Varicose Veins of the Lower Extremities: Etiology, Pathogenesis, Classification, Diagnosis, Treatment Methods

Varicose veins are a condition in which the vein wall becomes thin and the veins dilate unevenly.

Epidemiology

Varicose veins of the lower extremities (VVLE) are among the most common chronic vascular diseases. According to epidemiological studies:

• Prevalence in the adult population reaches 20–30%.
• Women are affected 2–3 times more often than men, associated with hormonal influences and pregnancy.
• The frequency increases with age: more than 50% of women and 30% of men over the age of 60 have signs of varicose veins.
• Ethnic differences are minimal, but there is evidence of a slightly lower incidence in Afro-Caribbean populations compared to Caucasians.

Etiology

The development of varicose veins is caused by a combination of factors, the main ones being:

• Heredity – genetic mutations affecting the structure of the venous wall and valves;
• Female sex and hormonal changes – progesterone reduces venous wall tone;
• Pregnancy – increased intra-abdominal pressure and hormonal effects;
• Occupations involving prolonged standing – impair venous outflow;
• Sedentary lifestyle and obesity – contribute to venous stasis;
• Trauma and previous deep vein thrombosis – impair valve function.

Pathogenesis

The core of pathogenesis is venous hypertension due to valve insufficiency and reduced vein wall elasticity.

• Primary valve insufficiency:

Malfunctioning venous valves → retrograde blood flow (reflux).

Reflux increases pressure on the vein wall, leading to its dilation, especially in superficial veins (great and small saphenous veins).

• Destruction of the venous wall:

Loss of collagen and elastin in the media → decreased tone → varicose transformation.

Activation of matrix metalloproteinases, inflammatory cytokines (IL-6, TNF-α) → vascular remodeling.

• Microcirculatory impairment:

Venous hypertension leads to capillary stasis, hypoxia, and transendothelial leakage of plasma and erythrocytes. This causes edema, trophic skin changes, and, with progression, varicose ulcers, especially in the area of the medial malleolus, where hydrostatic resistance is the lowest.

Classification

The CEAP classification is used to assess the stage and severity of chronic venous disease: C – Clinical signs; E – Etiology; A – Anatomic location; P – Pathophysiologic mechanism.

Clinical manifestations

Symptoms range from cosmetic changes to severe trophic skin disorders:

• Dilated, tortuous superficial veins;
• Heaviness, fullness, and burning sensations in the legs;
• Evening pain;
• Ankle and lower leg edema;
• Night cramps and paresthesias;
• Skin changes: hyperpigmentation, induration, eczema;
• Trophic ulcers (commonly in the medial ankle).

Symptoms worsen with prolonged standing and improve with rest or leg elevation.

Diagnosis

Physical examination: Inspection and palpation of veins while standing;

Assessment of reflux (Trendelenburg test, Sheinis test).

Instrumental methods: Ultrasound angioscanning (duplex ultrasound) – the gold standard of diagnosis.

• Imaging: Duplex ultrasound — the gold standard; reveals reflux, occlusions, vein diameter, and anatomy;
• Pathologic reflux: >0.5 seconds post-compression

Laboratory tests (in complications):

• Coagulation panel — for suspected thrombosis;
• Glucose, HbA1c — if diabetic angiopathy suspected;
• Wound microbiota — if infected ulcers are present.

CEAP classification helps stratify risk and guide treatment decisions.

Treatment

1. Conservative Treatment

Compression therapy:

• Elastic stockings come in different compression levels and are selected based on the stage of the disease and the severity of symptoms. An improperly selected garment may be ineffective or even harmful, so the type and class of compression should be prescribed by a doctor based on the examination.
• They improve venous return, reduce edema, and alleviate subjective symptoms.

Venoactive drugs:

• Diosmin, hesperidin, and troxerutin reduce capillary permeability and improve microcirculation.
• They are used as symptomatic treatment, but do not address the underlying cause.

Lifestyle modifications:

• Weight control;
• Moderate physical activity;
• Avoiding prolonged sitting or standing

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2. Surgical and Minimally Invasive Treatment

Indications:

• Symptomatic varicose veins with confirmed reflux;
• CEAP stages C2–C6;
• Ineffectiveness of conservative therapy.

2.1. Endovenous laser ablation (EVLA)

• Most common method;
• Minimally invasive;
• Laser causes thermal coagulation and vein sclerosis;
• Performed under ultrasound and tumescent anesthesia.

2.2. Radiofrequency ablation (RFA)

• Alternative to EVLA;
• Uses radiofrequency energy;
• Often better tolerated but more expensive.

2.3. Sclerotherapy

• Injection of a sclerosing agent (foam or liquid) to close the vein;
• Used for reticular veins and telangiectasias.

2.4. Miniphlebectomy (Müller technique)

• Removal of varicose tributaries through micro-incisions.

2.5. Crossectomy and stripping

• Resection of the great saphenous vein;
• Used less often, when endovenous techniques are contraindicated.

Contraindications:

• Acute thrombosis;
• Decompensated chronic diseases;
• Pregnancy (relative contraindication);
• Active skin infections at the intervention site.

With timely and appropriate treatment, the prognosis is favorable. Modern endovenous techniques result in remission in 90–95% of cases. Recurrence is possible if technique is flawed or disease progresses.

Possible complications:

• Thrombophlebitis;
• Deep vein thrombosis (DVT);
• Hyperpigmentation and hyperkeratosis;
• Ulcerative and necrotic skin changes;
• Bleeding from a varicose vein.