Wound Bed Preparation....

Before any kind of wound dressing is applied, the wound should be appropriately prepared to enhance both the effectiveness of the dressing and the self-healing ability of the wound. To achieve optimal healing, wounds must not be infected, they should contain as much vascularized wound bed as possible, and they should be free of exudate.
Wound bed preparation in both acute wounds and chronic wounds is currently a part of the overall wound healing cascade, including (1) local blood coagulation, (2) vascular supply, (3) inflammation, (4) granulation tissue formation and revascularization, (5) epithelialization, (6) wound contraction, and (7) scar formation (see the first and second images below). However, the way of wound bed preparation in acute wounds differs from that of chronic wounds. For example, in acute wounds, debridement is an effective way to remove both damaged tissue and potential bacteria. Once performed, the acute wound should be clean and prepared to heal easily by primary intention. However, in the case of chronic wounds, debridement is usually an ongoing process (see the third image below).
Wound healing phases. Image courtesy of Wikimedia Commons. Wound healing phases. Image courtesy of Wikimedia Commons. Neuropathic heel ulcer. A 68-year-old diabetic female on dialysis presented with a chronic right heel ulcer (3.4 cm X 3.1 cm) of greater than 3 months duration. Photograph of the wound after thorough wound bed preparation over the course of 2 weeks. Image courtesy of Wikimedia Commons. Unlike acute wounds, chronic wounds have what is termed necrotic burden consisting of nonviable tissue and exudate. This is usually a result of many, mostly long-standing local or systemic abnormalities, such as diabetes, arterial or venous insufficiency, and local tissue compression, leading pathogenetically to chronic wounds.
Drs Falanga^[2] , Sibbald, and Harding introduced the concept of wound bed preparation in the late 1990s. Wound bed preparation is defined as the global management of the wound to accelerate endogenous healing or to facilitate the effectiveness of other therapeutic measures, including wound debridement, bacterial balance, and moisture balance. This concept leads to more effective strategies to address the reasons why chronic wounds fail to heal. Wound bed preparation as a strategy allows physicians to break into individual components in various aspects of wound care, while maintaining a global view of what they wish to achieve.
Chronic wounds have always been overshadowed by acute wounds. Scientific breakthroughs and therapeutic measures would generally be developed or envisioned first for wounds caused by trauma, scalpel, or other types of acute injury. For instance, stimulation of reepithelialization by dressings providing moist conditions was first observed experimentally in acute wounds. The acceleration of healing by peptide growth factors was first formally demonstrated in experimental acute wounds in animals. These observations provided proof of principle for the effectiveness of topically applied growth factors, and they led to testing and commercialization of these agents in chronic wounds. Many other examples exist, but the point is that knowledge accumulated about acute injury has been the anchor on which one has relied for developing a therapeutic strategy for chronic wounds.
The common error is to view wound bed preparation as the same as wound debridement. In acute wounds, wound debridement is a good way to remove necrotic tissue and bacteria. This is not the case for chronic wounds, where much more than debridement needs to be addressed for optimal results. Chronic wounds can be intensely inflammatory (eg, venous ulcers) and, thus, produce substantial amounts of exudate that interfere with healing or with the effectiveness of therapeutic products, such as dressings, growth factors, and bioengineered skin substitutes. Therefore, in the context of wound bed preparation, the concerns are not only the removal of actual eschars and frankly nonviable tissue but also the removal of the exudative component.
Another important aspect of chronic wounds, which make them different from acute wounds in the context of wound bed preparation, is the possible need for a maintenance debridement phase. Debridement, whether it is performed by surgical, enzymatic, or autolytic means, is usually considered a procedure or a therapeutic step with defined time frames. This may be true of acute wounds that have become colonized and necrotic and, thus, need to be revitalized. However, with chronic wounds, debridement is generally unable to fully remove the underlying pathogenic abnormalities; necrotic material, nonviable tissue, and exudate (ie, necrotic burden) continue to accumulate.
Within the context of wound bed preparation, the notion of an initial debridement phase followed by a maintenance debridement phase may be adopted. For example, after the initial debridement of chronic wounds, a temporary positive outcome on wound closure may be observed. However, often, a healing arrest occurs, with a return to a poor wound bed. One explanation may be that, because of the underlying and uncorrected pathogenic abnormalities, necrotic tissue and exudate, which now cause the healing arrest, continue to accumulate. Rather than always starting from the beginning, with periodic debridement and exudate control, one might consider a steady state removal of the necrotic burden that should continue throughout the life of the wound.
In the concept of wound bed preparation, the biologic microenvironment of chronic wounds has to be clearly understood. For example, after an appropriate dressing is used, optimal compression therapy for edema control in venous ulcers decreases the amount of exudate and, thus, clears the macromolecules that may be trapping growth factors. Similarly, correction of the bacterial burden decreases the possibility of infection, but it also diminishes the ongoing inflammation that often characterizes many chronic wounds. Some chronic wounds may be "stuck" in one of the phases of the normal healing process, such as the inflammatory or proliferative phase. Eliminating the bacterial burden by the use of debridement, some antibacterial products, or adequate dressings can help this situation.
As another example, appropriate debridement removes tissue and, therefore, cells that have accumulated and are no longer responsive to signals required for optimal wound healing. In this respect, fibroblasts from chronic wounds, including venous and diabetic ulcers, have been shown to become senescent and are unresponsive to certain growth factors. The term cellular burden has been created to describe this phenomenon. When a wound is debrided, this cellular burden is removed and wound responsiveness is restored. In the future, some specially developed chemical or biologic agents will probably help for normalizing such cells rather than removing them.
In aiming at a well-vascularized wound bed, much can be achieved by removing necrotic or fibrinous tissue, by controlling edema, by decreasing bacterial burden, by performing compression therapy (especially for venous ulcers), and by off-loading (in the setting of pressure-induced ulcers). Further improvements in the vascularization of the wound bed can also be achieved by applying growth factors (eg, platelet-derived growth factor [PDGF]), by applying bioengineered skin, or even by using occlusive dressings. Indeed, one of the most important effects of occlusive dressings in chronic wounds, in addition to pain relief and absorption of exudate, may be stimulation of granulation tissue formation. Some growth factors, not yet available commercially, have the potential to greatly stimulate angiogenesis. These agents include fibroblast growth factors (FGFs) and vascular endothelial growth factor (VEGF).
Bioengineered skin and autologous or allogeneic skin can stimulate the formation of granulation tissue and, perhaps indirectly, the process of reepithelialization. Particularly noteworthy is the so-called edge effect (migration of the wound's edge toward the wound's center) after the application of bioengineered skin to previously unresponsive chronic wounds. These clinical effects have been observed with bioengineered skin and with simple keratinocyte sheets. It has been hypothesized that these stimulatory effects are due to the synthesis and the release of certain cytokines by the donor cells. However, the situation is probably highly complex, with cross-talk developing between the donor cells and the recipient resident wound cells. This cross-talk leads not only to the release of cytokines but also to the recruitment of other cell types from surrounding tissue and the circulation, to the formation of new blood vessels, and to the laying down of a more ideal extracellular matrix.
The concept of wound bed preparation can help to recognize that chronic wounds have a complex life of their own and that they are not simply an aberration of the normal healing process. This concept allows examination of the different components that need to be addressed in chronic wounds and development of long-term strategies for the more complex issues that lead to failure to heal.
The authors recommend the daily use of the concept of wound bed preparation, which, together with an appropriately chosen wound dressing or tissue substitute, will lead to more effective treatment of acute and chronic difficult-to-treat wounds. Moreover, this area of wound care is also critical to the assessment and evaluation of any new advanced wound healing technologies.