 0.5–0.8:** modified compression (20–25 mmHg) with close monitoring *ABI >0.8:** standard compression safe^[8]

Adjunctive conservative measures:

Patients should be counseled on exercise (walking improves calf pump function), weight reduction (reduces venous pressure), and leg elevation (facilitates venous return). Venoactive drugs such as micronized purified flavonoid fraction (MPFF) or horse chestnut extract may reduce symptoms but do not replace compression therapy ^[6],[1].

Interventional (Superficial System)

Long-term outcomes:

Endothermal ablation techniques (EVLA and RFA) demonstrate durable anatomic closure rates of 85–95% at 3–5 years. Success rates depend on device selection, energy delivery parameters, operator experience, and vein diameter. Contemporary meta-analyses and randomized trials confirm sustained clinical improvement with low recurrence rates ^[10],[11].

Interventional (Deep Venous System)

• Iliocaval stenting:
• For iliac vein compression (May–Thurner) or post-thrombotic obstruction.^[7]
• Patency >80% at 5 years with symptom relief ^[7].
• Valve reconstruction (rare):
• Neovalve or transplant techniques in severe reflux.^[1]

Ulcer Management

Compression as primary therapy:

Compression remains the cornerstone of venous ulcer management. Multilayer compression bandaging or high-pressure stockings (targeting approximately 40 mmHg at the ankle) should be applied consistently. As with all compression therapy, the ankle-brachial index (ABI) must be checked first, with compression pressure reduced or withheld in patients with significant arterial disease.^[8]

Pharmacologic adjuncts:

Pentoxifylline, a hemorrheologic agent, may accelerate ulcer healing when used as an adjunct to compression therapy, though the effect size is modest.^[8]

Early intervention:

The EVRA (Early Venous Reflux Ablation) trial demonstrated that early endovenous ablation of superficial truncal reflux, combined with compression, significantly accelerates ulcer healing and reduces recurrence compared to compression alone. This has established early ablation as standard of care for C6 patients with superficial reflux ^[6],[12].

Follow-up

• DUS surveillance after ablation or stenting.^[8]
• Compression stockings long-term in advanced disease.^[1]
• Multidisciplinary ulcer care for CEAP C6.^[1]

Guidelines

• SVS/AVF Guidelines (2011, updated 2022):
• Endovenous ablation preferred over surgery for GSV/SSV reflux.
• ESVS Guidelines (2015):^[6]
• Compression in all CEAP ≥C3.
• Endovenous therapy first-line for symptomatic varicose veins.
• Stenting indicated for significant iliac obstruction with symptoms.
• NICE Guidelines (UK, 2013):
• Offer endothermal ablation as first-line, foam sclerotherapy if unsuitable.

Tables

Table 11.1. Comparison of Interventions for Superficial Reflux*

*Success rates represent anatomic closure of treated vein; clinical improvement often occurs despite anatomic recurrence.^[11]

†Cyanoacrylate demonstrates non-inferiority to RFA at 12 months; longer-term data are emerging ^{[10],[11],[13]}.

Complete CEAP classification (E, A, P components) and Venous Clinical Severity Score (VCSS)

The complete CEAP classification system extends beyond the clinical C0–C6 scale to include three additional descriptors that provide comprehensive characterization of venous disease:

Etiology (E): * Ec: congenital venous disorders * Ep: primary venous insufficiency * Es: secondary (post-thrombotic) venous disease * En: no identifiable venous cause

Anatomy (A): * As: superficial veins (GSV, SSV, tributaries) * Ap: perforator veins * Ad: deep veins (femoral, popliteal, iliac) * An: no venous anatomic location identified

Pathophysiology (P): * Pr: reflux * Po: obstruction * Pr,o: combined reflux and obstruction * Pn: no identifiable venous pathophysiology

Each classification includes a symptomatic (S) or asymptomatic (A) suffix. A complete CEAP designation might read: "C2, Ep, As, Pr, S" (symptomatic varicose veins from primary superficial venous reflux).

Venous Clinical Severity Score (VCSS):

The VCSS complements CEAP by providing a quantitative severity assessment. This 10-item instrument scores pain, varicose veins, edema, pigmentation, inflammation, induration, number of active ulcers, ulcer duration, ulcer size, and use of compression therapy. Each item is graded 0 (absent) to 3 (severe), yielding a maximum score of 30. The VCSS enables longitudinal tracking of disease progression and objective comparison of treatment outcomes ^[3],[6].

Ultrasound reflux thresholds and testing protocol

Duplex ultrasound assessment for venous reflux requires standardized patient positioning and provocation techniques. The examination should be performed with the patient standing or positioned in reverse Trendelenburg to maximize venous column height and facilitate reflux detection. Reflux is provoked using manual distal compression and release (calf squeeze), distal augmentation, or Valsalva maneuver.

Pathologic reflux thresholds:

Reflux duration thresholds differ by venous system: *Superficial and perforator veins:** >0.5 seconds of retrograde flow *Deep veins:** >1.0 seconds of retrograde flow

These thresholds are based on correlation with clinical disease and have been validated in multiple studies.

Systematic reflux mapping:

A comprehensive venous duplex examination should systematically evaluate: *Junctional reflux:** saphenofemoral junction (SFJ) and saphenopopliteal junction (SPJ) *Truncal reflux:** great saphenous vein (GSV) throughout the thigh and calf; small saphenous vein (SSV) in the calf *Accessory saphenous veins:** anterior and posterior accessory GSV (AAGSV, PAGSV) *Perforator veins:** particularly medial calf perforators (Cockett I-III), mid-thigh (Hunterian), and distal thigh (Dodd)

For each refluxing segment, the operator should document anatomic location, vein diameter, and reflux duration ^[8],[6].

Endothermal heat-induced thrombosis (EHIT) and post-ablation DVT surveillance/management

Endovenous thermal ablation carries a risk of endothermal heat-induced thrombosis (EHIT), in which thrombus extends from the treated saphenous vein into the adjacent deep venous system.^[8]

EHIT Classification:

• Class I: thrombus protrudes into but does not occlude the deep vein
• Class II: thrombus occludes the deep vein
• Class III: thrombus extends into the common femoral vein or above
• Class IV: thrombus extends into the iliac veins or inferior vena cava^[8]

Risk Factors:

EHIT is more likely with: * Large great saphenous vein (GSV) diameter (>8–10 mm) * Higher energy delivery during ablation * Proximity of the ablation endpoint to the saphenofemoral junction * Concomitant thrombophilia or hypercoagulable state^[8]

Surveillance and Management:

Post-ablation duplex ultrasound should be performed within 1 week to detect EHIT early. Management depends on EHIT class: *Class I:** observation with repeat duplex in 1–2 weeks; often resolves spontaneously *Class II:** anticoagulation for 3 months; repeat imaging to document resolution *Class III–IV:** full therapeutic anticoagulation as for 12VTE; consider thrombectomy in selected cases^[8]

True deep vein thrombosis (occurring independently of the ablation site) should be treated with standard anticoagulation protocols (see 12VTE) ^[6].

Management of tributaries: ambulatory phlebectomy and ultrasound-guided foam sclerotherapy

While endovenous ablation addresses truncal reflux, residual varicose tributaries often require additional treatment. Two approaches are commonly used:

Concomitant phlebectomy:

Ambulatory phlebectomy of large tributary varicosities can be performed during the same procedure as truncal ablation. This approach provides immediate cosmetic improvement and symptom relief in a single session. Small stab incisions are made along the course of tributary varicosities, and the veins are removed using phlebectomy hooks.

Staged treatment:

Alternatively, tributaries may be treated in a staged fashion 6–12 weeks after truncal ablation. Some tributary varicosities may regress spontaneously after truncal ablation, potentially reducing the extent of subsequent treatment needed. Staged treatment allows assessment of which tributaries persist and require intervention.

Foam sclerotherapy:

Ultrasound-guided foam sclerotherapy offers a minimally invasive alternative to phlebectomy for tributary varicosities. It is particularly useful for veins that are technically challenging for phlebectomy due to location or depth.

Outcomes:

Randomized trials demonstrate that adjunctive treatment of tributaries—whether by concomitant or staged phlebectomy or foam sclerotherapy—significantly improves patient-reported outcomes, quality of life scores, and cosmetic satisfaction compared to truncal ablation alone ^[11],[6].

Perforator vein disease: indications and techniques

Perforator vein incompetence contributes to venous hypertension and is particularly relevant in advanced chronic venous disease.

Diagnostic Criteria:

Pathologic perforator veins are identified by duplex ultrasound as: * Diameter >3.5 mm * Reflux duration >0.5 seconds * Located beneath areas of lipodermatosclerosis or ulceration

Indications for Treatment:

Perforator ablation is most beneficial in: *CEAP C5–C6:** patients with healed or active venous ulcers *Recurrent varicose veins** after prior superficial venous treatment *Persistent symptoms** despite treatment of superficial reflux

Perforator ablation is typically performed after or concomitantly with treatment of superficial truncal reflux, as isolated perforator treatment rarely succeeds if major superficial reflux persists.

Ablation Techniques:

• Endothermal ablation: radiofrequency or laser ablation under ultrasound guidance, often using a modified technique with lower energy than truncal ablation
• Foam sclerotherapy: ultrasound-guided injection of sclerosant foam
• Mechanochemical ablation: in selected cases

Expected Benefits:

Studies demonstrate that perforator ablation in appropriately selected C5–C6 patients accelerates ulcer healing, reduces ulcer recurrence rates, and improves venous clinical severity scores. The benefit is most pronounced when combined with treatment of superficial reflux ^[6].

Combined superficial reflux and iliac outflow obstruction

Patients with advanced chronic venous disease may have concomitant superficial venous reflux and deep venous outflow obstruction, most commonly from post-thrombotic changes or iliac vein compression (May-Thurner syndrome).

When to Suspect Iliofemoral Obstruction:

• Unilateral limb swelling disproportionate to superficial venous findings
• Venous claudication (bursting leg pain with walking, relieved by rest and elevation)
• Advanced venous disease (C4–C6) refractory to standard treatment
• History of iliofemoral deep vein thrombosis

Diagnostic Evaluation:

When clinical features suggest outflow obstruction, advanced imaging is warranted: *CT or MR venography:** assess iliocaval patency and collateral formation *Intravascular ultrasound (IVUS):** gold standard for detecting hemodynamically significant iliac vein stenosis (>50% diameter reduction)^[7]

Treatment Strategy:

In patients with combined superficial reflux and iliac obstruction: *Address obstruction first or concurrently:** iliac vein stenting should be performed before or at the same time as superficial ablation, as outflow obstruction may prevent adequate decompression of the superficial system *Stenting outcomes:** iliocaval stenting for post-thrombotic or compressive obstruction demonstrates patency rates >80% at 5 years and significant symptom relief *Superficial ablation:** once outflow is restored, superficial reflux can be treated with standard endovenous techniques

Failure to address significant outflow obstruction may result in suboptimal outcomes from superficial venous intervention alone ^[7],[6].

Pregnancy and varicose veins

Varicose veins commonly develop or worsen during pregnancy due to increased blood volume, hormonal effects on vein wall compliance, and mechanical compression of pelvic veins by the gravid uterus.^[1]

Management During Pregnancy:

Conservative management is appropriate for most pregnant women with varicose veins: *Compression therapy:** graduated compression stockings (20–30 mmHg) reduce symptoms and limit progression *Leg elevation:** frequent elevation reduces venous hypertension *Exercise:** walking and calf exercises improve venous return

Timing of Intervention:

Invasive treatment (endovenous ablation, sclerotherapy, or surgery) should be deferred until after pregnancy and completion of lactation^[1] because: * Many pregnancy-related varicosities regress spontaneously postpartum (typically within 3–6 months) * Endovenous procedures are relatively contraindicated during pregnancy due to concerns about anesthesia, positioning, and thromboembolic risk * Sclerosants cross the placenta and are contraindicated

Indications for Intervention During Pregnancy:

Rarely, acute complications may necessitate intervention: *Bleeding varix:** requires urgent compression and may require suture ligation *Superficial thrombophlebitis:** managed with compression, anti-inflammatory agents, and anticoagulation in selected cases *Severe, refractory symptoms:** phlebectomy of specific symptomatic veins may be considered in the second trimester

Patients should be counseled that definitive treatment is best postponed until after pregnancy and lactation ^[6].

Ulcer Care: Compression Levels and Adjuncts

Venous ulcer management requires a multifaceted approach combining compression therapy, wound care, and when appropriate, correction of underlying venous reflux or obstruction.

Compression Therapy:

Compression remains the cornerstone of venous ulcer treatment: *Target pressure:** 30–40 mmHg at the ankle, with approximately 40 mmHg recommended for active ulcers^[8] *Delivery systems:** + Multilayer compression bandaging (Profore, Coban) + High-compression graduated stockings (once ulcer size allows) + Compression wraps (adjustable as edema resolves) *Application:** ensure sustained compression 24 hours daily; reapply bandages as limb volume decreases

Arterial Assessment:

Before applying high-pressure compression, arterial perfusion must be assessed (see 10PAD): *ABI >0.8:** full compression safe *ABI 0.5–0.8:** reduced compression (20–25 mmHg) with close monitoring *ABI <0.5:** high-pressure compression contraindicated; refer for vascular evaluation and potential revascularization^[9]

Patients with mixed arterial-venous ulcers require individualized compression strategies in consultation with a vascular specialist.

Adjunctive Pharmacotherapy:

Pentoxifylline (400 mg three times daily) demonstrates modest benefit as an adjunct to compression. It may accelerate healing through improved microcirculatory flow and reduced inflammation, with an absolute improvement of 10–15% in healing rates when added to compression.^[8]

Early Venous Intervention:

The EVRA (Early Venous Reflux Ablation) trial established that early endovenous ablation of superficial truncal reflux, combined with compression therapy, significantly accelerates ulcer healing and reduces recurrence compared to compression alone. Current guidelines recommend identifying and treating superficial venous reflux early in the course of C6 disease rather than deferring intervention until after ulcer healing ^[12],[6].

Venous disease classification (CEAP) and outcomes

Chronic venous disease is classified using the CEAP system, which stratifies patients based on Clinical manifestations (C0–C6), Etiologic factors, Anatomic distribution, and Pathophysiologic mechanisms. The clinical classification ranges from C0 (no visible venous disease) to C6 (active venous ulcer). The Venous Clinical Severity Score (VCSS) provides a validated instrument for tracking disease severity and response to treatment ^[3].

Typical progression follows a sequence from telangiectasias and varicosities (C1–C2) to edema (C3), skin changes including pigmentation and lipodermatosclerosis (C4), healed ulceration (C5), and active ulceration (C6). However, not all patients progress through all stages, and some present with advanced disease without prior symptoms.

Prognostically, higher CEAP classes correlate with reduced quality of life, increased healthcare utilization, and greater difficulty achieving ulcer healing. The classification helps guide treatment intensity and set realistic expectations for outcomes.