Mark Collier, BA (Hons), RN, ONC, RCNT, RNT.
Lead Nurse/Consultant - Tissue Viability, United Lincolnshire Hospital NHS Trust (ULHT), Pilgrim Hospital, Boston, Lincolnshire
Wound-bed management or preparation is a concept that has been introduced to professionals working in wound care in recent years (Collier, 2001; Collier, 2002). It can be argued that wound-bed management is simply overall good wound care (Dowsett, 2002). However, this author believes that it allows the practitioner a focused perspective of the problems associated with chronic wounds, which can ultimately assist in resolving the same, while also keeping in mind the principle of moist wound healing.
Wound-bed management or preparation is a concept that has been introduced to professionals working in wound care in recent years (Collier, 2001; Collier, 2002). It can be argued that wound-bed management is simply overall good wound care (Dowsett, 2002). However, this author believes that it allows the practitioner a focused perspective of the problems associated with chronic wounds, which can ultimately assist in resolving the same, while also keeping in mind the principle of moist wound healing.This Study paper seeks to clarify the meaning of wound-bed management, highlight the rationale underpinning the concept and discuss the clinical relevance of it for all health-care practitioners involved in caring for patients with a variety of wound management needs in the UK.Moist wound healing, a principle which is accepted by health-care professionals in most settings, can be compared with the concept of wound-bed management. This comparison is similar to comparing the concepts of excoriation and maceration.Excoriation and maceration both involve the presence of fluid on the skin over a period of time; however, the effects of that fluid on the skin, in particular surrounding a wound, can be very different. The nature of excoriation is dependent upon the components (toxins) within the fluid and will result in the stripping of the top layers of the epidermis (Collier, 2000) and requires a healing process to correct. Maceration is the softening or sogginess of the tissues due to the retention of ‘excessive’ moisture (Cutting, 1999), which might simply be caused by tap water such as from a prolonged bath, only requiring the tissues to ‘dry out’ to correct.Moist wound healing (Bloom, 1945; Bull et al, 1948; Winter, 1962) and wound-bed management (Falanga, 2000a) both involve the presence of fluid - this time within the margins of a wound. Ensuring the presence of a moist wound-healing environment (through the use of interactive materials for example) should create the ideal environment for wound healing to take place (Turner, 1985). Wound-bed management differs as it involves practitioners taking both decisions and actions, not only to facilitate a moist wound bed, but also to facilitate the presence of components within the moisture which have been reported to have a positive influence on wound healing, such as growth factors (Calvin, 1998; Robson et al, 1998).The normal wound-healing process
The process of normal wound healing is a complex one that involves interacting cells, cytokines/growth factors, carbohydrates and proteins, all of which cascade into and act within the wound margins and across the wound bed at different rates and at different speeds. The process as a whole has been identified as involving three major phases: inflammation, a phase that can be further subdivided into early and late phases, regeneration and maturation (Calvin, 1998).The main cells that are involved in the process of wound healing have been identified as:- Platelets, neutrophils, lymphocytes, macro-phages and epithelial (during inflammation)- Macrophages and fibroblasts (during regeneration and maturation). Fibroblasts are linked with the deposition and regulation of collagen as well as wound contraction (Calvin, 1998).Wound-bed management explained
The aim of wound-bed management can be summarised as the active creation of an optimal wound-healing environment through planned interventions; essentially in order to maximise the benefits of chosen advanced dressing materials. It could be argued that it is not cost effective or efficacious to use expensive wound-management products unless the optimum environment has been created or is already present in the wound bed. In the opinion of this author, wound-bed management should be considered for chronic wounds that are not progressing through a normal wound-healing process (Calvin, 1998; Collier, 1996). The overall management goal is to achieve a stable wound - characterised by a well-vascularised, moist wound bed with minimal ‘excess’ exudate (Falanga et al, 1994). The chronicity of a wound is the result of an imbalance within systems, for example cellular alterations - increased enzyme levels (matrix metalloproteases (MMPs)), a decreased number of available active macrophages and/or a decreased number of active growth factors (Calvin, 1998).It has been previously reported that effective wound-bed management involves the:- Removal of necrotic/fibrinous tissue- Control of oedema- Achievement of a well-vascularised wound bed- Decrease of bacterial burden- Minimisation of wound exudate (Collier, 2002; Falanga, 2000b).Principles for practice
The removal of necrotic/fibrinous tissue - This can be achieved by a variety of practical interventions that should involve various members of the multidisciplinary team. These include:- Surgical: generally acknowledged to be the fastest and most effective way of removing wound debris and necrotic tissue, this is usually under-taken in a hospital setting by a surgeon. If, however, sharp debridement is being carried out in a hospital ward or community environment, the nurses involved should ensure that they have had the appropriate training and are following a local policy or guideline that has been approved. The need to use local anaesthetic should be considered.- Autolytic: Autolysis is a process that occurs naturally to some extent in most wounds. It involves the separation of dead tissue from healthy tissues as a result of macrophage and proteolytic enzyme activity that liquefies dead tissue. A number of modern wound-management products can also assist the autolytic debridement process such as hydrogels (Jones and Milton, 2000a), occlusive (Jones and Milton, 2000b) and semi-occlusive (Jones and Milton, 2000c) materials.- Enzymatic: involves the application to the wound surface of proteolytic and other exogenous enzymes via wound-management materials such as Varidase (incorporates streptokinase and streptodornase) and collagenase (Tong, 2000)- Mechanical: the use of physical force or wound-‘cleansing’ techniques such as ‘wet to dry’ (Tong, 2000) to remove sloughy and necrotic tissue from the wound bed. Generally this technique is observed in use in the USA. Recent guidelines from the National Institute for Clinical Excellence (NICE) do not recommend this technique, primarily because of the associated pain reported by patients at the time of dressing changes (NICE, 2001; Collier and Hollinworth, 2000)- Larval: the use and value of Lucilia sericata larvae (the greenbottle fly) commonly referred to as ‘maggot therapy’ has been widely recognised and reported (Dowsett, 2002; Thomas, 1996). One of the main roles of the nurse before undertaking this form of treatment is to ensure that the patient has given informed consent, as well as to ensure that all other nurses involved with the care of the patient have the required knowledge and skills to perform the technique and are comfortable in facilitating the recommended treatment.Previous research recognises that if the debridement process - removal of necrotic/fibrinous tissue - is accelerated, more rapid wound healing takes place (Steed et al, 1996).The control of oedema
Before considering how to control oedema, it is first important to assess and identify its cause and nature. Appropriate treatment objectives must also be identified, such as ‘To reduce the dead space within the tissues of the wound bed/margins.’ Only after this can suitable medical (drugs) and wound-management interventions (absorbent wound dressing products) be initiated. For example: if what was thought to be oedema is ultimately identified as lymphoedema, then the use of manual lymph drainage (MLD) and compression garments would be indicated (Moffatt and Harper, 1997). As with all planned interventions, the techniques/ materials to be used to both the patient and his or her relatives/carers (health education/promotion) should be explained in order to increase compliance.Achievement of a well-vascularised wound bed
The treatment objective underpinning this can be identified as: ‘To increase the availability of active cells/growth factors within the wound bed.’ In summary, the techniques that can be considered for improving the blood supply to the chronic wound bed are as follows:- Surgical debridement: fresh bleeding within the wound margin can be initiated due to the surgical debridement of dry necrotic tissue (eschar). This should only be done in the operating theatre (patient anaesthetised) by surgeons- Graduated compression therapy: can be facilitated by the use of short-stretch or multi-layered bandage systems (for the management of patients with venous leg ulceration) (Morison et al, 1997)- Topical negative pressure (TNP) therapy: facilitated by the vacuum-assisted wound closure system (VAC) (Collier, 1997; Baxter and Ballard, 2001)- The use of appropriate wound management products designed to alter the osmotic pull/capillary permeability (White, 2001).Decrease bacterial burden
Much has been written recently and in the past about how to define, recognise and manage wound infection (Beldon, 2001; Ayton, 1986); however, more recently, a new term is being incorporated into the literature, that of critical colonisation. This describes wounds that are moving between the spectrums of colonisation and local infection. It has been suggested that, during critical colonisation, subtle clinical signs of infection such as increasing pain/tenderness, increasing serous exudate and friable granulation tissue may be present before the classical signs of surrounding erythema, increased temperature, pain and swelling, pus production and associated odour (Cutting and Harding, 1994).It could therefore be argued that critical colonisation, as a concept, has a particular relevance to all practitioners who may be involved with preparing the wound bed for healing.The treatment objective underpinning the interventions with the aim of decreasing the bacterial burden present within the chronic wound bed can be identified as: ‘To prevent colonised wounds from becoming critically colonised; thereby reducing the risk of local/systemic infection.’ Appropriate interventions would include:- Surgical debridement- Use of appropriate ‘interactive’ wound management materials- Use of TPN (VAC therapy)- Use of antimicrobials such as cadexomer iodine and silver sulphadiazine.The role of antimicrobials (such as iodine) has been revisited within the past few years (Gilchrist, 1997) and, in the opinion of this author, their use should be considered for wound-bed management in order to manage critical colonisation.Animal studies involving cadexomer iodine in 1994 highlighted a marked decrease in the presence of methicillin-resistant Staphylococcus aureus (MRSA) within wounds (Falanga et al, 1994).In 1995 Schmidt demonstrated that the presence of cadexomer iodine helped to positively modulate the wound environment (Schmidt et al, 1995). In addition, other clinical studies have demonstrated that cadexomer iodine successfully cleared pseudomonas (Danielson et al, 1996), is not harmful to tissues within chronic non-healing wounds (Gruber et al, 1975) and has been reported as assisting with the control of excess exudate production (Falanga, 2000a).The minimisation of wound exudate
This is an important issue when preparing wound beds for healing, as an excessive amount of fluid within the wound margins will create a ‘dead’ space. Stotts reports that bacterial invasion and impaired healing results from unfilled dead spaces (Stotts, 1997) and cells involved in normal wound healing require a moist, not soggy, wound-healing environment (Winter, 1962; Calvin, 1998; Collier, 1996). In addition, should exudate leak from the wound margins onto the surrounding skin then both excoriation (Collier, 2000) and maceration (Cutting, 1999) may be noted - the effects of which have been explained previously. To summarise, an appropriate treatment objective could be identified as: ‘To achieve an optimal moist wound-healing environment - not too wet, not too dry - and reduce the risks of complications on the surrounding skin.’ This can be achieved by the use of:- Appropriate absorbent wound management materials- Graduated compression therapy once the patient’s arterial status has been assessed (Moffatt and Harper, 1997)- TNP (VAC therapy) and chemotherapy to reduce the patient’s inflammatory response, as it has been acknowledged that most chronic wounds are stuck in the late inflammatory phase of healing (Calvin, 1998).The correction of matrix abnormalities
As has been previously discussed, the chronicity of a wound can be as a result of an imbalance within systems such as cellular alterations, and in order for these to be corrected they need to be assessed.If any deficiency is identified or suspected then there is some evidence to indicate that the correction of matrix abnormalities can be assisted by the use of growth factors such as platelet-derived growth actor (PDGF) applied topically (Falanga, 1999).Wood et al have demonstrated accelerated wound healing following the topical application of epidermal growth factor (EGF) derived from a patient’s own cultured keratinocytes, delivered in a fluid compress (Wood et al, 1997). Additionally, studies involving a combination of collagen and oxidised regenerated cellulose (ORC) in a freeze-dried dressing form have indicated both an increase in the presence and improved utilisation of growth factors within the wound margins (Johnson & Johnson, 2000).To date, however, it is important to remember that clinical investigations in relation to wound healing have concentrated on a limited range of growth factors. In addition to EGF and PDGF these have included basic fibroblast growth factor (bFGF) and transforming growth factor-beta2 (TGF-b2).For a brief review of the role of these growth factors within the normal wound healing process, see Table 1.Conclusion
This paper has sought to explain wound-bed management. It highlights associated relevant principles for practice and identifies some of the techniques that can be used to achieve desired treatment objectives, with the rationale underpinning them explained.It could be argued that wound-bed management is not just moist wound healing once removed, but a concept with which all practitioners should become familiar as their exposure to wounds and wound management increases over time. Practitioners should not leave it to the few nurse specialists in the field. Only then will wound-bed management become a familiar phrase heard in all health-care settings where patients with wounds are cared for.- This is the final in a series of articles based on presentations at the Professional Nurse Wound Healing Masterclass events 2002.ACTIVITY 1
Before reading the main body of this text, write down the terms you would use to describe the process of normal wound healing to a colleague and briefly highlight the nature and role of growth factors actively linked with this process (15 to 20 minutes).ACTIVITY 2
Read the following article, which highlights in detail the process of wound healing and the role of both cells and growth factors associated with the ‘normal’ process (30 minutes):Kingsley, A. (2002) Wound healing and potential therapeutic options. Professional Nurse 17: 9, 539-544.ACTIVITY 3
Write down all the debridement techniques that you have used recently and identify the rationale that underpinned your decision at the time (20-30 minutes).ACTIVITY 4
Now that you have completed reading this article, write down the terms you would now use to describe the process of normal wound healing to a colleague and highlight the nature and role of growth factors actively linked with this process. Compare your answers with those you gave in response to the first Activity (20 minutes).Discuss any differences you may have noted between your answers with a colleague and discuss how your future practice may be altered in the light of any new knowledge (15 to 20 minutes).Key points
All practitioners involved in wound-bed management should:- Understand the role of cells within the normal wound-healing process- Consider the role of various debridement options- Consider the evidence for wound-cleansing techniques and solutions used: ‘do not put in a wound what you would not put in your eye’ (Falanga, 2000b)- Remember that most chronic wounds are stuck in the late inflammatory phase of wound healing and have not progressed to the regenerative phase- Consider the place of cadexomer iodine (for the absorption of fluid/bacteria)- Understand the need to manage wound fluid using absorbent interactive wound management materials/TNP (VAC therapy).- This educational hand-out can be photocopied and used in teaching sessions on this subject.
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