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Wound care

Wound bed preparation and the diabetic foot

Lynne Watret

ARTICLE POINTS Introduction The philosophy of is now widely accepted as a valuable Patients with 1will often present concept when implementing a wound management treatment plan. Wound with a compromised bed preparation involves identifying individual patient issues, treating healing wound. underlying causes whenever possible, and wound diagnosis. The philosophy also questions the differences between acute and healing, leading to Wound bed a greater understanding of the barriers that may compromise the healing 2preparation using the process. Wound bed preparation, therefore, provides us with a rational TIME acronym can help strategy to plan the care of a patient with a complex wound. plan a rational approach to wound management. raditionally the acute wound The wound bed preparation paradigm healing cascade was used as an ideal has ‘led to independence of chronic TIME stands for: 3Tissue management; Thealing model and the management from models of acute ’ / of this type of wound was transferred to (Falanga, 2003). Surgical of control; Moisture balance the chronic wound. However, the underlying granulating tissue may convert and Edges/epithelial differences between acute and chronic the chronic wound to acute, however, due advancement of the wounds have been given greater credence to compromised healing problems with wound. when underlying patient co-morbidity diabetes, the patient’s wound will still problems have been taken into account present the challenges of a compromised Wound bed (Table 1) as well as individual patient factors healing wound. 4preparation provides that may compromise (Table a framework that can be 2). Furthermore, on analysis of acute and Wound bed preparation understood by taking a chronic wound fluid there are profound in practice – using TIME holistic view of the differences that may promote healing in the In order for a diabetic foot lesion to progress to management of the patient with diabetes acute wound in the ‘healthy individual’ but healing there must be well-vascularised with a foot lesion. may result in imbalance which may result in to provide oxygen and barriers to healing for compromised for the proliferating epidermal cells to patients (Kirstner et al, 2001; Schultz et al migrate and promote wound closure. ‘Wound KEY WORDS 2003; Ayello and Cuddigan, 2004; Keast et bed preparation provides us with a holistic Wound bed al, 2004). The International Working Group structure to plan a rational approach to patient Compromised healing on the Diabetic Foot identified that wound management, whilst within this wound impairment of , abnormalities of framework the introduction of the TIME TIME growth factor production, and an increase acronym focuses assessment and management Infection in the amount of degrading enzymes on the wound bed’ (Watret, 2004). TIME stands Management present all result in a complex biological for Tissue management; Infection/inflammation healing process in the person with diabetes. control; Moisture balance and Edges/epithelial A common feature of the compromised advancement of the wound (Schultz et al, 2003). wound is that it appears to be arrested at the stage of inflammation and granulation Tissue management formation (Moore, 2004). The presence of Each component will have an effect on the slough, and increased bacterial ability of the wound to move forward in the burden further compromise the wound’s healing cascade. If, for example, sloughy ability to heal. Barriers to healing are tissue is the dominant factor (T) then Lynne Watret is a Nurse Tissue therefore preventing the wound healing will be delayed and increased risk of Viability Specialist, Primary Care infection may result unless debridement Division, Greater Glasgow NHS progressing towards epithelialisation in a Trust timely fashion. takes place (Jones et al, 2004). Wet slough

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WOUND BED PREPARATION AND THE DIABETIC FOOT

may result in high levels of and PAGE POINTS Table 2. Individual patient factors odour. Once the dominant factor is that may compromise wound Aggressive surgical addressed and slough removed, the exudate healing 1debridement can be and odour should diminish. Conversely if used as a means to the slough or necrotic tissue is dry, unless it Social isolation/depression accelerate closure of is hydrated to facilitate removal or sharp Low self-esteem diabetic foot ulcers. debridement takes place, the wound will Alcohol misuse not epithelialise due to the splinting effect of Smoking Infection is a major the dessicated tissue (Figure 1). There is also Unemployment/inability to work 2problem in people an increased risk of infection. Poor glycaemic control with diabetes so the In complex wounds it is generally not challenge is prevention possible to remove the underlying cause systemic infection but can prevent or early diagnosis. pathogenic abnormalities and consequently healing progressing. Critical colonisation If the wound necrotic burden continues to accumulate. (Kingsley, 2001) may respond to topical 3becomes critically Aggressive surgical debridement can be antimicrobials that reduce the bacterial colonised it can prevent used as a means to accelerate closure of burden (Jones et al, 2004). The wound may healing progressing. diabetic foot ulcers (Saap and Falanga, then progress to healing. If critical 2002). Regular maintenance debridement colonisation persists in the presence of an The diabetic foot may also be necessary to ensure that a inappropriate host response, clinical 4ulcer tends to be build up of slough does not recur (Ayello infection may result. This situation may polymicrobial and and Cuddigan, 2004). Recurrence of slough occur rapidly in a patient with diabetes and microbial interactions may also indicate poor perfusion to the a clinically effective response to infection is may create a more area and a vascular referral may be of value essential, as infection may be life threatening. favourable environment if this has not already been initiated. The diabetic foot tends to be for anaerobic . polymicrobial in nature. The longer a Anaerobic bacteria Infection/inflammation control wound is in existence the greater the 5and their metabolites Infection (I) is a major problem in patients change in the microbial flora, resulting in a may significantly impair with diabetes. Greater difficulty arises in ‘microbial soup’ of different organism types the normal wound wound diagnosis in that signs and (Bowler et al, 2004). Polymicrobial healing process. symptoms of infection may be absent or interactions may well play a crucial role in reduced in many (Edmonds et al, 2004). wound healing – for example, less invasive The challenge in the diabetic foot is micro-organisms can be synergistic with prevention or early diagnosis of infection more virulent forms (Bowler et al, 2004). A (Table 3). A glossary of associated terms is further example of synergy, cited by Percival provided in Table 4. and Bowler (2004), is that ‘as the aerobic All wounds are colonised with bacteria bacteria grow they consume oxygen and and in a healthy individual this may not result create a more favourable environment for in clinical infection. However, with an anaerobic bacteria’. He also argues that impaired host response infection could ‘some anaerobes may impair the host occur without a significant change to the to improve the survival wound population. If the wound moves from chances for both themselves and other co- colonised to critically colonised it may not habiting organisms’. Wound management strategies often Table 1. Additional underlying overlook the potential role of anaerobic co-morbidity problems that may organisms in chronic wounds, instead compromise healing in a person focusing on aerobic organisms. Anaerobic with diabetes bacteria and their metabolites may interfere with aspects of the wound healing Increasing age process. Unfortunately, identifying Increased anaerobic bacteria to provide meaningful results is not always possible in the clinical Peripheral vascular disease situation (Bowler et al, 2001). Renal disease are being discussed more frequently in chronic wound management

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WOUND BED PREPARATION AND THE DIABETIC FOOT

at low bacterial cell numbers there is a low PAGE POINTS concentration of auto-inducer molecules Bacteria proliferate and the bacteria remain dormant, helping 1forming micro them to evade the . As the colonies that attach to bacterial burden increases, the auto-inducer the wound bed and concentration in the local environment secrete a sugary coating reaches a threshold at which point the (glycocalyx) that protects bacteria are sufficient in numbers to mount them from antimicrobial an attack on the host and switch on key agents and . virulence factors. The key to controlling this virulent attack would be to block the It is often difficult quorum sensing system, thereby tricking the to establish what 2 bacteria into behaving as if they had the causative micro- organisms are. insufficient numbers to successfully mount Figure 1. Slough is a dominant factor an attack. Further research is required in providing a barrier to healing. Management of this area. 3bacterial burden (Percival and Bowler, 2004; Edwards and Despite a greater understanding of the involves wound Harding, 2004). Biofilms occur when potential action of bacteria on wounds, it is irrigation, maintenance bacteria proliferate and form micro often difficult to establish what the causative debridement and use of colonies that become attached to the micro-organisms are and therefore ‘foot topical antimicrobials. wound bed and secrete a sugary coating infection must be diagnosed primarily on (glycocalyx) that protects the micro- clinical grounds’ (Armstrong et al, 1995). If moisture balance is organisms from antimicrobial agents and Management of bacterial burden involves viewed as the 4 antibiotics, which in turn can contribute to wound irrigation (Sibbald et al, 2003), dominant factor in the maintenance debridement (Falanga, 2003) chronic wound due to delayed healing. and use of topical antimicrobials (Edwards excess exudate ‘Biofilms are resistant to antibiotics and Harding, 2004; Murray, 2004; Wright et producation, it should administered orally, intravenously or not result in a topically’ (Wysocki, 2002). al, 1999). Antibiotics continue to be being used simply to required in the presence of clinical infection. absorb excess exudate. This provides a major challenge in the prevention of infection in vulnerable Moisture balance patients. If moisture balance (M) is viewed as the Quorum sensing is a method of dominant factor in the chronic wound due communication used by bacteria that allows to excess exudate production, it should not them to coordinate their group behaviour result in a dressing being used simply to and ‘form a slimy ’ (Wysocki, 2002). absorb excess exudate. We should instead D. McCulloch and N.P. Bannister at the consider asking the question ‘Why is the Smith and Nephew Research Centre wound continuing to exude?’. Exudate in (personal communication, 2004) argue that chronic wound healing is inextricably linked with the presence of slough and bacterial Table 3. Indicators of infection in diabetic foot ulcers (adapted burden. from Edmonds et al, 2004) Gray and White (2004) state that assessment of the wound should involve the wound exudate continuum which takes into Ulcer base yellowish/grey account not only the volume of exudate but Blue discolouration of surrounding tissue the viscosity, which may be an indicator of Fluctuance or crepitus on palpation the presence or absence of infection. Keast Purulent exudate et al (2004) state that the ‘Conversion of Sloughing of ulcer and surrounding tissue exudate to seropurulent and then to Sinuses with undermined or exposed bone purulent drainage suggests bacterial Odour proliferation or progression to wound Wound breakdown infection’. The presence of tracking, with Delayed healing pockets of undermining slough, may be the cause of the continued high level of exudate.

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In this case it may be beneficial to cleanse and prevented from contracting due to a build PAGE POINTS drain the wound with hydrogel or have up of callus or necrotic tissue, and frequent Once the underlying further sharp/surgical debridement. removal by the podiatrist is essential to 1reasons for the Thorough systematic assessment is therefore encourage epithelialisation. Maceration exudate are addressed, required to identify the reason for the around the wound edges may also delay moisture balance may be exudate. Once the underlying reasons are healing and cause further tissue breakdown restored. addressed moisture balance may be restored. due to the destructive components of The same may be said of odour, which chronic wound exudate (Rodgers and Build up of callus or may be masked by the use of a ‘simple’ Watret, 2003). There is therefore a need 2necrotic tissue may charcoal dressing. This will not remove the for the appropriate use of dressings to prevent wound edges from underlying reason for the odour, namely absorb excess exudate whilst preventing contracting and so should presence of sloughy, necrotic tissue, maceration to surrounding tissue. be frequently removed by bacterial burden or need for more frequent a podiatrist to encourage dressing changes due to excess exudate. Conclusion epithelialisation and restoration of the Wound bed preparation provides a barrier. Edges/epithelial advancement framework that may be universally Edges (E) are a particularly important area understood by taking a holistic view of the The use of the wound in the management of the diabetic foot. patient with a compromised healing wound. 3bed paradigm is a ‘There must be a source of viable epidermal The use of the TIME acronym promotes a valuable concept in cells capable of undergoing repeated cycles structured, focused view on the wound within managing the patient of cell division’ (Dodds and Hayes, 2004) to the wound bed preparation framework. The with diabetes with a foot promote epithelialisation and restoration use of the wound bed preparation paradigm is lesion. of the skin barrier (Figure 2). In the diabetic a valuable concept in the management of the foot lesion the wound edges may be patient with diabetes with a foot lesion.

Table 4. Glossary of terms associated with bioburden

Bacterial effect Definition Anaerobic bacteria Wounds with a sufficiently hypoxic environment are susceptible to colonisation with a wide variety of anaerobic bacteria (Bowler, 2001). With good microbial techniques, anaerobes have been isolated in 95 % of diabetic wounds (Gerding, 1995). Colonisation Presence of multiplying bacteria with no overt host response. Continued exposure of devitalised tissue associated with a slowly-healing chronic wound is likely to facilitate the colonisation and establishment of a wide variety of endogenous micro-organisms (Bowler, 2001). Critical colonisation/ Inability of the host to maintain a balance of organisms at the wound bed whereby ‘wound local infection healing may be delayed in the absence of typical clinical features of infection’ (Edwards and Harding, 2004). Infection Overpowering of host response, presence of multiplication and increased virulence of organisms with spreading cellular damage, provoking systemic response. Synergy Interdependent action of bacterial strains that may affect the pathogenicity of the organisms. They have the capacity to have a direct effect on wound healing through the production of destructive enzymes and toxins. Mixed communities of organisms may also indirectly affect healing by promoting a chronic inflammatory state. Biofilm Biofilms occur when bacteria proliferate and form micro colonies that become attached to the wound bed and secrete a sugary coating (glycocalyx), which in turn helps protect the micro-organisms from antimicrobial agents. The presence of channels allows the transfer of nutrients and waste products between colonies. Quorum sensing Production of signaling molecules within a bacterial population that enables bacteria to communicate with each other and initiate a response to their surrounding environment once a critical population density has been reached (Percival and Bowler, 2004). Host response The ability of an individual’s (host) immune response and ability to respond to bacteria during good health. When illness occurs the host response may be impaired (resulting in immunocompetency failure).

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Figure 2. Frequent removal of callus or necrotic tissue by a podiatrist is required to encourage epitelialisation. Armstrong DG, Liswood PL, Todd WF et al (1995) Keast DH, Bowering CK, Evans AW, MacKean GL, of mixed in the diabetic pedal Brrows C, D’Souza L (2004) MEASURE: A proposed wound. A retrospective review of 112 infections. assessment framework for developing best practice Journal American of the Podiatric Medical Association recommendations for . Wound 85: 533–37 Repair and Regeneration 13(3): S1–S17

Ayello EA, Cuddigan JE (2004) Conquer chronic Kingsley A (2001) A proactive approach to wound wounds with wound bed preparation. The Nurse infection. Nursing Standard 15(30): 50–58 Practitioner 29(3): 8–25 Kirster RS, Orsted H, Wright BJ (2001) Matrix Bowler PG, Duerden BI, Armstrong DG (2001) Wound metalloproteinases in normal and impaired wound microbiology and associated approaches to wound healing: a potential role of nanocrystalline silver. management. Clinical Microbiology Reviews 14(2): 244–69 Wounds 13(3): S4–S14

Bowler PG (2003) The 105 bacterial growth guideline: Moore K (2004) compromised wound healing: a reassessing its clinical relevance in wound healing. scientific approach to treatment. In: Trends in Wound Ostomy/wound management 49: 44–53 Care Volume III Quay Books, Salisbury: 132–44

Bowler PG (2004) Management of wound bioburden. Murray F (2004) Can the new generation dressings aid Presentation at: Convatec Tissue Interest Group patient involvement? Diabetic Foot 7(1), Suppl: S2–S6 Symposium, Scotland Percival, S, Bowler P (2004) Understanding the effects of Dodds S, Hayes S (2004) The wound edge epithelialisation bacterial communities and biofilms on wound healing. and monitoring wound healing. A journey through (available at www.worldwidewounds.com, accessed TIME wound bed preparation in practice. British Journal on 20.1.05) of Nursing (Supplement) Sapp LJ, Falanaga V (2002) Debridement performance Edmonds M, Foster AVM, Vowden P (2004) Wound bed index and its correlation with complete closure of preparation for diabetic foot ulcers. European Wound diabetic foot ulcers. Wound Repair and Regeneration Management Association. Position document: Wound 10(6): 354–59 Bed Preparation in Practice. London, MEP Ltd Schultz GS, Sibbald RG, Falanga G (2003) Wound bed Edwards R, Harding KG (2004) Bacteria and wound preparation: a systematic approach to wound healing. Current Opinion in Infectious Diseases 17(2): management. Wound Repair and Regeneration 11: 91–96 (Supp1): S1–S28

Falanga V (2003) Wound bed preparation: future Sibbald RG, Williamson D, Orsted HL, Campbell K, Keast approaches. Ostomy/Wound Management D, Krasner D, Sibbald D (2000) Preparing the wound 49(Supplement 5A): 30–33 bed – debridement, bacterial balance and moisture balance. Ostomy/wound management 46(11): 14–35 Gerding DN (1995) Foot infections in diabetic patients: the role of anaerobes. Clinical Infections Watret L (2004) Wound bed preparation and the and Diseases 20(Suppl 2): S283–88 journey through TIME. Wound bed preparation in practice. British Journal of Nursing Supplement Gray D, White R (2004) The wound exudate continuum: an aid to wound assessment. Applied Wright JB, Lam K, Hansen D, Burrell RE (1999) Efficacy Wound Management Supplement, Wounds UK of topical silver against fungal burn wound . American Journal of Infection Control 27: 344–50 Jones SA, Bowler PG, WalkerM, Parsons D (2004) Controlling wound bioburden with a novel silver- Wysocki A (2002) Evaluating and Managing open skin containing Hydrofiber dressing. Wound Repair and wounds: colonization versus infection. AACN Clinical Regeneration 12: 288–94 Issues 13(3): 382–97

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