Short note on varicose veins with definition, epidemiology, symptoms, signs, investigation and treatment

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"varicose veins"[MeSH Terms] AND treatment

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Varicose Veins

Clinical photograph demonstrating varicose veins - Gray's Anatomy for Students

Definition

Varicose veins are dilated, bulging, tortuous superficial veins measuring at least 3 mm in diameter, typically occurring in the lower limbs. They are distinct from:

Reticular veins: dilated intradermal veins, 1-3 mm diameter, blue-green, do not protrude from the skin surface
Telangiectasias (spider veins): <1 mm diameter, near the skin surface, forming blue/purple/red linear or web patterns

Varicose veins are classified as:

Primary: originate in the superficial system; result from defective valve structure and function in the saphenous veins, intrinsic wall weakness, or high intraluminal pressure
Secondary: result from venous hypertension due to deep-venous insufficiency, deep-venous obstruction, incompetent perforating veins, or arteriovenous fistulas

(Harrison's Principles of Internal Medicine 22E, p.2223; Bailey and Love's 28th Ed.)

Epidemiology

Adult prevalence of visible varicose veins: 30-50% (Bailey and Love's 28th Ed.)
At least 10% of the general population is affected (Schwartz's 11th Ed.)

Risk factors:

Factor	Detail
Gender	Higher prevalence in women in most studies
Age	Prevalence rises sharply with age; Edinburgh Vein Study: 11.5% (18-24 yrs) rising to 55.7% (55-64 yrs)
Pregnancy	Increases risk due to hormonal changes and elevated intra-abdominal pressure
Family history	~50% have a family history; genetic susceptibility is well-documented
Obesity/BMI	Increasing BMI associated with higher prevalence
Prolonged standing	Inconclusive but commonly cited occupational factor
Ethnicity	Influences prevalence; Western populations more affected
Hormonal therapy	Exogenous estrogens associated with increased risk

Symptoms

Symptoms may be absent (asymptomatic) or significant. Typical complaints include:

Aching, heaviness, throbbing, burning, or bursting sensation over affected areas or the whole limb
Pruritus (itching) - more frequent in the presence of complications
Ankle swelling (edema) - mild in early disease
Early fatigue of the affected leg
Cosmetic concern - unsightly dilated veins

Key feature: Symptoms typically worsen throughout the day or with prolonged standing and improve with leg elevation or compression hosiery. Symptoms are independent of the degree of venous incompetence and can significantly impair health-related quality of life.

Telangiectasias and reticular veins without significant reflux rarely cause physical symptoms but patients often seek cosmetic treatment.

(Bailey and Love's 28th Ed., p.1052; Schwartz's 11th Ed.)

Signs

On examination (standing position):

Tortuous, dilated subcutaneous veins - usually clinically obvious
Distribution helps identify the affected system:
- Medial thigh and calf varicosities → Great Saphenous Vein (GSV) incompetence (~60% of cases)
- Posterolateral calf varicosities → Small Saphenous Vein (SSV) incompetence (~20% of cases)
- Anterolateral thigh and calf → Anterior accessory GSV (AAGSV) incompetence
Saphena varix: large dilated vein at the saphenofemoral junction (SFJ) presenting as a lump in the groin - disappears when recumbent, may transmit a cough impulse (can mimic a groin hernia)
Pitting edema - may extend from ankle to knee or thigh in severe disease
Signs of chronic venous insufficiency (CVI):
- Stasis dermatitis / eczema (corona phlebectatica)
- Hyperpigmentation (hemosiderin deposition)
- Lipodermatosclerosis: induration + hemosiderin deposition + inflammation, just above the ankle
- Atrophie blanche: white scar patches with focal telangiectasias, near medial malleolus
- Phlebectasia corona: fan-shaped intradermal veins near the ankle
- Venous ulceration: shallow, irregular border, medial/lateral malleolus

Bedside clinical tests (now largely replaced by duplex ultrasound):

Brodie-Trendelenburg test: leg elevated to empty veins, tourniquet placed on proximal thigh, patient stands - rapid filling after tourniquet release = superficial venous insufficiency (primary); filling before release = deep-venous incompetence (secondary)
Perthes test: tourniquet on midthigh while standing, patient walks 5 min - collapse of superficial veins = patent deep system; distension = deep venous obstruction

(Bailey and Love's 28th Ed.; Harrison's 22E, p.2224)

Investigations

Duplex Ultrasound Scanning (gold standard)

Tourniquet tests and hand-held Doppler have now been abandoned. Duplex ultrasound is recommended for all patients prior to any intervention. It should be performed with the patient standing, using a 7.5-13 MHz high-frequency linear array transducer.

Duplex scanning establishes:

Presence of reflux in deep and superficial venous systems
Exact distribution and extent of reflux in the superficial system (affected junctions, perforators)
Presence of obstruction in the deep venous system
Suitability of incompetent veins for various treatment options (based on diameter, tortuosity, presence of saphena varix)
Presence of thrombus within superficial veins
Indication of a pelvic source of reflux

Reflux definitions on duplex:

Superficial/crural vein reflux: retrograde flow lasting ≥0.5 seconds
Proximal deep vein reflux: retrograde flow lasting ≥1 second

The "Mickey Mouse sign" on transverse view shows the GSV and CFV lying medial to the common femoral artery.

Other investigations (occasionally required):

MR venography (non-invasive) - for pelvic or iliac vein assessment
Contrast venography / IVUS - invasive, reserved for complex cases
Varicography is now historical

(Bailey and Love's 28th Ed., p.1053-1054)

Treatment / Management

1. Conservative Management

Compression hosiery - the cornerstone of conservative treatment:

Graduated external compression (20-30, 30-40, or 40-50 mmHg)
Stockings range from knee-high to waist-high
Provides sufficient symptomatic relief in many patients
First-line trial before interventional management

Other conservative measures: weight loss, leg elevation, regular exercise, avoiding prolonged standing.

2. Sclerotherapy

Destroys the venous endothelium to obliterate the vein
Sclerosants used:
- Hypertonic saline (11.7-23.4%)
- Sodium tetradecyl sulfate (STS) (0.125-1%)
- Polidocanol (0.5-1.0%)
Foam sclerotherapy: ultrasound-guided foam injection - randomized trials show significant symptom relief and improved cosmetic appearance
Elastic bandaging after injection worn for 3-5 days (to appose inflamed walls), then compression stockings for ≥2 weeks
Complications: allergic reaction, hyperpigmentation, thrombophlebitis, DVT, skin necrosis

3. Endovenous Thermal Ablation

Catheter-based minimally invasive techniques, performed under tumescent local anaesthesia under ultrasound guidance. Both have similar outcomes and have largely replaced open surgery.

a) Endovenous Laser Ablation (EVLA):

A laser fibre is introduced via catheter; energy delivery of ~60-80 J/cm causes thermal occlusion
Compression applied post-procedure

b) Radiofrequency Ablation (RFA):

Electromagnetic current heats the vein wall to 120°C in 20-second treatment cycles
Most popular device: ClosureFast™ (Medtronic)
Multiple RCTs show EVLA and RFA have comparable efficacy and safety; recent meta-analysis (Jiang et al., 2024) confirmed this

4. Non-Thermal, Non-Sclerosant Ablation (Newer Techniques)

Mechanochemical ablation (MOCA): combines catheter-based mechanical endoluminal injury with liquid sclerosant - no tumescent anaesthesia required
Cyanoacrylate adhesive (VenaSeal): proprietary glue injected under ultrasound guidance - promising early results, avoids heat and sclerosants

5. Surgical Treatment

High ligation and stripping (Trendelenburg operation): ligation of the SFJ or SPJ + stripping of the GSV or SSV - now less commonly performed, reserved for cases not amenable to endovenous techniques
Phlebectomy (avulsions): removal of tributary varicosities through small stab incisions; often performed alongside thermal ablation as a combined procedure

Indications for intervention (beyond conservative therapy):

Symptoms not relieved by compression
Lipodermatosclerosis
Venous ulceration
Bleeding from varicosities
Superficial vein thrombosis (thrombophlebitis)

(Bailey and Love's 28th Ed., p.1054-1055; Schwartz's Principles of Surgery 11th Ed.; Harrison's 22E)

Complications

Acute	Chronic
Superficial vein thrombosis (thrombophlebitis)	Lipodermatosclerosis
Haemorrhage (spontaneous or traumatic)	Venous eczema/stasis dermatitis
	Venous ulceration
	Hyperpigmentation
	Atrophie blanche

Recent evidence note: A 2024 meta-analysis (PMID 38316290) comparing endovenous RFA vs. EVLA confirmed comparable efficacy, safety, and quality-of-life outcomes - supporting either technique as first-line interventional treatment for GSV/SSV reflux over open surgery.

Classification of varicose vein in detail

Varicose veins are classified by etiology (primary/secondary/congenital), by the affected anatomical system (GSV/SSV), and by the CEAP classification system which is the internationally accepted standard grading from C0 (no signs) to C6 (active venous ulcer). Let me pull the detailed classification from the textbooks.

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Classification of Varicose Veins

Varicose veins are classified across several overlapping frameworks: by etiology, by morphology/type, by anatomical system, and most comprehensively by the internationally accepted CEAP classification system (updated 2020). Two additional scoring tools - the Venous Clinical Severity Score (VCSS) and the Venous Segmental Disease Score (VSDS) - supplement CEAP for outcomes assessment.

I. Classification by Etiology

This is the most fundamental and clinically practical division.

1. Primary Varicose Veins (Ep)

Arise from intrinsic abnormalities of the venous wall (structural weakness) or venous valve leaflets
Result in valvular incompetence and reflux within the superficial venous system
No identifiable underlying deep venous disease
Approximately 50% have a positive family history, suggesting genetic susceptibility
Other contributing factors: aging, female sex, pregnancy, obesity, hormonal therapy, prolonged standing
The most common type encountered in clinical practice

2. Secondary Varicose Veins (Es)

Result from an identifiable acquired cause that elevates venous pressure and drives dilation of superficial veins.

The 2020 CEAP revision further subclassifies secondary causes as:

Subtype	Meaning	Examples
Esi	Secondary - intravenous	Post-thrombotic syndrome (previous DVT leading to valve destruction and reflux), intraluminal obstruction
Ese	Secondary - extravenous	External compression of deep veins (May-Thurner syndrome, Nutcracker syndrome, pelvic tumours, pregnancy), arteriovenous fistula

Arteriovenous fistulas cause varicose veins in the affected limb by raising venous pressure directly.

3. Congenital Varicose Veins (Ec)

Present from birth; result from a developmental defect in the venous system
Associated syndromes include:
- Klippel-Trenaunay syndrome: port wine stain + varicose veins + bony/soft tissue hypertrophy of a limb
- Parkes-Weber syndrome: similar but with arteriovenous fistulas
- Ehlers-Danlos syndrome: connective tissue disorder with venous fragility
- Clonal trisomies and other chromosomal anomalies

4. No Cause Identified (En)

Venous disease present but no etiology can be established after workup

II. Classification by Morphology / Type of Vessel

Type	Diameter	Appearance	Protrudes?
Telangiectasias (spider veins)	< 1 mm	Blue, purple, or red; linear, branching, or spider-web patterns	No
Reticular veins	1-3 mm	Dilated intradermal/subdermal veins; blue-green	No
Varicose veins (trunk varicosities)	≥ 3 mm	Dilated, tortuous, bulging subcutaneous veins	Yes
Saphena varix	Variable	Dilated vein at the saphenofemoral junction; disappears supine; cough impulse present	Yes (groin lump)

(Harrison's Principles of Internal Medicine 22E, p.2223)

III. Classification by Anatomical System

Based on which superficial venous axis is incompetent (confirmed by duplex ultrasound):

System	Distribution of Varicosities	Approximate Frequency
Great Saphenous Vein (GSV) incompetence	Medial thigh and calf varicosities	~60% of cases
Small Saphenous Vein (SSV) incompetence	Posterolateral calf varicosities	~20% of cases
Anterior Accessory GSV (AAGSV) incompetence	Anterolateral thigh and calf varicosities	Less common
Perforator vein incompetence	Localised clusters of varicosities at specific perforator sites	May coexist with above
Pelvic/gonadal vein reflux	Perineal, posterior thigh, or bilateral varicosities	Especially in parous women

(Bailey and Love's Short Practice of Surgery 28th Ed., p.1152)

IV. Classification by Presentation / Complication Status

From clinical practice (Bailey and Love's):

Varicose Veins
├── Uncomplicated
│   ├── Asymptomatic
│   └── Symptomatic (aching, heaviness, itching, etc.)
└── Complicated
    ├── Chronic (skin changes, venous eczema, lipodermatosclerosis, ulceration)
    └── Acute (superficial vein thrombosis / thrombophlebitis, haemorrhage)

V. CEAP Classification (International Standard, Updated 2020)

Devised in 1994 by the American Venous Forum (AVF); revised in 2004 and again in 2020 (Lurie et al., J Vasc Surg Venous Lymphat Disord. 2020;8:342-352). Modelled after the TNM cancer staging system. Classifies chronic venous disease (CVD) across four domains: Clinical (C), Etiologic (E), Anatomic (A), Pathophysiologic (P).

The 2020 update added:

C4c (corona phlebectatica) as a new subclass
The "r" modifier for recurrent varicose veins and recurrent venous ulcers
Replacement of numeric venous segment descriptions with standard abbreviations

C - Clinical Classification

C6 active venous ulcer - Current Surgical Therapy 14e

C Class	Description	Clinical Features
C0	No visible or palpable signs of venous disease	Normal appearance; patient may have symptoms
C1	Telangiectasias or reticular veins	Spider veins (<1 mm) or reticular veins (1-3 mm)
C2	Varicose veins	Dilated, tortuous, subcutaneous veins ≥3 mm
C2r	Recurrent varicose veins	Varicosities recurrent after previous treatment
C3	Edema	Pitting or non-pitting edema; no skin changes yet
C4	Skin and subcutaneous tissue changes secondary to CVD	(subdivided below)
C4a	Pigmentation or eczema	Hemosiderin staining; stasis dermatitis/eczema
C4b	Lipodermatosclerosis or atrophie blanche	Induration + inflammation above ankle; white scars
C4c	Corona phlebectatica	Fan-shaped pattern of intradermal veins near ankle/foot (new in 2020)
C5	Healed venous ulcer	Ulcer previously present but now healed; residual scar
C6	Active venous ulcer	Open ulcer; shallow, irregular edges, granulation tissue
C6r	Recurrent active venous ulcer	Active ulcer in a patient with previously healed venous ulcer

Each limb is further designated:

"s" = symptomatic (e.g., C2s)
"a" = asymptomatic (e.g., C2a)

Important: C3-C6 reflects progressive chronic venous insufficiency (CVI). Skin changes (C4b) and ulceration carry significant morbidity - venous disease accounts for ~85% of all chronic lower limb ulcers.

E - Etiologic Classification

Code	Etiology
Ep	Primary (intrinsic valve/wall defect)
Es	Secondary (acquired cause)
Esi	Secondary - intravenous (e.g., post-DVT)
Ese	Secondary - extravenous (e.g., compression syndromes)
Ec	Congenital (present since birth)
En	No cause identified

A - Anatomic Classification

The 2020 revision uses standard venous abbreviations rather than numbered segments.

Code	Location	Key Veins Included
As	Superficial	Great saphenous vein (GSV), small saphenous vein (SSV), anterior accessory GSV (AAGSV), non-saphenous superficial veins, telangiectasias, reticular veins
Ap	Perforator	Thigh perforators, calf perforators (e.g., Cockett's perforators above medial malleolus)
Ad	Deep	Inferior vena cava (IVC), iliac veins (common, internal, external), femoral veins, popliteal vein, tibial veins (anterior, posterior, peroneal), gastrocnemius/soleal veins
An	No venous anatomic location identified

Multiple anatomic locations can be listed together (e.g., As,p,d).

P - Pathophysiologic Classification

Code	Pathophysiology	Mechanism
Pr	Reflux	Incompetent valves → retrograde flow → venous hypertension
Po	Obstruction	Thrombosis or extrinsic compression blocking outflow
Pr,o	Reflux and obstruction	Combined (e.g., post-thrombotic syndrome)
Pn	No pathophysiology identified

How to Write a Full CEAP Code

A complete CEAP classification is written as: C_E_A_P

Examples:

C2s,Ep,As,Pr = Symptomatic varicose veins; primary etiology; superficial system; reflux only - classic uncomplicated primary varicose veins
C6,Es,Ad,Pr,o = Active venous ulcer; secondary etiology (post-DVT); deep system affected; both reflux and obstruction - severe post-thrombotic syndrome
C4a,Ep,As,p,Pr = Pigmentation/eczema; primary; superficial + perforators; reflux - CVI with skin changes
C2r,Es,As,Pr = Recurrent varicose veins after treatment; secondary; superficial; reflux

VI. Supplementary Scoring Systems

CEAP classifies but does not quantify severity for outcomes tracking. Two validated tools complement it:

Venous Clinical Severity Score (VCSS / r-VCSS)

Assigns a quantitative score to 10 clinical attributes (pain, varicose veins, edema, skin pigmentation, inflammation, induration, ulcer count, duration, size, compression use)
Each attribute scored 0-3 (absent/mild/moderate/severe)
Total score 0-30; used to track treatment outcomes before and after intervention
Current standard for validated patient-reported outcomes following endovascular and open surgical interventions

Venous Segmental Disease Score (VSDS)

Maps the anatomic extent and severity of reflux and obstruction across individual venous segments
Complements CEAP and VCSS for research and complex cases

Aberdeen Varicose Vein Score (AVVS)

Patient-reported outcome measure (PROM) specific to varicose veins
Helps identify patients most likely to benefit from intervention and assess treatment expectations

(Sabiston Textbook of Surgery; Fischer's Mastery of Surgery 8th Ed.; Current Surgical Therapy 14th Ed.)

Summary Diagram

VARICOSE VEIN CLASSIFICATION
│
├── 1. By ETIOLOGY
│   ├── Primary (intrinsic valve/wall defect)
│   ├── Secondary
│   │   ├── Intravenous (post-DVT, intraluminal)
│   │   └── Extravenous (compression syndromes, AV fistula)
│   └── Congenital (Klippel-Trenaunay, Parkes-Weber, etc.)
│
├── 2. By MORPHOLOGY
│   ├── Telangiectasias (<1 mm)
│   ├── Reticular veins (1-3 mm)
│   ├── Varicose veins (≥3 mm)
│   └── Saphena varix
│
├── 3. By ANATOMICAL SYSTEM
│   ├── GSV system (60%)
│   ├── SSV system (20%)
│   ├── AAGSV
│   └── Perforator/Pelvic source
│
├── 4. By COMPLICATION STATUS
│   ├── Uncomplicated (asymptomatic / symptomatic)
│   └── Complicated (acute: thrombophlebitis, bleed | chronic: ulcer, LDS)
│
└── 5. CEAP CLASSIFICATION (International Standard 2020)
    ├── C0 → C6r  (Clinical severity)
    ├── Ep/Es/Ec/En  (Etiology)
    ├── As/Ap/Ad  (Anatomic location)
    └── Pr/Po/Pr,o  (Pathophysiology)

(Sources: Bailey and Love's 28th Ed.; Harrison's Principles 22E; Sabiston Textbook of Surgery; Current Surgical Therapy 14e; Fischer's Mastery of Surgery 8th Ed.; Lurie et al. 2020 CEAP Update)

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