VOL: 98, ISSUE: 02, PAGE NO: 55
Mark Collier, BA, RGN, ONC, RCNT, RNT, is nurse consultant/senior lecturer, tissue viability, Thames Valley University, London, and honorary consultant, Hinchinbrooke Healthcare NHS Trust, Cambridgeshire
Moist wound-healing is now accepted by professionals in the majority of health care settings. Both excoriation and maceration 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 depends on the components (toxins) within the fluid and will result in the stripping of the top layers of the epidermis (Collier, 2000). It requires a healing process to correct, whereas 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 prolonged bathing, only requiring the tissues to ‘dry out’ to correct.
Moist wound-healing (Bloom, 1945; Bull et al, 1948; Winter, 1962) and wound-bed preparation (Falanga, 2000) also involve the presence of fluid - this time within the margins of a wound - but the difference is that ensuring the presence of a moist wound-healing environment (through the use of ‘interactive’ wound management materials, for example) should create the ideal environment for wound healing to take place (Turner, 1985). Wound-bed preparation, however, involves practitioners in 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 (Calvin, 1998; Robson et al, 1998), such as growth factors.
Wound bed preparation explained
The aim of wound-bed preparation can be summarised as the active creation of an optimal wound-healing environment through planned interventions in order to maximise the benefits of chosen advanced materials, as it could be argued that it would not be cost-effective or efficacious to use expensive wound management products unless the optimum environment for them to operate in has been previously created or is already present in the wound bed.
Therefore wound-bed preparation should be considered for chronic wounds that are not progressing through a normal wound-healing process (Calvin, 1998; Collier, 1996), with the overall management goal being 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 as a result of an imbalance within ‘systems’ such as cellular alterations - increased enzyme levels or matrixmetalloproteases (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 preparation involves the following:
- The removal of necrotic/fibrinous tissue;
- The control of oedema;
- The achievement of a well-vascularised wound bed;
- The decrease of bacterial burden;
- The minimisation of wound exudates (Collier, 2001; Falanga, 2000).
Removing necrotic/fibrinous tissue
This can be achieved by a variety of practical interventions that should involve various members of the multidisciplinary team.
These include the following:
- Surgical - if this is not being undertaken in an operating theatre the need for the use of local anaesthetic should be considered;
- Autolytic - use of hydrogels (Jones and Milton, 2000a), occlusive (Jones and Milton, 2000b) and semi-occlusive (Jones and Milton, 2000c) wound management products;
- Enzymatic - use of products incorporating streptokinase/streptodornase - for example Varidase and collagenase (Tong, 2000)
- Mechanical - wound-cleansing techniques such as ‘wet to dry’);
- Larvae - commonly referred to as ‘maggot therapy’ (Thomas, 1996).
It has previously been acknowledged that if the debridement process - removal of necrotic/fibrinous tissue - is accelerated, more rapid wound-healing takes place (Steed et al, 1996).
Before considering how to control oedema it is important to assess and identify the cause and nature of any oedema present, while also identifying an appropriate treatment objective, such as ’to reduce the dead space within the tissues of the wound bed/margins. Only after this can suitable medical and wound management interventions be initiated. For example, if what was thought to be oedema is ultimately identified as lymphoedema the use of manual lymph drainage and compression garments would be indicated (Moffatt and Harper, 1997).
As with all planned interventions, it is important to explain the techniques/materials to be used to both patients and their relatives/carers in order to increase concordance.
Achieving a well-vascularised wound bed
The treatment objective underpinning the achievement of a well-vascularised wound bed can be identified as ‘to increase the availability of active cells/growth factors within the wound bed’. 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 by surgical debridement of dry necrotic tissue (eschar). This procedure should only be undertaken in the operating theatre, with the patient anaesthetised, by surgeons;
- Graduated compression therapy - this can be facilitated by the use of short-stretch or multi-layered bandage systems (Morison et al, 1997);
- Topical negative pressure therapy (TNP) - facilitated by the vacuum-assisted wound-closure (VAC) system (Collier, 1997; Baxter and Ballard, 2001);
- The use of appropriate wound management products designed to alter the osmotic pull/capillary permeability (White, 2001).
Decreasing the bacterial burden
Much has been written about how both to define, recognise and manage wound infection (Beldon, 2001; Ayton, 1986). However, more recently a new term has been incorporated into the literature - that of critical colonisation. This term can be used to describe 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 for all practitioners who may be involved with preparing wound beds for healing.
The treatment objective underpinning the interventions that can be considered in order to decrease the bacterial burden present within the chronic wound bed can be identified as preventing colonised wounds from becoming critically colonised, thereby reducing the risk of local/systemic infection. Appropriate interventions would include the following:
- 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 (iodine) has been revisited within the past few years (Gilchrist, 1997) and their use should be considered for wound-bed preparation 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 in wounds (Falanga et al, 1994), and 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, 2000).
Minimising wound exudate
The minimisation of wound exudate 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 (1997) reports that bacterial invasion and impaired healing results from unfilled dead spaces, and cells involved in normal wound-healing require a moist, but not soggy, wound-healing environment (Winter, 1962; Calvin, 1998; Collier, 1996). In addition, should exudate leak from the wound margins on to the surrounding skin both excoriation and maceration may be noted.
In summary, 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), and TNP/VAC therapy and chemotherapy to reduce the patient’s inflammatory response, as it has been widely acknowledged that the majority of chronic wounds are stuck in the late inflammatory phase of wound-healing (Calvin, 1998).
Correcting matrix abnormalities
As has been previously discussed, the chronicity of a wound can be a result of an imbalance within ‘systems’, such as cellular alterations, and in order for these to be corrected it is important that first they must 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 factor (PDGF) applied topically (Falanga, 1999). Additionally it has been demonstrated (Woods, 1997) that accelerated wound-healing follows the topical application of epidermal growth factor (EGF) derived from a patient’s own cultured keratinocytes, delivered in a fluid compress.
However, it is important to remember that to date 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 in the normal wound-healing process see Table 1.
It could be argued that wound-bed preparation is not just moist wound-healing once removed but a concept that all practitioners should become familiar with as their exposure to wounds and their management increases over time. it should not be left to the few nurse specialists in the field. All practitioners who are, or will, become involved in both assessing patients for and initiating techniques relevant to wound-bed preparation should:
- Understand the role of cells in the normal wound-healing process;
- Consider the role of various debridement options, including surgery;
- Consider the evidence for wound-cleansing techniques and solutions used;
- Remember that ‘you should not put in a wound what you would not put in your eye’;
- Remember that most chronic wounds are stuck in the late inflammatory phase of wound-healing and have not progressed to the regenerative phase;
- Consider when cadexomer iodine has its place (absorption of fluid/bacteria);
- Understand the need to manage wound fluid;
- Consider what appropriate interventions may be required - for example, absorbent interactive wound management materials or TNP/VAC therapy.
Only then will wound-bed preparation become a familiar phrase in all health care settings in which wound management techniques are undertaken. It is to be hoped that it will not take as long as the arrival of the concept of moist wound-healing.