MedVellum
MedVellum
Back to Library
Vascular Surgery
Dermatology
General Practice

Venous Leg Ulcers

High EvidenceUpdated: 2025-12-24

On This Page

Red Flags

  • Rapidly Expanding Pain (Pyoderma Gangrenosum mimic)
  • Exposed Bone/Tendon (Unusual for VLU -> Suspect Arterial/Malignancy)
  • Marjolin's Ulcer (SCC change in chronic wound -> Biopsy edges)
  • Systemic Sepsis (Admit for IV Abx)
  • Critical Ischaemia (ABPI <0.5 -> Urgent Vascular Referral)
Overview

Venous Leg Ulcers

1. Clinical Overview

Summary

Venous Leg Ulcers (VLU) are the most common cause of lower limb ulceration (70-80%). They result from Chronic Venous Insufficiency (CVI)—sustained ambulatory venous hypertension caused by valvular incompetence (reflux), outflow obstruction (DVT), or calf muscle pump failure. The classic presentation is a shallow, exuding ulcer in the "Gaiter Area" (medial malleolus), surrounded by signs of CVI (haemosiderin, lipodermatosclerosis, varicosities). The Gold Standard treatment is High Compression Therapy (to oppose the hydrostatic pressure) combined with Superficial Venous Ablation (to fix the reflux). Healing is slow (weeks to months), and recurrence is common without lifelong stockings. [1,2]

Key Facts

  • Prevalence: ~1% of the adult population.
  • Mechanism: Ambulatory Venous Hypertension.
  • Classic Site: Medial Gaiter Area (2cm above medial malleolus).
  • Gold Standard Tx: 4-Layer Compression Bandaging (e.g., Profore).
  • Prerequisite: Must confirm adequate arterial supply (ABPI >0.8) before compressing.
  • Key Trial: EVRA Trial (Early Venous Reflux Ablation accelerates healing).
  • Recurrence: 70% if compression stopped.

Clinical Pearls

"It's not just the veins": The lymphatic system is always overwhelmed in severe venous disease ("Phlebolymphedema"). Compression treats both by forcing fluid out of the interstitium.

"Check the ABPI": NEVER apply high compression without checking pulses or ABPI. If the patient has significant arterial disease (ABPI <0.8), high compression will strangle the leg, reduce perfusion pressure below capillary closing pressure, and cause gangrene.

"The Champagne Bottle Leg": In chronic disease, the calf becomes hard and woody (lipodermatosclerosis) and tapers narrowly to the ankle, while the calf muscle remains bulky above. This simulates an inverted champagne bottle.

"Pain Relief": Venous ulcers ARE painful, but the pain is relieved by elevation (draining the pressure). If pain is severe and constant even with elevation, suspect infection, arterial component, or Pyoderma Gangrenosum.

"The Malignant Change": Any ulcer present for >3 months or with raised/rolled edges needs a BIOPSY to exclude Marjolin's Ulcer (Squamous Cell Carcinoma).


2. Epidemiology

Incidence

  • Prevalence: 1% of population; increases to 3% in >80 year olds.
  • Cost: Consumes 2-3% of total healthcare budgets in Western countries (mostly nursing time for dressing changes).
  • Age: Disease of ageing (valve failure) + immobility.

Risk Factors

  • History of DVT: Post-Thrombotic Syndrome (valve destruction). 30% of DVT patients develop CVI.
  • Varicose Veins: Superficial incompetence feeding the gaiter area.
  • Obesity: Increases intra-abdominal pressure.
  • Immobility: "Shuffle walking" inactivates the calf pump.
  • Pregnancy: Valve damage (Progesterone laxity + Uterine compression).
  • Trauma: Minor knock to a congested leg starts the ulcer.

3. Pathophysiology: The Pressure Cooker

The Physiology of Return: The Calf Muscle Pump

Blood must defy gravity (80-100mmHg column) to return to the heart.

  1. The Pump: Calf muscles contract, squeezing deep veins.
  2. The Valves: One-way valves prevent backflow.
  3. The Perforators: Connecting veins that allow flow only from Superficial (Low pressure) -> Deep (High pressure).

The Pathology: Venous Hypertension

When valves fail (reflux) or veins are blocked (DVT):

  • Pressure in the veins at the ankle remains high even when walking (Ambulatory Venous Hypertension).
  • Normally, walking drops venous pressure to ~20mmHg. In CVI, it stays >60-90mmHg.
  • The "blowout" usually happens at Cockett's Perforators (lower calf).

Why does the skin break? (Theories)

  1. Fibrin Cuff Theory: High pressure pushes fibrinogen out of capillaries. It forms a "cuff" around vessels, blocking oxygen diffusion -> Skin hypoxia.
  2. White Cell Trapping: WBCs get stuck in congested capillaries, become activated, and release proteolytic enzymes / free radicals -> Tissue destruction.

4. Clinical Presentation

Ulcer Characteristics

Signs of Chronic Venous Insufficiency

  1. Haemosiderin Deposition: Brown staining. RBCs leak out -> Macrophages eat them -> Iron deposits stay.
  2. Varicose Eczema: Red, scaly, itchy skin (Stasis Dermatitis). Immune reaction to proteins in oedema fluid.
  3. Atrophie Blanche: White, porcelain-like scars with red dots (capillaries). Signs of healed ulcers/infarcts.
  4. Lipodermatosclerosis (LDS): Fibrosis of the subcutaneous fat. The leg feels "woody" and hard. "Champagne Bottle" shape.
  5. Corona Phlebectatica: Fan of small veins at the medial ankle ("Malleolar flare"). Early sign.

Site
Medial Gaiter area (most common). Lateral represents LSV disease or trauma.
Edge
Slopey, shallow, irregular. (Punched out = Arterial. Rolled = Malignant).
Base
Granulating (red) or Sloughy (yellow). Heavy exudate (wet).
Pain
Aching, relieved by elevation. Worse at end of day.
5. Clinical Assessment

The Vascular Exam

  1. Palpate Pulses: DP and PT. If palpable, ABPI is likely >0.8, but measure to be safe.
  2. Trendelenburg Test: Assessing superficial vs deep reflux (largely replaced by Duplex).
  3. Doppler / ABPI: Mandatory.
    • ABPI 0.8 - 1.2: Safe to compress (Standard 40mmHg).
    • ABPI 0.5 - 0.8: Mixed disease. "Reduced Compression" (20mmHg).
    • ABPI <0.5: Critical Ischaemia. Compression CONTRAINDICATED. Urgent referral.
  4. Sensation: Check with 10g monofilament (exclude Neuropathic ulcer).

6. Investigations

Non-Invasive

  • Venous Duplex Ultrasound: The roadmap.
    • Checks Deep System (Patency, Reflux).
    • Checks Superficial System (Long Saphenous / Short Saphenous reflux).
    • Checks Perforators (Incompetent?).
  • Swab: Only if clinical signs of infection (Cellulitis, Pyrexia, Rapid expansion). Bacterial colonisation is normal and does not need antibiotics. "Don't treat the swab, treat the patient."
  • Biopsy: If atypical appearance or non-healing >3 months.

Bloods

  • FBC/CRP: Infection?
  • HbA1c: Diabetes (Mixed ulcer?).
  • Autoimmune: Vasculitis screen if atypical (Rheumatoid factor, ANCA).

7. Management Algorithm
          LEG ULCER PRESENTATION
                   ↓
        CLINICAL ASSESSMENT + ABPI
                   ↓
     ┌─────────────┴───────────────┐
  ABPI &lt;0.8                     ABPI &gt;0.8
(Arterial/Mixed)               (Venous)
     ↓                             ↓
VASCULAR REFERRAL         CLEAN & DRESS (Simple)
(Do not compress)                  ↓
                          COMPRESSION BANDAGING
                          (4-Layer / Hosiery)
                                   ↓
                          REFER FOR VENOUS DUPLEX
                                   ↓
                          EARLY ENDOVENOUS ABLATION
                          (If reflux found - EVRA)

1. Compression Therapy (The Engine)

  • Mechanism: Applies external pressure to vein walls -> Reduces diameter -> Restores valve competence -> Reduces hypertension. Reduces oedema.
  • Gold Standard: 4-Layer Bandaging (e.g., Profore).
    1. Padding (Wool): Protects bony prominences, absorbs exudate.
    2. Crepe: Smooths the layer.
    3. Class 3a Elastic: Provides compression at rest.
    4. Cohesive: Outer layer to hold it all together.
  • Pressure: Generates 40mmHg at ankle, graduating to 20mmHg at calf.
  • Duration: Left on for 1 week.

2. General Measures

  • Elevation: "Toes above nose". Gravity assists drainage.
  • Exercise: Activate calf pump (Tip-toe exercises).
  • Pentoxifylline: Oral drug (400mg TDS). Improves white cell deformability / microcirculation. Modest benefit as adjunct.

3. Surgical Intervention (The EVRA Trial)

  • Principle: If superficial reflux (LSV varicosities / Sapheno-femoral junction) is "feeding" the ulcer, shutting it down reduces pressure.
  • Finding: Early ablation (within 2 weeks) accelerates healing compared to waiting until ulcer heals.
  • Technique: Endovenous Laser (EVLT) or Radiofrequency (RFA) or Foam Sclerotherapy under local anaesthetic.

8. Complications

Non-Healing (Chronic)

  • Ulcer >6 months duration.
  • Consider: Missed arterial disease? Malignancy (Marjolin)? Non-compliance?

Infection

  • Cellulitis: Sepsis, spreading erythema. Needs systemic antibiotics (Flucloxacillin).
  • Biofilm: Sloughy layer preventing healing. Needs debridement.

Contact Dermatitis

  • Allergy to dressing components (Lanolin, Latex, Preservatives).
  • Leg becomes red/itchy UNDER the bandage.

9. Surgical Atlas: Skin Grafting

Sometimes, large venous ulcers are clean but "stuck" (stalled). A skin graft can speed up closure.

  • Pinch Grafting: Small islands of skin taken from thigh (under local) and placed on ulcer.
  • Mesh Grafting: Sheet graft meshed to expand surface area.
  • Pre-requisite: The bed must be granulating and clean (no slough, no infection). Compression MUST continue over the graft.

10. Technical Appendix: ABPI Protocol

The Ankle Brachial Pressure Index.

  • Equipment: Manual sphygmomanometer + Handheld Doppler (8MHz).
  • Steps:
    1. Patient supine for 10 mins.
    2. Measure Brachial SBP in BOTH arms. Take the HIGHEST.
    3. Measure Ankle SBP (Dorsalis Pedis AND Posterior Tibial). Take the HIGHEST for that leg.
    4. Calculation: Highest Ankle / Highest Brachial.
  • Interpretation:
    • >1.2: Calcified/Stiff arteries (Diabetic). Non-compressible. Unreliable.
    • 1.0: Normal.
    • 0.5-0.9: PAD. Reduced compression (check with vascular).
    • <0.5: Critical Limb Ischaemia. Compression CONTRAINDICATED.

11. Technical Appendix: Bandaging Science

Laplace's Law

Pressure = (Tension x Layers x 4630) / (Circumference x Width)

  • Tension: Pull harder = More pressure.
  • Layers: More overlap = More pressure. (Spiral 50% overlap = 2 layers).
  • Circumference: Smaller limb = HIGHER pressure. Beware the bony shin/ankle (high pressure points). Padding increases circumference to lower pressure.
  • Width: Wider bandage = Lower pressure.

12. Evidence and Guidelines

Key Guidelines

  1. NICE CG168: Management of Varicose Veins.
  2. Cochrane Reviews: "Compression increases ulcer healing rates compared with no compression". "Multi-component systems are more effective than single component".

Landmark Trials

  1. EVRA Trial (NEJM 2018):
    • Intervention: Early endovenous ablation (within 2 weeks) vs Deferred/Conservative.
    • Outcome: Time to healing significantly shorter in Early group (median 56 days vs 82 days).
    • Impact: Changed guidelines to recommend immediate referral for Duplex/Surgery for all venous ulcers.
  2. ESCHAR Trial (2007):
    • Surgery + Compression vs Compression alone.
    • Surgery reduced recurrence rates significantly (12% vs 28% at 4 years), but did not speed up initial healing (unlike EVRA).

13. Patient/Layperson Explanation

What is a Venous Ulcer?

The veins in your leg have one-way valves that help blood flow up to the heart. If these valves break (varicose veins) or are blocked (clot), gravity pulls blood down, pooling in your ankle. This high pressure acts like a "water hammer", damaging the skin from the inside out, causing a sore that won't heal.

Why do I need tight bandages?

The ulcer is caused by high pressure in the veins. The only way to lower that pressure is to squeeze the veins from the outside. The bandages act like a second skin, helping your muscles pump blood back up towards your heart. Without compression, the ulcer will not heal. It might feel tight, but it needs to be tight to work.

Will it come back?

Yes, there is a high chance it will come back. To prevent this, once the ulcer is healed, you usually need to wear compression stockings (tight socks) every day for life.

Can surgery help?

Yes. If we find "leaky" veins feeding the ulcer, we can seal them off with a laser treatment. This helps the ulcer heal faster and stay healed longer.


14. Detailed Drug Monographs

Pentoxifylline (Trental)

  • Class: Methylxanthine derivative.
  • Mechanism: Improves red blood cell deformity (makes them squishier), reduces blood viscosity, decreases platelet aggregation.
  • Indication: Venous leg ulcers (Adjunct to compression).
  • Evidence: Cochrane review shows it serves as an effective adjunct to compression.
  • Dose: 400mg TDS.

Potassium Permanganate (KMnO4)

  • Role: Soaks for weeping/infected ulcers.
  • Mechanism: Astringent (dries it out) and Antiseptic.
  • Dose: Dissolve tablet in bucket (Light pink colour). Soak leg for 10-15 mins.
  • Caution: Can stain skin/bath brown. If solution is brown/purple, it is too strong and will burn.
15. Examination Focus (The Viva Vault)

Q1: What are the components of the CEAP classification? A: Clinical (C0-C6), Etiology (Congenital/Primary/Secondary), Anatomy (Superficial/Deep/Perforator), Pathophysiology (Reflux/Obstruction). Venous Ulcer is C6. Healed ulcer is C5.

Q2: What is the significance of the EVRA trial? A: It proved that early superficial venous ablation (within 2 weeks) improves healing time in venous ulcers. Previously surgery was delayed until healing.

Q3: Describe Lipodermatosclerosis. A: Chronic inflammation and fibrosis of the dermis and subcutaneous fat due to venous hypertension. The leg becomes hard, woody, and pigmented, often tapering at the ankle ("Champagne bottle").

Q4: When is compression contraindicated? A: When there is significant arterial disease (ABPI <0.5 is absolute; 0.5-0.8 is relative - reduced compression used). Also in decompensated heart failure (fluid overload shifting to lungs).

16. Rehabilitation Protocol

Phase 1: Active Ulcer

  • Compression bandaging (Changed weekly).
  • Maximize elevation.
  • Nutritional support (Protein, Zinc, Vitamin C).

Phase 2: Healed Ulcer

  • Measurement for Class 2 or 3 Made-to-measure hosiery (RAL standard).
  • Daily skin hygiene (Emollients).
  • Life-long compliance education.
17. Historical Perspectives
  • Hippocrates: Described "fluxes" of humours causing ulcers. Recommended bandaging.
  • Wiseman (1676): Described the "varicous ulcer" and the benefit of a "laced stocking".
  • Unna (1840): Paul Gerson Unna developed "Unna's Boot" (Zinc paste bandage) - still used today for venous eczema/ulcers.

(End of Topic)

Last updated: 2025-12-24

At a Glance

EvidenceHigh
Last Updated2025-12-24

Red Flags

  • Rapidly Expanding Pain (Pyoderma Gangrenosum mimic)
  • Exposed Bone/Tendon (Unusual for VLU -> Suspect Arterial/Malignancy)
  • Marjolin's Ulcer (SCC change in chronic wound -> Biopsy edges)
  • Systemic Sepsis (Admit for IV Abx)
  • Critical Ischaemia (ABPI &lt;0.5 -> Urgent Vascular Referral)

Clinical Pearls

  • **"It's not just the veins"**: The lymphatic system is always overwhelmed in severe venous disease ("Phlebolymphedema"). Compression treats both by forcing fluid out of the interstitium.
  • **"The Malignant Change"**: Any ulcer present for &gt;3 months or with raised/rolled edges needs a BIOPSY to exclude Marjolin's Ulcer (Squamous Cell Carcinoma).
  • Deep (High pressure).
  • Macrophages eat them -
  • Restores valve competence -

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines