Venous Ulcer - Surgery Case Presentation Guide

1. CASE INTRODUCTION (Opening Statement)

2. HISTORY OF PRESENTING COMPLAINT

• Site: lower leg, medial aspect, around medial malleolus (gaiter region)
• Duration: usually months to years
• Onset: often preceded by minor trauma, itching, or skin changes
• Pain: initially painful, then becomes relatively painless once chronic
• Discharge: seropurulent, occasionally blood-tinged
• History of preceding skin changes: pigmentation, eczema, skin thickening (lipodermatosclerosis)
• H/o varicose veins in the same limb

• Leg heaviness, aching, swelling (especially at end of day)
• Previous episodes of DVT (post-thrombotic syndrome)

3. PAST HISTORY

• Previous DVT or thrombophlebitis
• Varicose vein surgery
• Similar ulcers in the past (recurrence is common)
• H/o hypertension, DM, rheumatoid arthritis (to rule out other causes)

4. SOCIAL/OCCUPATIONAL HISTORY

• Prolonged standing (risk factor for venous hypertension)
• Obesity
• Pregnancy history (in women)
• Mobility status

5. PHYSICAL EXAMINATION

General Examination

• Obesity, oedema of legs, anaemia

Local Examination (most important - follow the surgical ulcer protocol)

• Lower third of the leg, medial aspect, above medial malleolus
• "Gaiter area" - between ankle and calf
• Never above the junction of the middle and upper thirds of the leg
• Never on the upper calf or foot (if so - rethink diagnosis)

• Any shape and size; usually shallow and flat

• Sloping (shelving) edge
• Pale purple-blue in colour
• Thin blue margin of growing epithelium

• Pale, unhealthy granulation tissue
• Covered by slough and exudate
• Seropurulent discharge
• Never penetrates the deep fascia (key differentiator from arterial ulcer)

• Fixed to deeper structures but does NOT involve deep fascia or tendons

• Haemosiderosis - brownish pigmentation from haemosiderin and melanin
• Lipodermatosclerosis (LDS) - fibrosis, thickening, induration of subcutaneous tissue ("inverted champagne bottle" appearance)
• Varicose eczema (venous eczema)
• Scars of previous ulcers

• May or may not be visible proximally

• Inguinal nodes - enlarged only if ulcer is infected

6. DIFFERENTIAL DIAGNOSIS

• Marjolin's ulcer (malignant transformation - raised, everted edge is the warning sign)
• Martorell's ulcer (hypertensive)
• Tropical ulcer
• Syphilitic/tuberculous ulcer

7. INVESTIGATIONS

• ABPI (Ankle-Brachial Pressure Index) using handheld Doppler - most important first investigation
  • Normal: >0.9 (confirms venous, allows full compression)
  • 0.5-0.8: mixed ulcer (modified compression)
  • <0.5: arterial disease - compression contraindicated

• Duplex Doppler ultrasound - assess reflux in superficial and deep veins, confirms venous incompetence, guides treatment. Performed in all new venous ulcer patients by vascular surgeons.

• CBC (anaemia, polycythaemia)
• Blood glucose (DM)
• ESR / CRP (vasculitis, RA)
• Sickle cell test (if appropriate ethnic background)
• Antibody screen (if RA suspected)

• Mandatory if edge appears raised/everted - to rule out Marjolin's ulcer (SCC arising in chronic venous ulcer)

8. MANAGEMENT

Conservative (First-line)

• Clean the ulcer with saline/antiseptic
• Debride slough
• Appropriate primary dressing (the exact dressing matters less than compression)
• Antibiotics only if cellulitis is present (not for wound colonisation)

• Two-layer compression hosiery OR four-layer compression bandaging (most effective)
  • Layer 1: Orthopaedic wool (distributes pressure, absorbs exudate)
  • Layer 2: Cotton crepe (smooths wool, holds it in place)
  • Layer 3: Elastic bandage (~1/3 of total interface pressure)
  • Layer 4: Cohesive bandage (~2/3 of total interface pressure)
• Target interface pressure: 35-40 mmHg for pure venous ulcer
• For mixed ulcer (ABPI 0.5-0.8): modified compression at 30 mmHg

• Reduce oedema and venous hypertension

• Pentoxifylline - increases microvascular perfusion, reduces cytokine-mediated damage; useful adjunct to compression
• Horse chestnut seed extract - improves symptoms, reduces leg volume

Surgical/Interventional

• Treats superficial venous incompetence (great saphenous/small saphenous)
• Methods: endovenous laser ablation (EVLA), radiofrequency ablation (RFA), or open surgery
• Accelerates healing and reduces recurrence - refer to vascular service promptly

• Pinch grafts or split-skin mesh grafting
• Good early healing (50% healed at 5 years)
• Biological dressings (fetal keratinocytes, collagen mesh) - improve healing but not cost-effective for most

Prevention of Recurrence

• Treat superficial incompetence definitively
• Long-term compression stockings (Class II - 23-32 mmHg)
• Avoid prolonged standing
• Weight reduction
• Regular follow-up

9. COMPLICATIONS

• Marjolin's ulcer - squamous cell carcinoma (most feared complication) arising at margin of long-standing venous ulcer; suspected if edge becomes raised, everted, hard, or growth changes
• Secondary bacterial infection / cellulitis
• Chronic osteomyelitis (rare)
• Haemorrhage
• Lipodermatosclerosis
• Recurrence (very common - major problem)

10. PROGNOSIS

• Healing rate with optimal compression: 60-70% at 6 months
• Recurrence rate is high without definitive venous treatment
• Mixed ulcers have lower healing rates
• Long-term recurrence can be reduced significantly with superficial venous ablation + lifelong compression stockings

VIVA TIPS - Likely Questions

1. What is the commonest cause of all leg ulcers? - Venous disease (85%)
2. What is the single most important investigation? - ABPI / Doppler
3. Why is compression the keystone of treatment? - Because the underlying cause is venous hypertension; compression reduces it
4. What is lipodermatosclerosis? - Fibrosis and induration of subcutaneous tissue of the gaiter area from chronic venous hypertension
5. When should you NOT give compression? - ABPI <0.5 or ankle pressure <60 mmHg (severe arterial disease)
6. What is Marjolin's ulcer? - Squamous cell carcinoma arising in a chronic venous ulcer; signs: raised, everted, hard edge
7. Why do venous ulcers NOT occur in the upper limb? - Because ambulatory venous hypertension only affects the lower limb (hydrostatic pressure)
8. Pathophysiology in one sentence? - Chronic ambulatory venous hypertension causes pericapillary fibrin cuffing, leukocyte activation, reactive oxygen species release, and ultimately tissue breakdown
9. What is the CEAP classification? - C0-C6 (C5 = healed venous ulcer, C6 = active venous ulcer)