5.2.1 Venous leg ulcers

Prevalence of all leg ulcers: 1-2% in the general population, 4-5% of individuals older than 80 years. CVI is considered to cause 60-80% of leg ulcers, mixed venous-arterial insufficiency (PAOD) is the cause in in 10-20%.

A chronic ulcer on the lower leg between knee and ankle joint resulting from improper functioning of venous valves and advanced chronic venous insufficiency (CVI). They are the most common cause of leg ulcers at all.

The common denominator of venous ulcers is ischaemia of the upper dermis. Ulcers occur in superficial CVI (30-40%), such as marked insufficiency of the great saphenous vein, combined superficial and deep CVI, deep CVI (60-70%), post-thrombotic syndrome (50-60%) of patients with a venous ulcer have post- thrombotic syndrome.

Venous hypertension is the first factor followed by fibrin cuff and inflammatory cytokine release. Thereafter, leukocytes get trapped in the capillaries releasing proteolytic enzymes and reactive oxygen metabolites, which finally cause endothelial damage.

In certain cases thrombophilia like factor V Leiden mutation, prothrombin mutations, deficiency of antithrombin, presence of antiphospholipid antibodies, protein C and S deficiencies and increased homocystein are co-morbidities complicating and driving the disease.

Moderate pain, which improves on elevation (unlike in PAOD).

Irregular edges, associated oedema due to increased hydrostatic pressure, which contributes to ‘atrophie blanche’, pigmentation, associated superficial CVI.

Peri-malleolar i.e. anterior to medial malleolus, pretibial area, lower third of leg and almost always medial.

• Chronic, recurrent. Duration of more than 1 year - recurrence rate in these ulcers is more than 70%

• larger wounds

• fibrin in >50% of wound surface

• ankle-brachial pressure index (ABPI) <0.8

• history of venous stripping/ligation and relapse.

• Dermatoliposclerosis.

• Cellulitis (erysipelas) with an ulcer as the entry site. Recurrent cellulitis is often relatively asymptomatic but may lead to chronic lymphedema and further impaired drainage.

• Allergic and irritative or protein dermatitis. In particular, the common allergic contact sensitizers such as lanolin, topical antibiotics (gentamycin, neomycin, bacitracin), antiseptics, preservatives, emulsifiers, resins and latex are responsible.

• Other factors are not sufficiently working muscle pumps (ankle, calf).

Additional clinical findings: oedema, atrophie blanche, varicose vein(s).

Identification of CVI: duplex (first choice), phlebography, doppler sonography: only low sensitivity.

For the assessment of the deep venous system the systolic ankle‐brachial‐pressure index for ruling out concomitant PAOD is recommended.

• Vascular: PAOD, lymphatic vasculitis.

• Haematological diseases: sickle cell anaemia, thalassaemia.

• Infections: bacterial ecthyma; mycobacterial - TB and leprosy; gumma (syphilis); parasitic (tropics); fungal (tropics).

• Traumatic/physical.

• Autoimmune: pyoderma gangrenosum, vasculitis, antiphospholipid antibody syndrome, systemic sclerosis, localized bullous pemphigoid, rheumatoid arthritis.

• Metabolic/endocrine: necrobiosis lipoidica, calciphylaxis, diabetes mellitus.

• Iatrogenic: radiation dermatitis, hydroxyurea treatment.

• Neoplasia: Primary ulcerated skin tumours: malignant melanoma; squamous cell carcinoma; basal cell carcinoma. Secondary: skin metastases; malignant change in chronic ulcer (squamous cell carcinoma).

• Congenital: Klinefelter’s syndrome, dysgenesis of the venous valves, primary lymphoedema.

• Improve general factors: Anaemia, hypoalbuminaemia, diabetes mellitus. Nutrition and physical activity should be optimized.

• Improve venous return by muscle pump activation and compression. No bed rest.

• Multicomponent compression systems are more effective than single-component compression systems; High compression is more effective than lower compression;

• Medical compression stockings are more effective than compression with short stretch bandages.

• Stripping of varicosities, selective vein surgery, endovascular ablative techniques and sclerotherapy.

• Necrotomy reduces the level of contamination and speeds up granulation. Maggots can be used in the early treatment phase.

• Enhance granulation in moist milieu. Encourage re-epithelialisation in non-occlusive, semi-moist milieu.

• Skin grafting when sufficient granulation tissue is present.