Leg Ulcer Assessment & Treatment

Dr Mary Costello PhD, RANP Tissue Viability and Lymphoedema Care, RNP, FFNMRCSI

Leg Ulcer Assessment in practice

This Clinical Focus  is presented by Dr Mary Costello. Mary is recognised as one of the foremost expert practitioners in Tissue Viability & Wound Care actively practicing in Ireland.  Mary began her wound-care career in 2010 as a community based TVN in the Midlands of Ireland.  On completion of an audit at this time it was evident that 84% of all wounds treated by Public Health Nurses were Lower Limb Ulcerations.  It also highlighted the fact that only 14% of Venous Leg Ulcers (VLU) were being actively managed through the application of compressions bandaging.  Following the completion of this audit Mary played a key role in the establishment of 6 Nurse led Leg Ulcer Clinics and the development of a team of 16 CRGNs who expanded their scope of practice to include Doppler and Clinical Assessment of clients with Lower Limb Ulceration.

  As a result of her practice Mary realised that there was an absence of referral pathways for a particular patient group within the clients being treated for lower limb ulceration within the health service.  These were clients with Lower Limb Lymphoedema, both primary and non cancer related secondary lymphoedema.  Inn 2013 Mary completed an MScN in Advanced Practice through the RCSI the focus of which was a systematic  review of the Role of Manual Lymph Drainage (MLD) in the treatment of Lymphoedema and subsequently became a certified MLD Therapist establishing a Lymphoedema Clinic in the midlands in 2015. 


In 2015 Mary became a PhD scholar and completing her research and graduating in 2019 and subsequently publishing her research ‘Exploring the experience of patients with primary and secondary, non cancer related lymphoedema during intensive and maintenance phases of Complex Decongestive Therapy and its’ impact on their lives’ in 2021.

Mary continues to play a key role in the provision of the Nurse Lead Assessment & Care of Lower Limb Oedema and Ulcer Service in the Midlands from a Clinical, Education and Service Development perspective ensuring patient access to immediate assessment and care as well as referral to specialised services and therapy pathways



A venous leg ulcer (VLU) is an open skin wound, or lesion, and that shows little progress towards healing within 4-6 weeks of when it initially occurred. Venous leg ulcers usually occur between the ankle and the knee (medial side of the lower leg) and are the most common type of chronic lower limb wound.

Venous ulcers arise from venous valve incompetence and calf muscle pump insufficiency which leads to venous stasis and hypertension. This results in microcirculatory changes and localised
tissue ischaemia.11,12

Venous ulceration is the most common type of leg ulceration. 60 to 80% of leg ulcers have
a venous component.1-7

A UK study comprising 600 patients with leg ulceration found that 76% of ulcerated legs had evidence of venous disease and 22% had evidence of arterial disease. Ten to 20% of cases had both arterial and venous insufficiency.  9% of ulcerated legs were in patients with rheumatoid arthritis. 5% of the patient group had diabetes.8

Chronic venous leg ulceration has an estimated prevalence of between 0.1% and 0.3% in the
United Kingdom.1-6,9 Prevalence increases with age.8 Approximately 1% of the population will
suffer from leg ulceration at some point in their lives.9

The natural history of the disease is of a continuous cycle of healing and breakdown over decades and chronic venous leg ulcers are associated with considerable morbidity and impaired quality of life.10 Leg ulcers in patients from the most deprived communities (social classes IV and V) take longer to heal and are more likely to be recurrent.11

Average Time to Healing – 5.9 Months for VLUs, 7.4 months for mixed aetiology ulcers.  In the community 45% of VLUs have a 6 month healing rate.  Specialist Clinics show a 45 to 70% heal rate at 6 months for VLUs.  Recurrence rates are relatively high with 26 to 69% 12 month recurrence rate. (Callum et al 2001)


Leg ulcer treatment pathway developed by Atkin and Tickle (2016)

60 to 80% of Leg Ulcers have a venous component

Timely & Efficient Assessment of Lower Limb Oedema and or Ulceration is vital in identifying the most appropriate Therapy Pathway and Treatment

Pathophysiology of Venous Ulceration

VLU’s are due to increased pressure within the veins of the lower leg caused by chronic venous insufficiency, occurring as a result of damage to the valves in the leg e.g. varicose veins or venous thrombosis.

Venous ulceration is the culmination of a cascade of complex cellular and humeral events that are magnified by genetic predisposition and initiated by venous hypertension. This concept highlights two connected but distinct aspects of venous ulcer pathophysiology—an open wound leading to chronicity and pathologic hemodynamics. Hemodynamic abnormalities are essential features of primary and secondary chronic venous diseases (CVD). Reflux in deep veins can be present in both of these.

A number of theories have been proposed to explain the development of venous ulcers. In reality, these theories are of historical interest only, because venous ulceration is a complex cascade of events initiated by venous hypertension.

Pathophysiology of Peripheral Vascular Disease & Underlying Venous Reflux

the Stages of Peripheral Vascular Disease

T.W.A. - Holistic Assessment

How to acurately measure a wound.

Wait! ..... We don't start with the wound?

The simple answer is…. No! 

By starting our assessment only looking at the wound in isolation we miss the opportunity to identify factors external to the wound and sometimes indeed the patient that may impede healing and possibly undermine the specific wound management strategies derived from our wound assessment.

We may also lose the opportunity to integrate ‘Supporting Actions’ into our overall care plan such as Nutritional support that can have a significant impact in improving and supporting the healing process.

Therefore inline with a holistic ethos we take time at the very beginning to identify factors from an Environmental/Social and Patient perspective that may negatively impact or retard the healing process and/or may require additional interventions to reduce their negative impact on wound healing or enhance and support the healing process.



“Underestimating the impact of Environmental or Systemic Factors on wound healing will often lead to an undermining of good Wound Care Practice and ultimately lead to a less than positive experience for both the Patient and Wound Care Practitioner”


Three Levels Of Assessment

Environment & Social

Here we look at factors external to the patient that may have an impact wound healing or the provision of optimal wound care. These may include:

  1. Where is care being provided – Hospital/Community
  2. Specialised Service Requirements
  3. Availability of Services / Materials
  4. Care Provider –
    • Professional(Nurse)
    •  Carer (Relative or HCA)
    • Self Caring


Here we look to gain an overview of the patient’s medical condition, including some baseline data on the wound. This should include Type/Diagnosis, Aetiology, Location, Duration and Current Status of the wound along with other systemic factors that may influence or impede healing.

  1. Age, Lifestyle & Psychological Status.
  2. Comorbidities; Diabetes, Coronary Vascular (CV) Disease, Circulatory disorders, malignancy
  3. Medications – Corticosteroids, Anticoagulants, Immunosuppressants etc
  4. Infection – Systemic or Localised
  5. Reduced Oxygenation & Tissue Perfusion
  6. Dietary & Hydration Status
  7. Pain Generalised or Specific to wound


The Wound is Assessed from the inside outwards.

  1. Wound Bed Assessment
  2. Wound Edge Assessment
  3. Peri-Wound Skin Assessment

Prior to assessing each of the wound tissue areas we must take some baseline data with regards to size, so a measurement of the Length ( Head to Foot direction), Width (From either L-R or R-L Lateral position), Depth can be measured using an appropriate wound probe.

CLick on the icon below to view brief video on proper wound measurement.





Focused Lower Limb Assessment

Lower Leg Changes Associated with Venous Hypertension

Changes associated with Lower leg Venous Hypertension are progressive and can be numerous and include the following.

  • Spider & Reticular Veins
  • Varicose
  • Oedema
  • Ankle Flare
  • Hyperpigmentation
  • Lipodermatosclerosis
  • Atrophie Blanche
  • Varicose Eczema
  • Hyperkeratosis  
Ankle Flare
Atrophie Blanche

Treatment Goals

Treatment of Venous Leg Ulceration will include both Symptomatic Relief and the address of the underlying causative factors.

  • Heal any active wound
  • Control of Chronic Venous Insufficiency and related skin changes.
  • Reduce oedema
  • Control symptoms
  • Address and or reduce the impact of any comorbidities
  • Encourage compliance with care and prevent recurrence.



Skin Care

Ulcerated Area

In order to maintain overall skin integrity of the ulcerated limb it is important that the clinician should ensure good skin and ulcer hygiene.

  • Cleanse the leg with a pH appropriate skin cleanser.
  • Showing in potable water
  • Washing the leg in a dedicated lined bucket of potable water.
  • Wiping the leg with a moist single use cloth.

(International Consensus document Defying hard to heal wounds with an early anti-biofilm intervention strategy: wound hygiene. JWC 2020)

Surrounding Skin

  • Peri Ulcer should be treated with an Emollient.
  • Consider a topical barrier preparation to protect from exudate.
  • Consider the following treatments for Varicose Eczema:
    • Topical Corticosteroids
    • Zinc Impregnated Bandages.


Hyperkeratosis refers to the increased thickness of the stratum corneum, the outer layer of the skin. Stratum corneum is composed of multiple layers of keratinocyte bodies that, during maturation, produced keratin and subsequently have lost their nucleus and cytoplasmic organelles.

It is essential that Hyperkeratosis is addressed with the gentle and gradual removal of the plaque build up down to the healthy skin beneath.  

Failure to do so may lead to traumatic dislodgement of thick plaques damaging the fragile epidermis beneath potentially causing further ulceration or extension of ulceration if already present. 

Treatment of Hyperkeratosis

  • Continuous moistening with Skin Conditioning Creams and Emollients.
  •  Creams containing 10% Urea (Eucerin) is beneficial.
  • Cleansing with Monofilament Pad (Debrisoft Pads) can aid in the gentle dislodgement of Hyperkeratotic Plaques.

Medicated Paste Bandages

Zinc Paste Bandages 


  • Oil based prep. Will Also assist removal of scale and seal in topical steroid.

Zinc Paste and Ichthammol – Ichthopaste

  • Useful for the treatment of irritated varicose eczema


  • Water based and provides decreased risk of allergy.
NOTE: Patch Test for at least 24 hours prior to applying in full.
Sensitivity may occur over time

Leg Ulcer Wound Bed Priorities

The Principles and approach to the Assessment and identification of Wound Bed Priorities for 'VLUs' are the same as for general wound assessment


Management Priorities

Treatment Option Examples

Tissue Type



Remove devitalised tissue and encourage proliferation of granulation tissue.

Debridement of devitalised tissue through Active Wound Cleansing, Autolytic Debridement or Sharp Debridement



Protect new Granulation & Epithelial Tissue and encourage angiogenesis and new tissue growth.

Encourage pinpoint bleeding of granulation tissue during wound cleansing.

Light Honey Dressing, Hydrocolloid



Rehydrate the wound bed.

Heavy Honey Dressing, Hydrogel

Reassess the suitability of the primary dressing and dressing frequency.




Appropriate management of wound exudate

Hydrofibre, Lite Foam

Foam Dressing

Superabsorbent Dressing


Clinical Signs of Infection

Proactive Management of WOund Bioburden and the prevention of Critical colonisation of the wound bed.

Implement ‘Wound Hygiene’ process from the start of treatment replacing Saline with a non-cytotoxic antiseptic wound cleansing solution (eg Microdacyn60)

Click here to view the ‘Wound Hygiene’ consensus document

Control of CVI and Oedema

Compression bandaging is the Gold Standard for the treatment of venous ulceration and the reversal of Venous Hypertension.

However there are challenges to the provision of compression therapy and a UK Based study showed that only 20% of patients with VLU’s received compression bandaging. (Petherick et al. 2013)

Furthermore it has been shown in France that  only 10.8% of GP’s followed the guidelines for VLU Management. (McGuckin & Kerstin, 1998)

Both present a strong case for the further development of Nurse Lead Early Intervention Community Based Leg Ulcer Clinics.

Compression - Mode Of Action.

(R) Without Compression (L) With Graduated Compression

Graduated Compression is clinically proven to be the most important factor when managin Chronic Venous Insufficiency, 40mmHg (at the ankle) is the widely accepted therapeutic ressure to heal aVLU (ABPI >0.8)

For Patients wit an ABPI 0.6 to 0.8 reduced compression applying 20mmHg at the ankle is recommended.

4main factorsaffect the effectiveness of the applied compression –

  • Bandage Tension
  • Limb Shape
  • Application Skill
  • Patient mobility
  • Patient Compliance with therapy.

Functions Of Compression Bandaging

External application of compression bandages impact the haemodynamic and lymphatic functions of the lower limb.

  •  Reduces vein diameter – improves valve function
  • Reduces Venous Reflux – Increases blood flow and venous return
  • Reduces Oedema – improves the reabsorption of interstitial fluid
  • Significantly improves the venous pump (Foot Pump) – Calf Muscles & Foot
  • Accelerates Blood Flow – Reduces risk of stasis
  • Improves Lymphatic function – Reduces Oedema
  • Improves skin condition – Reduces friability & risk of ulceration.

Types of Compression Bandaging.

Long Stretch Bandages (LSB)

Short Stretch Bandages (SSB)

Bandages (MLB)

  • Elastic –
  • Maintain pressure even when patient is at rest.
  • Low SSI <10
  • Particularly indicated for immobile patients as @Squeezes the leg.
Examples – Profore – Graduated Compression
  • Inelastic
  • Pressure rapidly dissipates
  • High SSI>10.
  • Dependent on calf muscle activity pressing against the bandage

Examples – Coban / Actico / Unna-boot / Coflex –

Low resting pressure/High working pressure

  • Original compression bandage system
  • Uses a combination of elastic and inelastic bandages
  • Maintains a medium resting pressure.
  • Gives a sustained graduated compression for up to 7 days
  • Required use skill and experience to apply correctly.
Examples – KTwo

Consideration When Selecting Compression Therapy

ABPI Results and Interpretation.

  • Training and competency of practitioners
  • Patient Mobility
  • Patient experiences
  • Patient Compliance & Education
  • Pain and Tolerance
  • Availability of bandaging systems
  • Employment and ability to attend clinic appointments
Special Precautions
  • Heart Failure
  • Diabetes & Peripheral neuropathy
  • Arterial insufficiency is a contraindication for the use of compression except in a modified form under specialist supervision.
  • The level of arterial insufficiency will determine the level of compression.
Doppler Assessment of ABPI
Promoting Patient Compliance Via Education
Interpretation of ABPI Values
Toe Pressure Assessment

Challenges For The Future

How Do We Increase Awarenes of VLU Treatment

  • Education –
    •  Patient
    • Family
    • Carers
    • Professionals
    • Nurses
    • Gp’s
  • Appropriate timing of referral
  • Equality of Assessment
  • Equality of access & availability of service
  • The further development of Nurse Lead specialist leg ulcer clinics.

Venous Leg Ulcer Product Focus

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Useful Documents

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Reference List

1. Baker SR, Stacey MC, Jopp-McKay AG, Hoskin SE, Thompson PJ. Epidemiology of chronic venous ulcers. Br J Surg 1991;78(7):864-7.

2. Baker SR, Stacey MC, Singh G, Hoskin SE, Thompson PJ. Aetiology of chronic leg ulcers. Eur J Vasc Surg 1992;6(3):245-51.

3. Callam MJ, Ruckley CV, Harper DR, Dale JJ. Chronic ulceration of the leg: extent of the problem and provision of care. Br Med J (Clin Res Ed) 1985;290(6485):1855-66.

4. Cornwall JV, Dore CJ, Lewis JD. Leg ulcers: epidemiology and aetiology. Br J Surg 1986;73(9):693-6.

5. Nelzen O, Bergqvist D, Lindhagen A. Leg ulcer etiology – a cross sectional population study. J Vasc Surg 1991;14(4):557-64.

6. Nelzen O, Bergqvist D, Lindhagen A. Venous and non-venous leg ulcers: clinical history and appearance in a population study. Br J
Surg 1994;81(2):182-7.

7. Nelzen O, Bergqvist D, Lindhagen A, Hallbook T. Chronic leg ulcers: an underestimated problem in primary health care among elderly patients. J Epidemiol Community Health 1991;45(3):184-7.

8. Callam MJ, Harper DR, Dale JJ, Ruckley CV. Chronic ulcer of the leg: clinical history. Br Med J (Clin Res Ed) 1987;294(6584):1389-91.

9. Callam. Prevalence of chronic leg ulceration and severe chronic venous disease in western countries. Phlebology 1992;7(Suppl1):6-12.

10. Persoon A, Heinen MM, van der Vleuten CJ, de Rooij MJ, van de Kerkhof PC, van Achterberg T. Leg ulcers: a review of their impact on daily life. J Clin Nurs 2004;13(3):341-54.

11. Callam MJ, Harper DR, Dale JJ, Ruckley CV. Chronic leg ulceration: socio-economic aspects. Scott Med J 1988;33(6):358-60.