Technology and product reviews


T E C H N O L O G Y U P D A T E : The role of ALLEVYNTM


Ag in the management of hard-to-heal wounds


Hard-to-heal wounds are challenging to treat and have a significant impact on a patient’s quality of life and healthcare resources [1,2,3]


. For clinicians,


hard-to-heal wounds pose the dual challenge of providing cost-effective management, while improving patients’ wellbeing and concordance with treatment [1,4,5]


Author: John Lantis, Patricia Price . This paper examines the impact of hard-to-heal wounds on


patients and reviews the clinical efficiency and cost-effectiveness of a topical antibacterial dressing containing silver sulfadiazine (ALLEVYNTM


Ag, Smith & Nephew) in the management of patients with infected hard-to-heal wounds.


INTRODUCTION The prevalence and costs of chronic wounds is increasing globally. This is reflected in the incidence of venous leg ulcers, which affect approximately 1% of the population worldwide[6]


year in the US alone[7] of closure by 24 weeks[12] . Others have shown


wound closure rates of 30–35% in ‘visually clean’ venous leg ulcers at 12 weeks using a standard care regimen[13,14,15]


and up to 2.5 million patients per . Pressure ulcers have an


overall prevalence rate of around 10%, although this is often higher in individual facilities[8]


. The References


1. Edwards H, Courtney M, Finlayson K, et al. Chronic venous leg ulcers: effect of a community nursing


intervention on pain and healing. Nurs Stand 2005; 19(52): 47–54.


2. Kotz P, Fisher J, McCluskey P, et al. Use of a new silver barrier dressing, ALLEVYN AgTM in exuding chronic wounds. Int Wound J 2009; 6(3): 186–94.


3. Persoon A, Heinen MM, van der


Vleuten CJ, et al. Leg ulcers: a review of their impact on daily life. J Clin Nurs 2004; 13(3): 341–54.


4. Jordan JL, Ellis SJ, Chambers R. Defining shared decision making


and concordance: are they one and the same? Postgrad Med J 2002; 78 (921): 383–4.


5. Price PE. Education, psychology


and ‘compliance’. Diabetes Metab Res Rev 2008; 24(Suppl 1): S101–5.


number of diabetic foot ulcers is expected to reach some 380 million by 2025, representing 7.1% of the adult population worldwide (www. idf.org). Venous leg ulcers alone typically consume 1–3% of healthcare budgets[9]


.


DEFINING HARD-TO-HEAL WOUNDS In the majority of cases, wounds close following a predictable sequence of overlapping stages[6]


. However, in some


wounds, despite the best efforts of clinicians using standard therapies, closure is prolonged or never achieved[6]


. The challenge for clinicians


is to predict when a wound is likely to become hard to heal. Typically investigators have defined hard-to- heal ulcers as wounds that have[10,11]


:


n Been present for over 12 months n A bioburden of more than 105 n A wound area of more than 10cm2 A review by Margolis et al[12]


venous leg ulcer larger than 10cm2


cfu/g .


identified that a and more


than 12 months old has only a 22% chance 29 Wounds International Vol 2 | Issue 4 | ©Wounds International 2011 . , while marginally


improved closure rates of 55% at 12 weeks have been achieved where active therapy has been used[13]


There is a lot of data to show that older


ulcers are more difficult to heal. There may be multiple reasons for this and the full picture is not clear, but as a consequence costs will be greater[16]


. Such low rates of closure place a premium


on: n Reducing bioburden[6,17] n Effective debridement[18] n Optimising the wound environment for closure [19]


.


These must all be achieved while maintaining adequate pain control[20] White and Cutting[21]


. state that bioburden


in a wound may be one of the most important barriers to wound closure. Bioburden refers to the bacterial load present on the surface of the wound or in the tissue. It is thought that the higher the load, the greater the risk of infection or delayed closure[22]


. The bacterial diversity


and density may also play a role in the delayed closure process[23]


bacteria linked to closure outcomes (including Pseudomonas aeruginosa, Staphylococcus aureus and β-haemolytic Streptococcus)[23]


.


The presence of biofilms in the wound bed has been suggested as a major contributory


, with the presence of specific


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