Chronic Venous Disease

Chronic venous disease is a spectrum of abnormalities of the venous system of the lower limbs, ranging from telangiectasia to venous ulceration, caused by valvular incompetence, venous obstruction, or both. Chronic venous insufficiency refers to the advanced stages (C3 to C6).

Epidemiology

• Varicose veins affect 20 to 30% of adults, and active or healed ulceration affects 1 to 2% of the population, rising to 4% in the elderly.
• Female sex, pregnancy, obesity, prolonged standing, family history, age and previous deep vein thrombosis are risk factors.

Pathophysiology

• Primary disease results from structural weakness of the vein wall and valves, with reflux of blood.
• Secondary disease follows deep vein thrombosis (post-thrombotic syndrome), trauma or pelvic venous obstruction.
• Reflux and obstruction cause ambulatory venous hypertension. In health the calf muscle pump lowers ambulatory pressure by 60 to 80% on exercise, while in disease the fall is blunted.
• Sustained pressure transmitted to the capillaries triggers leukocyte activation, endothelial injury, fibrin cuff formation, haemosiderin deposition and dermal fibrosis.

Duplex definition of reflux: reversal of flow lasting more than 0.5 seconds in superficial and perforator veins, and more than 1 second in the femoral and popliteal veins.

CEAP classification (clinical grade)

• C0: no visible disease.
• C1: telangiectasia or reticular veins.
• C2: varicose veins (3 mm or more).
• C3: oedema.
• C4a: pigmentation or eczema. C4b: lipodermatosclerosis or atrophie blanche.
• C5: healed ulcer. C6: active ulcer.
• Suffixes: S (symptomatic) or A (asymptomatic), then aetiology (primary, secondary, congenital), anatomy (superficial, deep, perforator) and pathophysiology (reflux, obstruction).

Complications include superficial vein thrombosis, bleeding from ruptured varices, cellulitis, deep vein thrombosis, and malignant change in chronic ulcers.

Symptoms

• Heaviness, aching, itching, throbbing, cramps and restlessness of the legs, worse after standing and in the evening, and relieved by elevation and walking.

Signs

• Dilated, tortuous superficial veins, ankle flare, and pitting oedema.
• Pigmentation, venous eczema, lipodermatosclerosis (inverted champagne bottle appearance of the lower leg), and atrophie blanche.
• Ulcers lie in the gaiter area above the medial malleolus. They are shallow with irregular margins, sloughy bases, moderate exudate, and surrounding eczema. Pain is mild and relieved by elevation.

Atypical features calling for another diagnosis or biopsy

• Severe pain, punched out ulcer, absent pedal pulses (arterial), neuropathic plantar location (diabetes), violaceous undermined border (pyoderma gangrenosum), palpable purpura (vasculitis), raised rolled edges (malignancy), and recurrent ulcers in sickle cell disease.
• Ulcers that fail to heal after 12 weeks of appropriate treatment warrant biopsy.

Features suggesting deep or pelvic obstruction include swelling of the entire limb, venous claudication, lower abdominal and pelvic varices, and vulval varices.

Differential diagnosis of leg swelling includes lymphoedema, lipoedema, heart failure, nephrotic syndrome, hypoalbuminaemia, drugs such as amlodipine, and deep vein thrombosis.

History and examination in the standing position, with documentation of CEAP class and the venous clinical severity score.

Investigations

• Ankle brachial index in all patients with ulcers or planned compression. Compression of 40 mmHg is safe when the index is above 0.8. Use reduced compression between 0.5 and 0.8, and avoid it below 0.5 without vascular review.
• Duplex ultrasound in the standing position with manual calf compression: assess great and small saphenous junction competence, reflux times, vein diameter, perforators, accessory trunks, and deep vein patency or post-thrombotic change.
• CT or MR venography, or intravascular ultrasound when iliac vein compression (May-Thurner), inferior vena cava obstruction, or pelvic venous disease is suspected.
• Biopsy of ulcer edge for atypical or non-healing ulcers.
• Wound swab only when there are clinical signs of infection (spreading erythema, pain, purulence, odour).
• Blood tests: CBC, HbA1c, albumin, creatinine and ferritin. Thrombophilia screening for ulcers with prior thrombosis or early onset.
• Photoplethysmography or air plethysmography is used for research and complex cases.

Conservative therapy for all patients

• Compression is the cornerstone. For C2 to C3 symptomatic disease, use knee-length stockings of 20 to 30 mmHg. For severe disease (C4 to C6), use 30 to 40 mmHg.
• Active ulcers: multilayer bandaging with sustained compression of about 40 mmHg at the ankle, changed once or twice weekly, until healing. Adjust for arterial status.
• Walking, calf muscle exercise, ankle mobility, leg elevation above heart level for 30 minutes three to four times daily, and weight loss.
• Skin care: emollients and low-potency topical steroids for venous eczema (betamethasone valerate 0.1% ointment for 1 to 2 weeks). Avoid sensitisers including neomycin, lanolin and fragrance.

Drug therapy

• Micronised purified flavonoid fraction (diosmin 450 mg with hesperidin 50 mg) 1000 mg daily reduces symptoms and oedema, and increases ulcer healing.
• Pentoxifylline 400 mg three times daily improves ulcer healing as an adjunct to compression.
• Diuretics are not indicated for venous oedema.
• Antibiotics only for clinical infection: flucloxacillin 500 mg to 1 g four times daily, or doxycycline 100 mg twice daily if penicillin-allergic, for 7 days. Cellulitis may need IV therapy.
• Analgesia with paracetamol. Avoid topical antibiotics.

Intervention for symptomatic reflux and for ulcers

• Endovenous thermal ablation (radiofrequency or laser) of incompetent great or small saphenous trunks under tumescent local anaesthesia is first line. Occlusion rates are above 90% at 5 years.
• Non-thermal non-tumescent options: cyanoacrylate glue and mechanochemical ablation.
• Ultrasound-guided foam sclerotherapy (polidocanol 1 to 3% mixed 1:4 with air, to a maximum of 10 mL per session) for tributaries, residual varices, recurrent disease, and ulcer-bearing segments.
• Phlebectomy for tributary varicosities. Open high ligation and stripping when endovenous therapy is not feasible.
• Venous ulcer with superficial reflux: early ablation (within 2 weeks of presentation) does not speed healing, but cuts 12-month recurrence by about half.
• Compression for 1 to 2 weeks after intervention, and duplex review at 1 week to detect endothermal heat-induced thrombosis.
• Complications: thrombophlebitis, saphenous nerve injury (paraesthesia in 5 to 10%), skin burns, residual pigmentation, deep vein thrombosis (under 1%).

Deep venous obstruction

• Iliac vein stenting (venoplasty with dedicated venous stents) for symptomatic iliac or May-Thurner compression, with antithrombotic therapy after the procedure (anticoagulation for at least 3 to 6 months, or lifelong in post-thrombotic disease).

Refractory ulcers

• Debridement of slough, skin graft or substitute for large clean ulcers, negative pressure therapy, and treatment of infection.
• Correct anaemia, nutrition and diabetes. Treat contributing arterial disease first.

Special circumstances

• Pregnancy: compression and elevation, defer intervention until about 3 months postpartum.
• Superficial vein thrombosis near the saphenofemoral junction or 5 cm or longer: fondaparinux 2.5 mg SC daily for 45 days, or rivaroxaban 10 mg daily for 45 days.
• Bleeding varix: elevation, direct pressure, then sclerotherapy or ligation.

Recurrence prevention

• Lifelong compression after healing (30 to 40 mmHg), exercise, weight reduction, and treatment of residual reflux. Ulcer recurrence rates fall below 15% when ablation is added.