Section: Vascular Curriculum: Curriculum, page 54

Definition

  • Area of epidermal loss that has not healed within 6 weeks
    • Ulcer = Persistent discontinuity of the epithelial surface

Incidence

  • 1-2% of the adult population in Western world
  • 3-5% of > 65yo
  • Incidence ↑ with age
  • F > M

Aetiology

  • Lymphovascular (90%)
    • Venous (50-70%)
    • Mixed venous & arterial (10-20%)
    • Arterial (10%)
    • Lymphoedema
    • DM → Microvascular disease (& secondary neuropathy)
  • Blood dyscrasias
    • Thalassemia, Sickle Cell disease, Polycythaemia Rubra Vera
  • Inflammatory
    • Vasculitis – RA/ SLE/ Polyarteritis Nodosa
    • Pyoderma gangrenosum (RA/ UC)
    • Infective: e.g. TB
    • Underlying Osteomyelitis
  • Neoplastic
  • Trauma
    • Obesity / Pressure sores – reduced mobility – won’t use calf muscle pump as much
    • Neuropathic ulcers = 2° to an inadequate sensory nervous system
      • E.g. DM, nerve injuries, leprosy, spinal cord lesions

Clinical

  • History
    • Pain (Lack of = neuropathic)
    • Systemic diseases
    • Hx of trauma
    • Hx of DVT/ varicose vein treatment
    • Mobility
    • Examine arterial system, nervous system & veins
    • Distribution of trophic & ischaemic ulcers may be similar (as the pressure points are same in both – e.g. over heel; distribution dependent on whether pt is bed-bound or ambulant)
  • Arterial ulcers
    • Painful, punched out, often on pressure areas
    • Ischemic ulceration
      • Large vessel disease; atherosclerosis or embolism
      • Small vessel disease: DM, Buerger’s disease, microembolism, pressure necrosis / trauma, Scleroderma, Raynaud’s
  • Venous ulcers
    • 90% - medial aspect of lower third of the leg, above medial malleolus = Gaiter area
    • May not be very painful, especially if chronic
    • Granulation tissue in base, uneven epithelial margins (peripheral healing)
    • Shallow with sloping edge
    • Raised/thickened edge in a chronic venous ulcer should raise the suspicion of malignant change (Marjolin ulcer)
    • Frequently colonized with bacteria, but may not be infected
    • Infection more likely if bacterial load is > 105 organisms/ gram of tissue or if β-haemolytic strep is present at level of 102 organisms/ gram

Pathology

  • Repeated pressure & trauma contribute the cause of both ischaemic & trophic ulcers
  • Microbiology
    • S. aureus (≈ 40%)
    • Pseudomonas Aeruginosa (≈ 25-30%)
  • Of the pts with venous ulceration
    • 50% have reflux in the superficial system alone
    • 38% have reflux in both superficial and deep venous system
    • 10% reflux in the deep system alone

Investigations

  • ABI/arterial studies
  • Test for glucose
  • Vasculitis screen: ESR, CRP, ANA, RhF, ANCAs
  • Consider punch Bx to rule out malignant ulcer / malignant change
  • Culture – Strep Group A, Staph aureus – colonisation common, routine bacterial cultivation not necessary
  • Imaging
    • Arterial system and venous system as indicated

Management

  • Consider all causes of leg ulcer (arterial disease, vasculitis, DM)
    • Stop smoking
  • Chronic venous ulceration
  • Elevation
  • Exercise
  • Dressings
    • Wounds heal 50% faster when moist
    • Occlusive dressing – Hydrocolloid (Duoderm, Comfeel)
      • Change every 5-7 days
      • Forms gelatinous barrier
      • Lower infection rate, equivalent healing time, less pain
      • Non-adherent - reforming epithelium does not get damaged when removed
  • Debridement of necrotic tissue (prevents epithelialization & encourages infection)
  • Infection treatment
    • if appropriate - no evidence for routine ABs
  • Manuka-honey
    • Non-sig improvement
    • Cochrane 2008: no benefit, except in burns?
  • DVT prophylaxis
  • Diuretics
  • Aspirin – evidence inconclusive
  • Diabetic ulcers
    • Hyperbaric oxygen ↓s amputation rates but is expensive
  • For mixed ulcers
    • If ABI > 0.8: Compression bandaging
    • If ABI 0.5 - 0.8: Modified compression ± consider for revascularization if ulcer not healing
    • If ABI < 0.5 → Refer for vascular revascularization surgery (before debriding)

Surgical management of venous disesae

  • Improves ulcer healing and lowers rates of recurrence
  • Goals
    • Definitively treat any refluxing axial veins, associated pathologic perforator veins, or associated varicose veins.
  • Types
    • Superficial axial venous ablation
    • Pathologic perforating veins
      • Mostly teated endovascular now but can use open ligation and subfascial endoscopic perforator ligation
    • Deep venous obstruction or insufficiency
      • Iliocaval venous obstruction 
      • Femoral or infrainguinal obstruction

Prognosis

  • Venous
    • Ulceration: Healing rates 70-80% at 24wks, ≈ 20% resistant
    • 12-month ulcer recurrence rates 30% (though may be up to 70%)
    • Recurrence rates ↓ in pts who have compression + surgery for their veins: At 3 yrs: recurrence rates = 10 vs 40% In those treated with compression alone
  • Risk factors for poor healing
    • Age
    • Ulcer chronicity (> 3 months)
    • Venous refill time ≤ 20s with a below knee tourniquet
    • Smoking
    • Ulcer size

ESCHAR

  • Effect of Surgery and Compression on Healing and Recurrence study by Gohel, BMJ 2007
    • RCT 500 patients with superficial and/or deep reflux and open or recently healed leg ulceration
    • 3 UK centres
    • Compared compression (multi-layered bandage for open ulcer, class 2 elastic stockings for healed) alone with surgery plus compression
    • Showed no difference in ulcer healing at 3 years (89% in compression vs 93% in surgery group)
    • Surgery group have lower recurrence rate at 3 years (31% vs 56%, NNT = 4), with most benefit for superficial and superficial plus deep segmental reflux, but no statistically significant benefit for deep reflux only
    • Ulcer free time to 3 years was significantly longer in surgery group (100 vs 85 weeks)

Dressings

Chemical debridement

  • Iodasrob
    • Good for wet
  • Hydrogel and Intrasite
    • Good for dry