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Varicose Veins — Comprehensive Overview

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1. Definition & Epidemiology

• Present in at least 10% of the general population
• Up to 20% of males and one-third of females develop lower extremity varicose veins
• By age 65, prevalence in the Western population exceeds 55% (Edinburgh Vein Study)

• Female sex (prolonged IVC compression from gravid uterus during pregnancy)
• Obesity
• Family history (faulty venous wall development — genetic predilection)
• Prolonged standing or inactivity
• Occupation (prolonged standing)
• Prior phlebitis destroying valve structure
• Congenital syndromes: Klippel-Trénaunay, Ehlers-Danlos, clonal trisomies
• Compressive syndromes: May-Thurner (iliac vein compression) and Nutcracker syndrome (left renal vein compression)

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2. Anatomy & Pathophysiology

Venous Return Physiology

1. Calf muscle pump: Contraction of calf muscles compresses the soleal sinuses and deep veins, generating pressures up to 300 cm H₂O, propelling blood proximally (the "ventricular" phase).
2. Perforating vein valves: During relaxation, blood flows from the superficial system through perforators into the deep veins. The superficial venous system acts like an atrium, and the deep calf veins like a ventricle.

Sites of Valve Incompetence

1. Saphenofemoral junction (SFJ) — saphena varix where the great saphenous vein (GSV) joins the femoral vein
2. Mid-thigh perforating vein — between GSV and femoral vein
3. Calf perforating veins (Cockett's perforators) — at 5, 10, and 15 cm above the medial malleolus
4. Saphenopopliteal junction (SPJ) — small saphenous vein (SSV) joining the popliteal vein

Mechanism of Varicosity Formation

1. Valve-first theory: A malfunctioning valve allows retrograde flow → increased venous pressure → vein dilation → progressive incompetence of distal valves (a cascade effect).
2. Wall-first theory (primary varicose veins): Intrinsic weakness of the vein wall causes primary dilation → valve leaflets separate and become incompetent → reflux develops.

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3. Classification

Primary vs. Secondary

CEAP Classification (2020 Revision)

Morphological Classification by Vein Size (Dermatology 5e)

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4. Clinical Features

Symptoms

• Unsightly cosmetic appearance
• Aching, heaviness, and fatigue in the affected leg
• Pruritus over varicosities
• Swelling (mild edema)
• Worsening with prolonged standing or sitting; relieved by leg elevation above heart level

Signs (Mild to Severe)

• Dilated, tortuous, visible subcutaneous veins
• Mild dependent edema
• Thrombophlebitis (superficial vein inflammation/thrombosis)
• Hyperpigmentation (stasis dermatitis / "brawny induration" — brownish discoloration from hemolysis of extravasated RBCs)
• Lipodermatosclerosis (fibrous thickening of subcutaneous fat)
• Venous ulceration — typically above medial malleolus; poor wound healing and superimposed infections are common
• Bleeding from attenuated vein clusters
• Stasis dermatitis ("brawny induration")

Important: Embolism from superficial varicose veins is very rare, unlike deep vein thrombosis which commonly leads to pulmonary embolism.

Pathology (Robbins)

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5. Diagnosis

Clinical Examination

• Patient lies supine; leg is elevated to drain veins
• Tourniquet placed around upper thigh below SFJ
• Patient stands up
• No filling below tourniquet → SFJ incompetence (reflux from femoral into GSV)
• A second tourniquet below the knee tests the SPJ and calf perforators

Duplex Ultrasound (Gold Standard)

• Performed with patient standing or in steep reverse Trendelenburg to allow accurate assessment of valve competency
• Pathologic reflux defined as: reversal of flow for >500 ms in perforators and truncal superficial veins; >1000 ms in deep veins
• Vein diameters >5 mm (>3.5 mm for perforators) correlate with symptomatic reflux
• Must identify the most proximal/central source of reflux
• Correlate duplex findings with symptoms — mild or isolated segmental reflux in a small vein rarely warrants intervention

Additional Investigations

• Venous Clinical Severity Score (r-VCSS) — validated tool for outcomes and treatment planning
• Aberdeen Varicose Vein Score — QoL assessment; identifies patients most likely to benefit from intervention
• In complex cases: CT venography, MR venography (for pelvic vein/gonadal vein incompetence)

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6. Management

Conservative (First-Line)

• Cornerstone of conservative management
• Compression classes:
  • 20–30 mmHg: mild symptoms, telangiectasias
  • 30–40 mmHg: moderate varicosities, edema
  • 40–50 mmHg: severe disease, venous ulcers
• Length: knee-high to waist-high, should cover symptomatic varices
• Provides sufficient symptom relief in many patients
• Lifestyle measures: weight loss, leg elevation, avoidance of prolonged standing

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Interventional Management

• Symptoms worsen or are unrelieved despite compression therapy
• Lipodermatosclerosis or venous ulceration present
• Patient desires treatment for cosmesis

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A. Sclerotherapy

1. Elastic bandages applied immediately after injection
2. Worn continuously for 3–5 days to oppose inflamed vein walls and prevent thrombus
3. Compression stockings for minimum 2 weeks after bandage removal

• Foamed detergent (liquid:gas ratio 1:4) is more potent — the concentrated sclerosant is on the outer micelle of each bubble
• Fewer injections needed; treats larger segments
• Varithena® (polidocanol 1% injectable foam): FDA-approved for incompetent GSVs, accessory saphenous veins, and visible GSV system varicosities above and below the knee; uses patented O₂:CO₂ (65:35) gas mixture producing cohesive microfoam <100 micron bubbles; provides circumferential endothelial destruction
• A multicenter RCT confirmed significant symptom relief and improved cosmesis with foam sclerotherapy vs. placebo

• Air bolus technique: Inject <0.5 mL air before sclerosant to displace blood and confirm intravascular needle position
• Multiple precannulation sites (MPS): Proximal and distal cannulation while patient stands (to distend veins), then veins treated in elevation

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B. Endovenous Thermal Ablation

1. Distal thigh or proximal calf GSV punctured with 21-gauge needle under US guidance
2. Guidewire inserted → sheath placed
3. Fiber/catheter advanced to just below (not at) SFJ
4. Tumescent anesthetic infiltrated circumferentially around GSV (thermal protection and compression)
5. Vein treated as catheter is withdrawn

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C. Non-Thermal, Non-Sclerosant Ablation

• Proprietary adhesive closes the vein lumen without heat or sclerosant
• No tumescent anesthesia required
• Promising early results; no thermal injury risk to surrounding structures

• Combines catheter-based mechanical endoluminal injury with simultaneous sclerosant injection
• No tumescent anesthesia required
• Lower risk of nerve injury or thermal damage

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D. Surgical Treatment

• Best for large branch varicosities
• Technique: 2-mm incisions directly over varicosities → varicosity dissected from subcutaneous tissue proximally and distally → simple avulsion (no ligation needed in most cases)
• Bleeding controlled by leg elevation, manual compression, and pre-procedure tumescent anesthesia

• Preferred for GSVs of very large diameter (>2 cm) or when endovenous techniques are not feasible
• Technique: Small medial groin incision + incision below the knee → GSV removed using blunt tip catheter or invagination pin stripper
• GSV stripping → lower recurrence rate and better QoL than saphenofemoral junction ligation alone
• Complications: Ecchymosis, hematoma, lymphocele, DVT, infection, saphenous nerve injury

• Historically performed alone, but higher recurrence than stripping
• Popliteal fossa dissection carries risk of common fibular nerve injury → footdrop (nerve lies superficial to popliteal vein)

Anatomical Warning: In the popliteal fossa — popliteal artery is deepest, popliteal vein is intermediate, sciatic nerve/divisions are most superficial. The common fibular nerve is at risk during SSV/SPJ surgery.

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Management of Specific Complications

Chronic Venous Insufficiency (CVI)

• Affects ~600,000 people in the US; costs ~$1 billion/year in healthcare
• 2 million workdays lost per year
• Management: graduated compression, wound care, endovenous/surgical treatment of reflux
• Venous ulcers: multilayer compression bandaging (Unna boot), moist wound healing, treatment of underlying reflux

Superficial Thrombophlebitis

• Warm compresses, NSAIDs, compression
• If propagating toward SFJ: low molecular weight heparin or anticoagulation

Variceal Bleeding

• Leg elevation, direct pressure
• Followed by sclerotherapy or surgical treatment

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7. Special Situations

Other Varicosities Sharing the Pathophysiology

Pelvic Varicosities

• Dilated, tortuous gonadal/ovarian veins (typically left-sided) cause chronic pelvic pain
• Diagnosed by CT/MRI venography or pelvic duplex
• Treated by endovascular embolization

Recurrence Mechanisms

• Neovascularization at the SFJ after stripping/ablation
• Accessory lymph node vessels serving as reflux conduits
• Incomplete ablation of all tributaries
• New incompetence at other junctions

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8. Recent Evidence Update (2024–2026)

• RFA vs. EVLA meta-analysis (PMID 38316290, 2024): Both techniques have comparable long-term ablation rates; RFA may have marginal safety advantages.
• Reflux patterns in primary CVD (PMID 39025298, 2024): Systematic review characterizing anatomical reflux patterns to guide treatment planning.
• Physiotherapy for venous ulcers (PMID 40504402, 2025): Exercise/physiotherapy interventions improve healing of chronic venous ulcers.
• Platelet-rich plasma for venous ulcers (PMID 41643347, 2026): Meta-analysis supports PRP as adjunct therapy improving venous ulcer healing rates.
• Restless legs syndrome and CVI (PMID 41306950, 2025): Systematic review confirms association — screening for CVI is warranted in RLS patients.

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Summary Algorithm

Varicose Veins Suspected
        ↓
Clinical Examination + Duplex Ultrasound
        ↓
CEAP Classification
        ↓
C1–C2: Conservative (compression, lifestyle)
        ↓ if symptomatic/refractory
C2–C3: Sclerotherapy (liquid for small, foam for larger)
        OR
        Endovenous ablation (RFA/EVLA for truncal reflux)
        OR
        Ambulatory phlebectomy (branch varicosities)
        ↓
C4–C6 (skin changes, ulcers):
        Aggressive treatment + wound care
        Deep vein assessment before ablation
        Multilayer compression for ulcers
        GSV stripping if vein diameter >2 cm

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Complications of Varicose Veins

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A. Disease Complications

1. Chronic Venous Insufficiency (CVI)

• AVP <35 mmHg: skin manifestations uncommon
• AVP >80 mmHg: 80% incidence of venous ulceration

• Primary CVI: Intrinsic vein wall abnormalities
• Secondary CVI (Postthrombotic Syndrome / PTS): Follows DVT; valve destruction from thrombus organization leads to combined reflux + obstruction — usually the most severe form

• Leg fatigue, heaviness, discomfort
• Progressive edema (initially pitting, later non-pitting)
• Varicosities

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2. Edema

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3. Stasis Dermatitis (Venous Eczema)

• Mechanism: Chronic venous congestion → extravasation of RBCs → haemolysis → haemosiderin deposition → local inflammatory reaction
• Appearance: Brown-bronze "brawny" pigmentation of the lower leg (especially medial malleolus); associated with eczematous pruritic rash, erythema, scaling
• Also called "brawny induration" — the brawny colour comes directly from haemolysis of extravasated red cells
• In CEAP: C4a (pigmentation or eczema)

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4. Lipodermatosclerosis

• Definition: Fibrotic thickening and induration of the subcutaneous fat of the lower leg, resulting from chronic venous hypertension and tissue ischaemia
• Appearance: Woody, board-like induration of the skin; often circumferential in the "gaiter zone" — classically giving an "inverted champagne bottle" or "champagne bottle" deformity of the lower leg
• In CEAP: C4b (lipodermatosclerosis or atrophie blanche)
• Predisposes to chronic non-healing ulcers and represents advanced CVI

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5. Atrophie Blanche (Livedoid Vasculopathy)

• Focal white, ivory-coloured, atrophic, stellate scars surrounded by hyperpigmentation and telangiectasias
• Located in the "gaiter zone" (lower third of leg)
• Represents end-stage scarring from microthrombi in dermal capillaries in the setting of venous hypertension
• In CEAP: C4b — clinically significant because the skin is extremely fragile and prone to ulceration with minor trauma
• Highly painful compared to standard venous ulcers

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6. Corona Phlebectatica

• Fan-shaped network of intradermal telangiectasias at the medial or lateral ankle/foot
• Also called "ankle flare"
• Reflects underlying perforator incompetence and advanced ambulatory venous hypertension
• In CEAP: C4c
• A clinical warning sign that severe CVI is present

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7. Venous Ulceration (Venous Stasis Ulcer)

• Treat the underlying venous reflux (sclerotherapy/endovenous ablation)
• Compression therapy is the cornerstone: 30–40 mmHg below-knee elastic stockings
  • 93% healing rate with compliant compression use
  • Compliance is critical: ulcer recurrence 29% at 5 years (compliant) vs. 100% at 3 years (non-compliant)
• Unna's Boot: Three-layer dressing (zinc oxide impregnated gauze + elastic wrap + cohesive bandage); applied from forefoot to below knee; changed weekly
• Multilayer elastic wraps: Provide sustained compression; reduce inflammatory cytokines and matrix metalloproteins
• Pneumatic compression devices: For immobile patients or adjunct therapy
• Wound care: Moist wound environment; débridement of slough; antimicrobials for infected ulcers
• Rule out arterial insufficiency (ABI) before high-compression therapy
• Optimise systemic factors: diabetes, nutrition, immunosuppression, heart failure

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8. Superficial Thrombophlebitis

• Definition: Thrombosis and inflammation of a superficial varicose vein
• Presentation: Tender, red, warm, indurated cord along the course of a varicosity; overlying erythema and induration
• Mechanism: Stasis within the dilated varicosity → spontaneous thrombosis → inflammatory response
• Risk: Rare embolism from superficial veins (contrast with deep vein thrombosis which commonly embolises)
• Important exception: If thrombus propagates to within 3–5 cm of the SFJ (saphenofemoral junction), risk of extension into the deep system (DVT + pulmonary embolism) increases significantly → anticoagulation warranted
• Management:
  • NSAIDs + warm compresses + compression
  • Low-molecular-weight heparin if propagating toward SFJ or extensive
  • Surgical drainage of large, tense thrombus for symptomatic relief

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9. Deep Vein Thrombosis (DVT)

• CVI and venous stasis are independent risk factors for DVT
• Venous wall damage, venous hypertension, and turbulent flow promote thrombosis
• Conversely, DVT is also a cause of secondary CVI (postthrombotic syndrome) — a bidirectional relationship
• DVT carries risk of pulmonary embolism — the major life-threatening complication in the venous disease spectrum

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10. Variceal Haemorrhage

• Rupture of a large subcutaneous varicosity, either spontaneously or from minor trauma
• Blood loss can be profuse and alarming, particularly in elderly patients on anticoagulants
• Attenuated, thin-walled vein clusters are at highest risk
• Immediate management: Leg elevation + direct pressure → rapid cessation in most cases
• Definitive treatment: sclerotherapy or surgical avulsion

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11. Secondary Infection / Cellulitis

• Chronic venous stasis and ulceration impair local immune defences
• The oedematous, poorly oxygenated skin is highly susceptible to bacterial invasion
• Cellulitis (most commonly Streptococcus pyogenes, Staphylococcus aureus) is a frequent complication of venous ulcers and stasis dermatitis
• Recurrent cellulitis can damage lymphatics → secondary lymphoedema — a devastating vicious cycle

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12. Contact Dermatitis

• From chronic application of topical agents (antiseptics, wound dressings, lanolin, rubber in compression garments) to sensitised, compromised skin
• A frequent and often under-recognised complication of long-standing venous ulcer management
• Patch testing may be required

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13. Restless Legs Syndrome (RLS)

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B. Complications of Treatment

Complications of Sclerotherapy

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Complications of Endovenous Thermal Ablation (EVLA/RFA)

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Complications of Surgical Treatment

GSV Stripping / Ligation

Popliteal Fossa Surgery (SSV/SPJ Ligation)

The popliteal fossa anatomy (superficial to deep): sciatic nerve divisions > popliteal vein > popliteal artery. The common fibular nerve diverges laterally around the fibular head — extreme care is essential during SPJ surgery.

Ambulatory Phlebectomy

• Complication rate is extremely low
• Minor haematoma, wound dehiscence, nerve injury (rare), infection, telangiectatic matting, hyperpigmentation

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Summary Table

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