Identification and management of biofilm in chronic wounds

Transcription

1 Identification and management of biofilm in chronic wounds Vincent Siaw-Sakyi Evidence suggests that biofilm is present in at least 78% of nonhealing wounds, and it is widely accepted that its presence may be a cause for delayed healing in some patients. As the majority of chronic wounds are managed in a community setting, it is important that clinicians have an understanding of what biofilm is, how to identify its presence in the wound, and how to carry out biofilm-based wound care (BBWC). AQUACEL Ag+ Extra is a unique dressing that has been specifically designed to manage biofilm. It combines antimicrobial and anti-biofilm components, which work in synergy to successfully disrupt biofilm, expose microorganisms to the broadspectrum antimicrobial activity of ionic silver in chronic wounds and to help prevent biofilm re-formation, thus making it worthy of inclusion in the biofilm care pathway. KEYWORDS: Biofilm Antimicrobial agents Chronic wounds AQUACEL Ag+ Extra Hydrofiber Technology Biofilm can simply be described as a community of microorganisms encased in a matrix that provides protection against antimicrobial treatment and the host s immune system. The National Institutes of Health (2002) estimated that more than 80% of human infections involve bacterial biofilm. The role that biofilm plays in delayed wound healing is becoming increasingly recognised and researched. At least 78% of chronic wounds contain biofilm (Malone et al, 2017), and its presence contributes to chronicity (Metcalf and Bowler, 2013). The protection that biofilm gives to the microbial community explains why repeated treatment with antibiotics and antiseptics often fails in some hard-to-heal wounds (Bowler and Parsons, 2016). Vincent Siaw-Sakyi, tissue viability nurse specialist, Kent Community Health NHS Foundation Trust This article describes what biofilm is, how it forms, and the characteristics that gives it protection against host immunity and antimicrobial agents. It presents evidence of its role in wound chronicity, and provides clinical guidance on how to identify and manage wounds with suspected biofilm, using biofilmbased wound care (BBWC). It also gives an overview of AQUACEL Ag+ Extra dressing, an award-winning dressing that helps to disrupt biofilm, kill infection-causing microorganisms and prevent biofilm re-formation (Parsons and Metcalf, 2014; Bowler and Parsons, 2016; Parsons et al, 2016), and presents clinical evidence to support its use in BBWC. MICROORGANISMS IN BIOFILM Planktonic microorganisms are single-celled, free-floating cells that are metabolically active and may multiply rapidly within a wound (Bjarnsholt et al, 2016; Bourdillon, 2016). They are the building blocks of biofilm, forming an initial attachment to the wound bed within minutes, and, in susceptible patients, can multiply and recruit other species of microorganisms to develop into mature biofilm communities. As most antibiotics act on single key components of microbial metabolism (Bowler and Parsons, 2016), the metabolic activity of planktonic microorganisms makes them susceptible to the action of these drugs. The exception to this is in the development of antibioticresistant strains, such as meticillinresistant Staphylococcus aureus (MRSA) or extended spectrum beta-lactamase (ESBL) producing Pseudomonas aeruginosa (Pastar et al, 2013; Bowler, 2018; Percival, 2018). It is now accepted that microorganisms prefer to exist as biofilm on and in the human body, since this provides protection from environmental threats such as the host immune system and antimicrobial agents, i.e. antibiotics and antiseptics (Bowler and Parsons, 2016). BIOFILM CHARACTERISTICS Biofilm microorganisms are contained in a protective matrix of self-produced extracellular polymeric substances (EPS). The EPS consists of a dense matrix of polysaccharides, proteins, lipids and extracellular DNA (of microbial or host origin). It encases the biofilm community and attaches to the wound bed, sometimes below the wound surface (Schultz et al, 2016), protecting the microorganisms 32 JCN 2018, Vol 32, No 5

2 Now it s time to confront the biofilm villain Lt d The dressing that gives you the weapons you need to attack the key local barriers to wound healing. AQUACEL Ag+ Dressing doesn t just manage exudate and infection*1-5. It helps destroy biofilm too*6-8. FI nd ou W *As demonstrated in vitro 1. Newman GR, Walker M, Hobot JA, Bowler PG, Visualisation of bacterial sequestration and bacterial activity within hydrating Hydrober wound dressings. Biomaterials; 27: Walker M, Hobot JA, Newman GR, Bowler PG, Scanning electron microscopic examination of bacterial immobilization in a carboxymethyl cellulose (AQUACEL ) and alginate dressing. Biomaterials; 24: Bowler PG, Jones SA, Davies BJ, Coyle E, Infection control properties of some wound dressings. J. Wound Care; 8: Walker M, Bowler PG, Cochrane CA, In vitro studies to show sequestration of matrix metalloproteinases by silver-containing wound care products. Ostomy/Wound Management. 2007; 53: Assessment of the in vitro Physical Properties of AQUACEL EXTRA, AQUACEL Ag EXTRA and AQUACEL Ag+ EXTRA dressings. Scientific background report. WHRIA3817 TA297, 2013, Data on file, ConvaTec Inc. 6. Antimicrobial activity and prevention of biofilm reformation by AQUACEL Ag+ EXTRA dressing. Scientific Background Report. WHRI3857 MA236, 2013, Data on file, ConvaTec Inc. 7. Antimicrobial activity against CA-MRSA and prevention of biofilm reformation by AQUACEL Ag+ EXTRA dressing. Scientific Background Report. WHRI3875 MA239, 2013, Data on file, ConvaTec Inc. 8. Physical Disruption of Biofilm by AQUACEL Ag+ Wound Dressing. Scientific Background Report. WHRI3850 MA232, 2013, Data on file, ConvaTec Inc. AQUACEL, AQUACEL Extra, ConvaTec, the ConvaTec logo, Hydrofiber and the Hydrofiber logo are trademarks of ConvaTec Inc. All other trademarks are the property of their respective owners ConvaTec Inc. AP GB C FE IN LM C ar e E XU DATE B IO Pe op le Find out more about AQUACEL Ag+ Dressings at T IO N

3 within from attack and destruction by host immune cells, such as neutrophils and macrophages (Hurlow, 2016). The EPS also allows microorganisms to withstand nutrient and moisture deprivation, as well as potentially harmful alterations in ph (Hurlow, 2016). Importantly, the EPS acts as a protective barrier that reduces the effective penetration of antibiotics and antiseptics. It has been estimated that microorganisms in biofilm are 100 1,000 times less susceptible to antimicrobial agents than their planktonic counterparts (Wounds International, 2017). Furthermore, microbial cells in the deeper layers of biofilm function at a slower metabolic rate. This allows them to be more tolerant of antibiotics, which target metabolically active cell sites (Bjarnsholt et al, 2017; Bowler and Parsons, 2016). Microorganisms within biofilm use a process called quorum sensing to communicate with each other, promoting their survival as they are able to respond to environmental changes to thrive and replicate (Figure 1). In biofilm, different microorganisms can group together to form a community. This means biofilm can vary in composition and characteristics, depending on the species involved. Although a wound may contain a biofilm consisting of different microbial species, individual patches of biofilm may contain only one species (Cooper, 2010; Bjarnsholt et al, 2017). Biofilm is not uniformly distributed across a wound bed and may exist in separate colonies. CHRONIC WOUNDS AND BIOFILM Figure 1. Planktonic microorganisms attach to a surface, such as a wound bed, and start to multiply and secrete the surrounding EPS matrix. As biofilm develops and matures, it attaches more firmly to the surface and can shed microorganisms and fragments of biofilm to seed biofilm elsewhere in the wound bed. The studies examined biopsy or debridement tissue from chronic wounds and used microscopy, with or without molecular analysis, to identify the presence of biofilm in a variety of chronic wound types. Six of the nine studies demonstrated biofilm in 100% of wounds examined. It is thought that at least 78% of chronic wounds contain biofilm (Malone et al, 2017), and that its presence contributes to chronicity in some patients. The authors concluded that biofilm was likely to be present in all chronic wounds, with the lower prevalence in three of the studies being a result of methodology when taking the sample, rather than the absence of biofilm (Malone et al, 2017). Biofilm can contribute to delayed wound healing by inducing the production of inflammatory mediators, such as neutrophil enzymes of the innate immune system (Watters et al, 2016), proinflammatory cytokines (Wolcott et al, 2008), and destructive proteases (Schultz et al, 2016). Box 1. DEFINITION OF BIOFILM A structured community of microbes with genetic diversity and variable gene expression (phenotype), which creates behaviours and defences used to produce unique infections (chronic infection) with characteristics of significant tolerance to antibiotics and biocides whilst also being protected from host immunity. (International Wound Infection Institute [IWII], 2016) production of and exposure to wound exudate, which itself may encourage the development of biofilm (Wolcott, 2017). As well as keeping the wound bed stuck in a chronic inflammatory state, the presence of biofilm clearly increases the risk of full-blown clinical infection developing. Several in vivo studies have also demonstrated that the physical presence of biofilm in the wound bed can delay healing by impeding granulation tissue formation and epithelial migration (Metcalf and Bowler, 2013; Bjarnsholt et al, 2017). A meta-analysis of nine studies by Malone et al (2017) determined that 78% of chronic wounds sampled contained biofilm. Prolonged inflammation can result in damage to healthy tissue and lead to increased wound size, as well as skin maceration through prolonged BIOFILM DEVELOPMENT RISK FACTORS Systemic and local wound factors 34 JCN 2018, Vol 32, No 5

4 that can result in delayed healing are well recognised (Bjarnsholt et al, 2017). Systemic factors include comorbidities such as diabetes, venous disease, malnutrition, malignancy and impaired immune response (James et al, 2008). Local factors in the wound bed include the presence of slough and necrotic tissue, wound infection, chronic wound exudate that contains potentially harmful enzymes and microorganisms and the presence of biofilm (Table 1). In some wounds, the presence of biofilm alone will be enough to result in delayed healing, yet in others, healing will eventually occur in the presence of biofilm, if the systemic/local factors delaying healing are addressed (Percival et al, 2015). This demonstrates the unique interaction between the patient and biofilm (World Union of Wound Healing Societies [WUWHS], 2016), and the need to continually review factors contributing to non-healing. Although there is limited information regarding specific risk factors for the development of biofilm, many of the same factors that delay wound healing are also thought to predispose to biofilm formation (Keast et al, 2014; Table 2). IDENTIFYING BIOFILM Recognising wound biofilm in clinical practice remains a challenge. Currently, the only way to detect biofilm involves advanced microscopy with or without molecular analysis in a laboratory setting (Keast et al, 2014). Standard clinical microbiology culturing procedures only detect readily culturable organisms. Tissue biopsy or swabbing may miss the area of biofilm entirely due to its non-uniform distribution in the wound bed (Wysocki and Grinnell, 1990; Keast et al, 2014; Hurlow, 2016). Table 1: Local barriers to wound healing Challenge Exudate Infection Biofilms Explanation Exudate in normal wound healing promotes denaturing of devitalised protein which supports autolysis (Hurlow, 2016). Chronic wound exudate does not have the active growth factors found in acute wound exudate and it can block the healing process, destroy the extracellular matrix (ECM) and become a wounding agent itself (Barrett, 2017). Chronic wound exudate can contribute to the integrity of biofilm (Hurlow and Bowler, 2012; Hurlow, 2016) Wound infection occurs when microorganisms start to increase in numbers and overwhelm the host s immune response. This response may be localised within the wound bed or systemic (IWII, 2016). It has also been suggested that infection is the most frequent complication in non-healing wounds (Gottrup et al, 2013; Barrett, 2017) Biofilm causes a prolonged inflammatory state (Schultz et al, 2016), is a source of infection, and hinders the effect of antimicrobial dressings and antibiotics on the wound bed Table 2: Risk factors for biofilm formation Patient-related Wound-related Environment Arterial disease Lower limb wounds Lifestyle choices Diabetes Sloughy tissue Smoking Venous disease Necrotic tissue Immobility Rheumatoid disease Excess exdate Pressure over bony prominences Immobility Oedema Excessive moisture on the skin Chronic cardiac disease Wound type, size, duration, location Medication Lymphoedema Obesity Renal disease Malnutrition Impaired immune status Surgical wounds healing by secondary intention There is currently debate about the visualisation of biofilm in the wound. Some clinicians claim it can be seen as a shiny, translucent layer on the wound surface that re-forms quickly once removed (Dowd et al, 2011; Wolcott, 2015). Others state that biofilm cannot be seen with the naked eye (WUWHS, 2016). There are indirect indicators for identifying biofilm. Following an algorithm (Figure 2) can help clinicians systematically to assess the potential for the presence of biofilm (Metcalf et al, 2014). It is currently recommended that biofilm should be presumed as a cause of delayed healing in chronic wounds that have not reduced in area >40% (or >50% for diabetic foot ulcers) after four weeks of optimal standard care for the wound type, including management of comorbidities and other factors that may be causing delayed healing (Wounds UK, 2017). If presence of biofilm is suspected, biofilm-based wound care (BBWC) should be implemented. Figures 3 and 4 show wounds that are non-healing, with biofilm suspected as a contributing factor to chronicity. BIOFILM-BASED WOUND CARE Management of a wound with suspected biofilm should aim to disrupt the biofilm, kill microorganisms and reduce the chances of biofilm re-forming (Wounds UK, 2017). BBWC is a term used for optimising several strategies to manage recalcitrant wounds and address factors that contribute to a delay in healing by targeting biofilm. JCN 2018, Vol 32, No 5 35

5 Probably with increasing Figure 2. Clinical algorithm to help identify wound biofilm (Metcalf et al, 2014; adapted from the Journal of Wound Care 2014: 23(3): 137 8, 140 2). This should involve a protocol of care that takes a three-step approach: Assessment Management Monitoring/reassessment. Assessment Full holistic patient and wound assessment should be undertaken to determine any underlying factors that may be contributing to delayed healing. These include diseases, e.g. arterial disease, venous disease, diabetes, autoimmune diseases, such as rheumatoid arthritis or underlying cancers, current and previous medication, lifestyle choices and psychological status. In some patients, removing these barriers may result in healing. Visual indicators 1. Does the surface substance detach easily and atraumatically from the underlying wound bed using physical removal techniques, such as swabs, pads or sharp debridement? 2. Does the surface substance persist despite use of autolytic or enzymatic debridement? 3. Does the surface substance re-form quickly (in 1 2 days) in the absence of frequent intervention (e.g. cleansing, debridement)? Indirect indicators 4. Does the wound respond poorly to topical or systemic antibiotics? 5. Does the wound respond poorly or slowly to dressings that contain antiseptic agents (e.g. silver, iodine, polyhexamethylene biguanide [PHMB]), including products that may reportedly control biofilm in vitro (e.g. cadexomer iodine, nanocrystalline silver, or ionic silver-containing carboxymethyl cellulose dressings)? 6. Does the wound respond favourably to multi-modal strategies, such as physical debridement, cleansing and topical antimicrobial agents and dressings (i.e. BBWC)? Probably host devitalised tissue, Probably planktonic bacteria Underlying comorbidity Healthcare professionals should also examine the wound and record the findings. This should include wound type, location, duration, tissue type present (with percentages of sloughy, necrotic and granulation tissue being recorded), size (length, depth and width), exudate (colour, consistency and volume), odour, and condition of the wound edge (i.e. is there evidence of maceration). It is also important to identify any signs and symptoms of infection or suspected biofilm and to ask about current and previous wound management regimens (e.g. dressings, devices, antimicrobial agents) (Wounds International, 2017). Management Disruption of biofilm can be Figure 3. Surgical wound dehiscence, where biofilm is likely to be present. Sloughy tissue is evident around the wound. Figure 4. A static ulcer of more than six months duration in a patient with diabetes. Photographs used with kind permission from their respective owners achieved by cleansing and debriding the wound. However, biofilm may be tolerant to gentle cleansing, so surgical or sharp debridement or the use of debridement pads or wipes to disrupt the biofilm is recommended. Wound debris, which may contain biofilm fragments and planktonic microorganisms, should be removed from the wound where possible. As biofilm is not evenly distributed on and in the wound bed, regular, multiple attempts may be required to ensure most biofilm is disrupted (Wounds UK, 2017). Biofilm can re-form daily, probably within hours, so regular debridement is key to disrupt and reduce the amount of biofilm present and prevent its re-formation (Metcalf and Bowler, 2013; Hurlow, 2016; Morris et al, 2016; Malone and Swanson, 2017). Currently, debridement every hours is recommended (Wolcott et al, 2010). Following debridement, an appropriate dressing, ideally 36 JCN 2018, Vol 32, No 5

6 Cost burden Among the findings of a seminal study by Guest et al (2015), it was revealed that more than 2.2 million wounds were being treating annually in the UK, equating to 4.5% of the adult population. The total annual cost of managing these wounds and associated comorbidities was estimated to be 5.3 billion, with non- or delayedhealing being a major factor in increasing costs, both in terms of resources used and nursing time. with anti-biofilm and an effective antimicrobial agent which can kill the biofilm and planktonic microorganisms released on disruption should be applied (Wounds UK, 2017). As with all dressing selection, other factors for consideration include the dressing s ability to conform to the wound bed and surrounding skin and manage local wound conditions, such as exudate volume and periwound skin. Monitoring/reassessment It is important to continue to monitor/reassess the wound, and use dressings which maintain a moist wound environment while providing an effective antimicrobial agent until the wound shows signs of wound progression. However, antimicrobial agents should not be used indefinitely (WUWHS, 2008). Wounds should be reassessed at every dressing change for signs of improvement, stasis or deterioration. Action to continue or cease antimicrobial use should be taken according to findings. In wounds where the infection has resolved, the antimicrobial agent can be discontinued. Where the wound has improved but there are also continuing signs of infection, continue treatment with the same or new topical antimicrobial and review again at two weeks (Edwards-Jones et al, 2016). With no improvement or deterioration of the wound, holistic assessment should be repeated and reasons for delayed healing/deterioration identified and addressed where possible. Ongoing assessment provides the opportunity to identify any changes in a patient s wound status, so that these can be managed in a timely manner to prevent further wound deterioration (Brown, 2017; Mahoney, 2017). It is highly unlikely that any protocol of care can eliminate all biofilm, but by carrying out BBWC, antimicrobial agents are able to work more effectively and reduce the bioburden enough to encourage wound healing. Even when the wound appears to be progressing, biofilm may re-form and result in delayed healing in the future, so this should always be considered (Wounds UK, 2017). AQUACEL AG+ EXTRA DRESSING was specifically developed to meet the challenges of slow-healing, static or deteriorating wounds, which are likely to be compromised by biofilm. The dressing contains a unique anti-biofilm formulation that is indicated for moderately to heavily exuding, infected chronic and acute wounds, or wounds at risk of infection. However, AQUACEL Ag+ Extra and Ribbon dressings can also be pre-moistened for use on lower exuding or drier wounds. This method should only be used in the absence of a more suitable dressing for the level of exudate being produced. contains two technologies that work together to manage key local barriers to wound healing (i.e. excess exudate, infection and biofilm), namely: Ag+ Technology Hydrofiber Technology. Ag+ Technology The Ag+ Technology used in has been specifically designed to help disrupt biofilm and prevent its re-formation (Parsons, 2014; Bowler and Parsons, 2016; Parsons et al, 2016). Ag+ Technology has an antibiofilm component that helps disrupt the biofilm structure, assisting the antimicrobial ionic silver (Ag + ) component to work more effectively to target and kill the exposed microorganisms without the need to increase the silver content of the dressing (Parsons et al, 2016; Metcalf et al, 2017). Hydrofiber Technology The Hydrofiber Technology in transforms into a gel on contact with wound exudate. In action, it: Locks in* wound fluid and bacteria to help minimise cross-infection and reduce lateral spread of fluid to help prevent maceration (Bowler et al, 1999; Walker et al, 2003; Newman et al, 2006; Walker et al, 2007; Walker and Parsons; 2010) Micro-contours* and forms an intimate contact with the uneven wound bed, helping to minimise the dead spaces in which microorganisms can grow (Jones et al, 2004; Bowler et al, 2010) Balances* wound fluid, adding and removing moisture to maintain a moist wound healing environment. The cohesive gel helps minimise pain associated with dressing changes (Barnea et al, 2004; Kogan et al, 2004; Foster et al, 2004). Clinical efficacy has facilitated wound healing in a number of real life clinical evaluations, studies and in vivo studies. For example, a real life clinical evaluation of AQUACEL Ag+ dressing was undertaken on 113 cases of challenging, at-risk, Practice point Effective biofilm, infection and exudate management enables wounds to progress to healing in a timely manner (Fletcher, 2013). JCN 2018, Vol 32, No 5 37

7 WOUND CARE A second study looked at the clinical safety and effectiveness of (Metcalf et al, 2017). The dressing was evaluated for a maximum of four weeks in 112 mixed wounds (111 patients), which had been present for an average of 12 months and were thought to be impeded as a result of suspected biofilm or infection. Biofilm was suspected in over half of the wounds (54%). Before the study, while iodine, honey and polyhexamethylene biguanide (PHMB)-containing dressings had been used, silver dressings were the most frequently used, with 16 patients being treated with antibiotics. Following local standards of care but introducing to replace the primary dressing previously used, biofilm suspicion fell from 54% to 27% of wounds. Exudate volume reduced from predominantly high or moderate to low or moderate. e. f. c. d. C ar e b. g. h. W ou nd a. Pe op The patient was admitted to an orthopaedic unit where excision and skin grafts were planned. Moistened AQUACEL Ag+ Extra dressing was used for the first time. After just 18 hours, visible improvement could be seen, with healthier tissue appearing at the wound edges (Figure e). Sharp debridement and moistened was used in a protocol of care for four days (Figure f). The dressing promoted wound progression to the extent that the operation was cancelled and the patient discharged (Figure g). In a protocol of care with debridement, the dressing achieved a positive patient outcome with notable estimated cost-savings (Figure h). Following elevation, moisturisation and compression socks at home, the patient returned to work. Lt d The patient (and author of this case) presented to hospital with an unknown insect bite on the lower left shin, cellulitis and systemic signs of infection (Figure a). Following oral then intravenous (IV) antibiotics, systemic signs resolved and the patient was discharged. Despite no comorbidities, a large blistering wound developed (Figure b). Silver gauze was used in the community, but the wound deteriorated, with slough, poor quality granulation, and necrosis at the margins (Figure c). After three days management with a foam dressing, the wound was painful, necrotic, odorous, oozing pus, with areas of poor quality granulation tissue (Figure d). infected acute and chronic wounds, of which 74% had suspected biofilm (Walker et al, 2015). Local standard protocols of care were followed except for the replacement of the current primary dressing with AQUACEL Ag+ dressing. Following an average treatment period of 4.1 weeks, the majority of wounds had either healed or improved (n=107, 94.7%), providing evidence of the benefits of AQUACEL Ag+ dressings for non-healing, chronic and acute wounds which may be impeded by suspected biofilm. le CASE REPORT ONE a. Spreading cellulitis eight days after an insect bite; b. Extensive blistering day 16; c. After non-antimicrobial gauze, day 19; d. Necrosis requiring (but not receiving) debridement (excision planned); e. 18 hours after pre-moistened AQUACEL Ag+ Extra was applied, day 24; f. facilitating debridement, day 27; g. Rear of leg after final debridement on discharge, day 27; h. Healed wound after elevation, moisturisation and reduced compression, day 38.?? 38 JCN 2018, 2015, Vol 32, 29, No 5 The results of this clinical evaluation provide evidence of the benefits of AQUACEL Ag+ Extra dressing for non-healing chronic and acute wounds that may be impeded by suspected biofilm. Seventy-eight percent of wounds progressed towards healing or went on to heal (65% improved, of which 13% healed), with an average management period of 3.9 weeks. CONCLUSION Chronic wounds pose a challenge to clinicians delivering wound care

8 in the community, and the role of biofilm should be considered in wounds that fail to heal within an expected timeframe despite best practice. For these wounds, BBWC should be implemented. contains two technologies Ag+ Technology and Hydrofiber Technology that work in synergy to help disrupt biofilm, exposing microorganisms to broad-sprectum ionic silver and preventing biofilm re-formation (Parsons et al, 2016). Its successful use in clinical practice makes it an attractive option for the management of biofilm in chronic wounds. JCN * As demonstrated in vitro winner of the World Union of Wound Healing Societies Most Innovative Dressing Award, REFERENCES Barnea Y, Amir A, Leshem D, et al (2004) Clinical comparative study of AQUACEL and paraffin gauze dressing for split-skin donor site treatment. Ann Plast Surg 53(2): Barrett S (2017) Wound-bed preparation: a vital step in the healing process. Br J Nurs 26(12): S24 S31 Bjarnsholt T, Schultz G, Kirketerp-Moller K, et al (2017) The role of biofilms in delayed wound healing. In: World Union of Wound Healing Societies (WUWHS) Florence Congress, Position Document. Management of Biofilm. Wounds International, London Bourdillon K (2016) Dressings and biofilms: interpreting evidence from in vitro biofilm models. Wounds Int 7(1): 9 14 Bowler P, Jones S, Towers V, Booth R, Parsons D, Walker M (2010) Dressing conformability and silver-containing wound dressings. Wounds UK 6: Bowler PG, Parsons D (2016) Combatting wound biofilm and recalcitrance with a novel anti-biofilm Hydrofiber wound dressing. Wound Med 14: 6 11 Brown A (2017) Managing exudate and maceration in venous leg ulceration within the acute health setting. Br J Nurs 26(Sup20): S18 S24 Cooper R (2010) Biofilms and wounds: much ado about nothing? Wounds UK 6(4): Dowd SE, Wolcott RD, Kennedy J, Jones C, Cox SB (2011) Molecular diagnosis and personalised medicine in wound care: assessment of outcomes. J Wound Care 20(5): Edwards-Jones V, Flanagan M, Wolcott RD (2016) Technological advancements in the fight against antimicrobial resistance. Wounds Int 6(2): Available online: www. woundsinternational.com/download/ wint_article/6897 Foster KN, Hermans MHE, Rick C (2004) AQUACEL Ag in the management of partial-thickness burns: results of a clinical trial. J Burn Care Rehabil 25: Fletcher J (2013) TIME for an update? Potential changes to wound assessment. Wounds Int 4: 8 Gottrup F, Apelqvist J, Bjarnsholt T, et al (2013) EWMA Document: antimicrobials and non-healing wounds evidence, controversies and suggestions. J Wound Care 22(5 Suppl): S1 S92 Guest JF, Ayoub N, McIlwraith T, et al (2015) Health economic burden that wounds impose on the National Health Service in the UK. BMJ Open 5: e doi: / bmjopen Hurlow J (2016) Understanding biofilm: what a community nurse should know. Br J Community Nurs 21 Suppl 9: S26 33 Hurlow J, Bowler PG (2012) Potential implications of biofilm in chronic wounds: a case series. J Wound Care 21(3): International Wound Infection Institute (2016) Wound infection in clinical practice. Wounds International, London James GA, Swogger E, Wolcott R, et al (2008) Biofilms in chronic wounds. Wound Repair Regen 16(1): Jones SA, Bowler PG, Walker M, Parsons D (2004) Controlling wound bioburden with a novel silver-containing Hydrofiber dressing. Wound Repair Regen 12(3): Keast D, Swanson T, Carville K, Fletcher J, Schultz J, Black (2014) Ten top tips... Understanding and managing wound biofilm. J Lymphoedema 5(2): 20 4 Kogan L, Modavsky M, Szvalb S, Govrin- Yehudain J (2004) Comparative study of AQUACEL and Silverol treatment in burns. Ann Burns Fire Disasters 17(4): Malone M, Bjarnshold T, McBain AJ, et al (2017) The prevalence of biofilms in chronic wounds: a systematic review and meta-analysis of published data. J Wound Care 28(1): 20 5 Malone M, Swanson T (2017) Biofilmbased wound care: the importance of debridement in biofilm treatment strategies. Br J Community Nurs 22(Suppl 6): S20 S25 Mahoney K (2017) Infection and inflammation: assessment and treatment. Wound Care Today 4(1): 20 7 Having read this article, Revalidation Alert Factors that result in delayed healing The importance of disrupting and preventing biofilm reformation Bowler PG (2018) Antibiotic resistance and biofilm tolerance: a combined threat in the treatment of chronic infections. J Wound Care 27(5): Bowler PG, Jones SA, Davies BJ, Coyle E (1999) Infection control properties of some wound dressings. J Wound Care 8(10): The key benefits of using Aquacel Ag+ Extra dressing to manage hard-to-heal wounds. Then, upload the article to the free JCN revalidation e-portfolio as evidence of your continued learning: JCN 2018, Vol 32, No 5 39

9 Metcalf D, Bowler P (2013) Biofilm delays wound healing: a review of the evidence. Burns Trauma 1(1): 5 12 Metcalf D, Bowler P, Hurlow J (2014) A clinical algorithm for wound biofilm identification. J Wound Care 23(3): Metcalf D, Parsons D, Bowler P (2017) Clinical safety and effectiveness evaluation of a new antimicrobial wound dressing designed to manage exudate, infection and biofilm. Int Wound J 14(1): Morris C, Timmons J, Sykes R (2016) The management of chronic wound biofilm with a monofilament fibre debridement biofilm pathway: results of an audit. Poster presentation. World Union of Wound Healing Societies (WUWHS) conference, Florence, Italy National Institutes of Health (2002) Research on Microbial Biofilms Guidance Report. National Institutes of Health Newman GR, Walker M, Hobot JA, Bowler PG (2006) Visualisation of bacterial sequestration and bacterial activity within hydrating Hydrober wound dressings. Biomaterials 27: Parsons D (2014) Designing a dressing to address local barriers to wound healing. In: Next-generation antimicrobial dressings: AQUACEL Ag+ Extra and Ribbon. Wounds International, London.Available online: www. woundsinternational.com Parsons D, Metcalf D (2014) Understanding local barriers to wound healing. In: Next-generation antimicrobial dressings: AQUACEL Ag+ Extra and Ribbon. Wounds International, London. Available online: www. woundsinternational.com Parsons D, Meredith K, Rowlands VJ, et al (2016) Enhanced performance and mode of action of a novel antibiofilm Hydrofiber wound dressing. BioMed Res Int ID: Pastar I, Nusbaum AG, Gil J, et al (2013) Interactions of methicillin-resistant Staphylococcus aureus and Pseudomonas aeruginosa in polymicrobial wound infection. PLoS ONE 8(2): e56846 Percival SL (2018) Restoring balance: biofilms and wound dressings. J Wound Care 27(2): Percival SL, Vuotto C, Donelli G, Lipsky BA (2015) Biofilms and wounds: an identification algorithm and potential treatment options. Adv Wound Care 4(7): Schultz GS, Bjarnsholt T, Kirketerp- Moller K, Cooper R (2016) Biofilm research: filling in the gaps in knowledge in chronic wounds. In: Position Document. Management of Biofilm. World Union of Wound Healing Societies Congress, Florence Congress Walker M, Hobot J, Newman G (2003) Scanning electron microsopic examination of bacterial immobilization in a carboxymethyl cellulose (AQUACEL ) and alginate dressing. Biomaterials 24: Walker M, Bowler PG, Cochrane CA (2007) In vitro studies to show sequestration of matrix metalloproteinases by silver-containing wound care products. Ostomy/Wound Management 53: Walker M, Parsons D (2010) Hydrofiber technology: its role in exudate management. Clinical review. Wounds UK 6(2): 31 8 Walker M, Metcalf D, Parsons D, Bowler P (2015) A real-life clinical evaluation of a next-generation antimicrobial dressing on acute and chronic wounds. J Wound Care 24(1): Watters C, Fleming D, Bishop D, Rumbaugh KP (2016) Host responses to biofilm. Prog Mol Biol Transl Sci 142: Wolcott R (2015) Disrupting the biofilm matrix improves wound healing outcomes. J Wound Care 24(8): Wolcott RD (2017) Biofilms cause chronic infections. J Wound Care 26(8): Wolcott RD, Rhoads DD, Dowd SE (2008) Biofilms and chronic wound inflammation. J Wound Care 17: Wolcott RD, Rumbaugh KP, James G, et al (2010) Biofilm maturity studies indicate sharp debridement opens a time-dependent therapeutic window. J Wound Care 19(8): World Union of Wound Healing Societies (2008) Principles of best practice: wound infection in clinical practice. An international consensus. MEP, London World Union of Wound Healing Societies KEY POINTS Biofilm has been microscopically observed in 78% of non-healing chronic wounds (Malone et al, 2017). Microorganisms prefer to exist as biofilm, since this provides protection from environmental threats such as the host immune response and antimicrobial agents. The role of biofilm should be considered in wounds that fail to heal within an expected timeframe despite best practice. Management of a wound with suspected biofilm should aim to disrupt and reduce the chances of it re-forming by following a protocol of care involving assessment, management and monitoring/ reassessment. AQUACEL Ag+ Extra dressing was developed to meet the need for an antimicrobial dressing with anti-biofilm activity, and contains two technologies that work synergistically to achieve this, namely Ag+ Technology and Hydrofiber Technology. (2016) Position Document. Management of Biofilm. Wounds International Wounds International (2017) AQUACEL Ag+ Extra Dressing Made Easy. Available online: www. woundsinternational.com/made-easys/ view/aquacel-ag-extra-made-easy (accessed 1 August, 2018) Wounds UK (2017) Best Practice Statement: Making day-to-day management of biofilm simple. Wounds UK, London. Available online: Wysocki AB, Grinnell F (1990) Fibronectin profiles in normal and chronic wound fluid. Lab Invest 63(6): JCN 2018, Vol 32, No 5