Leg Ulcers

Chronic wounds of the lower leg persisting >2 weeks. Venous ulcers account for ~70%, arterial ~15%, and mixed ~10–15%. Venous ulcers are managed with compression bandaging (after excluding arterial disease with ABPI). NICE NG168 provides guidance. Estimated prevalence ~1% of UK adults, costing the NHS ~£1 billion/year.

Key Facts

Venous ulcers (~70%): gaiter area (medial malleolus), shallow, irregular, with venous eczema, lipodermatosclerosis, haemosiderin staining Arterial ulcers (~15%): distal (toes, dorsum of foot), punched-out, painful, associated with absent pulses and claudication ABPI (ankle-brachial pressure index): >0.8 = safe for compression; <0.5 = significant arterial disease — do NOT compress Compression therapy: cornerstone of venous ulcer management — multilayer compression bandaging (ABPI >0.8) NICE NG168: leg ulcer management — assessment, ABPI, compression Pentoxifylline 400 mg TDS: adjunct to compression for venous ulcers — improves healing rates Malignant transformation (Marjolin's ulcer): SCC in chronic ulcer — biopsy non-healing ulcers >4–6 weeks Cost to NHS: ~£1 billion/year; affects ~1% of UK adult population

Overview

Key Facts

Chronic leg ulcers are extremely common, particularly in elderly patients. Accurate diagnosis of the underlying cause is essential as management differs fundamentally between venous and arterial ulcers. Compression therapy is the mainstay for venous ulcers but is dangerous in arterial disease.

Epidemiology

  • Prevalence: ~1% of UK adults; increases with age (~3.6% in >65s)
  • F > M
  • Venous ulcers: ~70% of all leg ulcers
  • Significant impact on quality of life and healthcare costs (~£1 billion/year NHS)

Aetiology

  • Venous (~70%): chronic venous insufficiency → venous hypertension
  • Arterial (~15%): peripheral arterial disease → ischaemia
  • Mixed (~10–15%): combined venous and arterial disease
  • Other: diabetic (neuropathic), vasculitic, malignant (Marjolin's), pyoderma gangrenosum, calciphylaxis

Pathophysiology

Venous:

  • Incompetent valves → venous reflux → sustained venous hypertension → capillary leak → fibrin cuff deposition → tissue hypoxia → ulceration
  • White cell trapping hypothesis: leucocytes trapped in capillaries → tissue damage

Arterial:

  • Atherosclerotic occlusion → reduced limb perfusion → tissue ischaemia → necrosis → ulceration

Clinical Presentation

Venous Ulcers

  • Location: gaiter area (between ankle and mid-calf), especially medial malleolus
  • Appearance: shallow, irregular, sloping edges; granulating or fibrinous base
  • Surrounding skin: venous eczema, haemosiderin staining (brown), lipodermatosclerosis (inverted champagne bottle), atrophie blanche, varicose veins, oedema
  • Pain: mild–moderate, improved by elevation

Arterial Ulcers

  • Location: distal — toes, dorsum of foot, heel, lateral malleolus; pressure points
  • Appearance: deep, punched-out, well-defined edges; pale/necrotic base
  • Surrounding skin: pale, shiny, hairless; absent/reduced pulses; prolonged capillary refill
  • Pain: severe; worse on elevation, improved by dependency (hanging legs off bed)
  • Claudication/rest pain history

Mixed Ulcers

  • Features of both venous and arterial disease
  • Require modified (reduced) compression

Red Flags

  • Non-healing ulcer >4–6 weeks despite appropriate treatment — biopsy to exclude SCC (Marjolin's ulcer)
  • Rapidly enlarging, undermined edges — consider pyoderma gangrenosum
  • Very painful ulcer with livedo reticularis — consider vasculitis
  • Calciphylaxis in dialysis/CKD patients — extremely painful, rapidly progressive

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Venous ulcerGaiter area, shallow, venous eczemaABPI, USS Doppler
Arterial ulcerDistal, punched-out, ischaemic signsABPI, CT angiography
Diabetic ulcerNeuropathic, painless, pressure pointsMonofilament test, HbA1c
Pyoderma gangrenosumRapidly enlarging, undermined violet edges, pathergyBiopsy, exclude IBD
Marjolin's ulcer (SCC)Non-healing chronic ulcer, raised edgesBiopsy
Vasculitic ulcerPurpura, livedo reticularis, systemic featuresANCA, biopsy

Diagnosis / Investigation

Bedside

  • ABPI (ankle-brachial pressure index): essential before applying compression
    • 0.8: venous — safe for full compression

    • 0.5–0.8: mixed — reduced/modified compression with specialist input
    • <0.5: significant arterial disease — NO compression; vascular referral
    • 1.3: calcified vessels (diabetes, CKD) — unreliable; use alternative assessment

  • Wound assessment: size, depth, base, edges, surrounding skin; photograph and document
  • Monofilament test: diabetic neuropathy assessment

Bloods

  • FBC: anaemia, infection
  • CRP/ESR: infection, inflammation, vasculitis
  • HbA1c: diabetes screen
  • Albumin: nutritional status (hypoalbuminaemia impairs healing)
  • U&Es: renal function
  • Rheumatoid factor, ANA, ANCA: if vasculitic ulcer suspected

Imaging

  • Venous duplex USS: assess venous incompetence — guide intervention
  • Arterial duplex/CT angiography: if ABPI <0.8 — assess for revascularisation

Special Tests

  • Wound swab: only if clinical signs of infection (not routine for colonisation)
  • Biopsy: non-healing ulcer >4–6 weeks — exclude malignancy, vasculitis, atypical infection
  • Patch testing: if suspected contact allergy to dressings/topical preparations

Management

Venous Ulcers

Compression therapy (ABPI >0.8):

  • Multilayer compression bandaging: first-line — aims for 40 mmHg at ankle
  • Compression hosiery (class 3): for prevention of recurrence after healing

Wound care:

  • Simple non-adherent dressings: changed as needed
  • Treat venous eczema: emollients, topical corticosteroids short-term
  • Avoid sensitising topical agents: lanolin, neomycin (high contact allergy rates in leg ulcer patients)

Adjunctive:

  • Pentoxifylline 400 mg TDS: improves venous ulcer healing — NICE recommended
  • Leg elevation above heart level: whenever resting

Surgical:

  • Venous intervention: endovenous ablation, foam sclerotherapy (EVRA trial — early intervention improves healing)
  • Skin grafting: for large, non-healing ulcers

Arterial Ulcers

  • Vascular surgery referral: revascularisation (angioplasty, bypass) is definitive
  • NO compression until arterial disease excluded/treated
  • Risk factor modification: smoking cessation, statin, antiplatelet, BP control
  • Wound care: moist wound healing, debridement, infection management

Mixed Ulcers (ABPI 0.5–0.8)

  • Modified/reduced compression: with specialist supervision
  • Vascular assessment: may benefit from revascularisation

Referral Criteria

  • Tissue viability nurse: all chronic leg ulcers
  • Vascular surgery: ABPI <0.8, arterial ulcer, failed conservative management
  • Dermatology: atypical ulcer, suspected vasculitis/pyoderma gangrenosum, biopsy needed
  • Diabetes team: diabetic foot ulcer

Prognosis

  • Venous ulcers: ~70% heal within 12 weeks with compression; recurrence ~30% within 1 year without compression hosiery
  • EVRA trial: early venous intervention accelerates healing
  • Arterial ulcers: healing dependent on revascularisation; poor prognosis without intervention
  • Marjolin's ulcer: aggressive SCC — 5-year recurrence ~30%, metastasis ~30%
  • Mixed ulcers: slower healing; require balanced approach
  • Prevention of recurrence: lifelong compression hosiery, leg elevation, weight management

Other Relevant Information

Leg Ulcer Comparison

FeatureVenousArterialNeuropathic (Diabetic)
LocationGaiter area, medial malleolusDistal toes, heel, pressurePressure points, sole
PainMild, improved by elevationSevere, improved by dependencyPainless
EdgesIrregular, slopingPunched-outCallused rim
Surrounding skinEczema, pigmentation, LDSPale, shiny, hairlessDry, fissured, neuropathic
PulsesPresentAbsent/reducedMay be present
ABPI>0.8<0.5May be falsely elevated

ABPI Interpretation

ABPIInterpretationAction
>1.3Calcified (unreliable)Use toe pressure/pulse oximetry
0.8–1.3NormalSafe for full compression
0.5–0.8Mixed diseaseReduced compression, vascular review
<0.5Severe arterial diseaseNO compression, urgent vascular referral