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Wound Bed Preparation and the Diabetic Foot

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Wound Bed Preparation and the Diabetic Foot DF81pg18,20,22,24,26 2/24/05 6:21 PM Page 1 Wound care Wound bed preparation and the diabetic foot Lynne Watret ARTICLE POINTS Introduction The philosophy of wound bed preparation is now widely accepted as a valuable Patients with diabetes 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 chronic wound 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 wounds from models of acute injury’ Infection/inflammation of this type of wound was transferred to (Falanga, 2003). Surgical debridement 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 wound healing (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 granulation tissue to provide oxygen and barriers to healing for compromised nutrients 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 neutrophils, 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, necrosis 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 18 The Diabetic Foot Vol 8 No 1 2005 DF81pg18,20,22,24,26 2/24/05 6:21 PM Page 2 WOUND BED PREPARATION AND THE DIABETIC FOOT may result in high levels of exudate 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 G Social isolation/depression accelerate closure of is hydrated to facilitate removal or sharp G Low self-esteem diabetic foot ulcers. debridement takes place, the wound will G Alcohol misuse not epithelialise due to the splinting effect of G Smoking Infection is a major the dessicated tissue (Figure 1). There is also G Unemployment/inability to work 2problem in people an increased risk of infection. G 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 ulcer tends to be for anaerobic bacteria. 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 immune response 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 G Increasing age process. Unfortunately, identifying G Increased obesity anaerobic bacteria to provide meaningful G Cardiovascular disease results is not always possible in the clinical G Peripheral vascular disease situation (Bowler et al, 2001). G Renal disease Biofilms are being discussed more frequently in chronic wound management 20 The Diabetic Foot Vol 8 No 1 2005 DF81pg18,20,22,24,26 2/24/05 6:21 PM Page 3 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 immune system. 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 antibiotics. 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).
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