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With the development of new and innovative products for enhancing the healing of chronic wounds, it is becoming increasingly clear that wound management must be optimal. In many ways, the need to take full advantage of advanced technological breakthroughs, i.e., topical growth factors, bioengineered skin, is forcing clinicians to be as good as they can be in managing wounds and getting them ready for these effective treatment modalities. Many of the steps we are now taking to optimize wound care were already known in the past, i.e., the need for wide debridement of diabetic ulcers, use of proper compression in venous ulcers, etc. Therefore, in large part, the progress being achieved consists of greater acceptance of previously known and sound wound care principles. In other cases, for example with the use of certain moist wound dressings, slow release antiseptics, or innovative surgical approaches, we are improving wound care from a more absolute standpoint. Ironically, it seems that the new and innovative products being developed are redefining basic wound care, the very thing they are competing with. Of course, patients are benefiting tremendously from this greater attention to what constitutes proper wound care, which is stimulated by the development of new products.

Optimal Preparation of Wound Bed

This area of wound care, i.e., preparation of the wound bed, is emerging as being critical to our assessment and evaluation of new advanced technologies. There are certain steps that should be adhered to when optimizing the wound bed. Wounds must not be infected, they should have as much as possible a vascularized wound bed, and should be free of exudate. Table 1 is an attempt at categorizing the critical targets in wound bed preparation and possible ways to achieve them. Table 1 has its limitations, but should be viewed as a starting point. The listed clinical targets are some of the critical ones which seem to be essential in the proper preparation of the wound bed. Certainly, the wound bed can improve with compression therapy alone, when the latter is indicated (i.e., in venous ulcers). Also, some clinical targets can be achieved with more than one of the modalities listed in Table 1. For example, debridement can be accomplished by surgical, chemical, and autolytic means. The choice of debridement agents or procedures is often dictated by the clinical circumstances. The use of dressings can be a useful adjunctive approach to debridement, but dressings have yet to show a convincingly major role in chronic wounds. In these wounds occlusive dressings seem to stimulate granulation tissue and, under appropriate circumstances, can lead to autolytic debridement (1).

Very importantly, it should be noted that the elimination of wound exudate is a concept that may be rather obvious but has actually not been properly emphasized. Clinicians often talk about optimizing the wound bed (i.e., granulation tissue, removing callus and fibrinous tissue, etc.) but do not normally incorporate the need to get rid of exudate in their discussion. However, the best looking wound bed will not fare well when also accompanied by moderate or copious amounts of exudate. In that situation, one should abstain from using advanced technological products, such as growth factors or bioengineered skin, until the exudate is controlled. Overall, as one considers other therapeutic options, the goal is to arrive at a stable wound which is characterized by an optimal well-vascularized wound bed and no or minimal exudate. Here are some aspects of wound care which need to be dealt with to achieve that goal.

Removal of necrotic/fibrinous wound tissue: This is a fundamental aspect of wound care. Certainly, it is highly unlikely that a wound will heal when covered by necrotic tissue. Indeed, there is evidence in diabetic ulcers that more aggressive surgical debridement leads to improved results with the use of a topically applied growth factor (PDGF) (2). It is also generally accepted that pressure (decubitus) ulcers need to be extensively debrided and their undermined tissue removed. What is not so clear is how aggressive surgical debridement should be in such wounds as venous ulcers, which are often covered by fibrinous material and which can be intensely fibrotic. The extent of debridement in these ulcers is a matter of some debate. For example, many clinicians feel that venous ulcers do not need to be aggressively debrided surgically. However, it may be that removal of the lipodermatosclerotic tissue is worthwhile in circumstances where there is failure to heal.

Besides surgical debridement, there are enzymatic ways to debride wounds. Collagenase and similar preparations are commonly used, particularly after the surgical removal of extensively necrotic tissue and eschars, which may prove difficult to eliminate by enzymatic means alone. Autolytic debridement can often be effective, particularly with the use of hydrocolloids, although formal studies using debridement as an endpoint have not been done with these occlusive dressings. Cadexomer iodine is proving to be an ideal means to clean up wounds and preparing them properly before the use of grafting or bioengineered skin. This agent combines the properties of slow-release antiseptics with that of being able to absorb substantial amounts of wound exudate. More recently, debridement with larval organisms is making a comeback in some circles.

Edema control: There is little question that edema interferes with the healing process. The reasons for this are unclear, but may represent a combination of impaired blood flow, increased bacterial colonization due to the accumulation of interstitial fluid, and perhaps trapping of growth factors and other key peptides and matrix proteins by the macromolecules which leak from the extravascular space. An interesting hypothesis is that the macromolecules accumulating in the dermis, as a result of venous hypertension for example, trap growth factors and other extracellular matrix material which are essential to the healing process. There is some evidence for this. For example, transforming growth factor-ß1 (TGF-ß1) is often found within the pericapillary fibrin cuffs characteristic of venous ulcers (3).

Clearly, leg elevation and compression therapy (i.e., for venous ulcers) are the main ways to control edema, while diuretics play a minor and more temporary role. Compression pumps can be very useful, especially in the setting of lymphedema. The issue of what constitutes optimal compression therapy is a very important one. Table 2 lists the different ways to achieve compression, categories of bandages, and combination systems. From systematic reviews of the literature, there is increasing evidence that elastic compression therapy, particularly with multilayered bandages, may be superior to other forms of compression bandages. Thus, in a recent analysis of 22 randomized clinical trials, it was found that compression is more effective than no compression alone, that single layer systems are less effective than multi-layered compression systems, and that elastic multi-layered systems are more effective than non-elastic ones (4,5). It should be noted that many different types of multi-layered systems are effective in removing edema, which helps in the preparation of the wound bed. Also, compression bandages help not only in removing edema, but also in stimulating a healthier granulation tissue. This stimulation of granulation tissue may be the result of removal of interstitial fluids or it may be due to other effects of compression on cellular activity which are not fully understood.

Well-vascularized wound bed:

In aiming at a well-vascularized wound bed, much can be achieved by removing necrotic or fibrinous tissue, controlling edema, decreasing bacterial burden, compression therapy (especially for venous ulcers), and off-loading (in the setting of pressure-induced ulcers). Clearly, it is important to note that all of the goals listed in Table 1 are interrelated and that there is substantial overlap among them. Further improvements in the vascularization of the wound bed can also be achieved by the application of growth factors, such as PDGF (2), bioengineered skin (6,7), or even the use of occlusive dressings (1). 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. There are some growth factors, not yet available commercially, which have the potential to greatly stimulate angiogenesis. These agents include fibroblast growth factors (FGFs) as well as vascular endothelial growth factor (VEGF) (8).

Bioengineered skin as well as autologous or allogeneic skin can also stimulate the formation of granulation tissue and, perhaps indirectly, the process of reepithelialization. Particularly noteworthy is the so-called edge effect (migration of the wounds 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 as well as with simple keratinocyte sheets (9). It has been hypothesized that these stimulatory effects are due to the synthesis and 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 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 more ideal extracellular matrix.

Bacterial wound colonization: Chronic wounds are inevitably colonized with bacterial organisms. The contribution bacteria make to the failure to heal remains unclear, but it is generally accepted that bacterial colonization must be brought to a minimum. Early evidence suggesting that high tissue bacterial counts interfered with engraftment has often been extrapolated to wounds in general. However, much more work needs to be done to decipher the significance of high bacterial counts in tissue, their correlation with failure to heal, and the contribution of specific micro-organisms. Also, there is emerging speculation that biofilms develop within chronic wounds and render the eradication of bacterial organisms very difficult with presently available antimicrobial approaches (10).

In simple terms, bacterial colonization can often be dealt with by the fundamental procedure of surgical debridement. In the case of diabetic ulcers, it is now standard therapy to debride the ulcers extensively by removing all of the surrounding callus and basically saucerizing the wound (2). In addition to the beneficial effect on bacterial burden, surgical debridement may have other advantages. Clinicians have often commented that extensive debridement turns a chronic wound into an acute wound. This notion is probably an oversimplification. However, in addition to its beneficial effect on removal of necrotic and infected tissue, it is possible that extensive debridement of ulcers might remove some of the cells that are no longer responsive to growth factors and no longer able to synthesize the right mix of extracellular matrix materials (11).

Some topical therapies are useful in decreasing the bacterial load, in containing wound exudate, and in improving the appearance of the granulation tissue. One way is to apply cadexomer iodine, a slow release iodine releasing agent (12,13). This agent is able to absorb the exudate from the wound and release iodine very slowly into the wound. Thus, cadexomer iodine has antiseptic and antimicrobial properties. Sometimes, after the initial use of this agent and exudate control, one can switch to topical enzymatic debridement for further optimization of the wound bed. In addition to cadexomer iodine, which also has the advantage of absorbing exudate (see below), there are now dressings capable of delivering silver ions as the antiseptic agents. Given the increasing problem of bacterial resistance to traditional antibiotics, it is likely that a number of products capable of delivering antiseptics slowly into wounds will become available. The slow-release feature of these products is a major advantage, for it decreases the chance of cellular and tissue toxicity. As understanding of whether and how biofilms play a role in chronic wounds increases, so will the development of more powerful agents and other approaches to deal with this problem.

Wound exudate:

Over the last several years, evidence has accumulated that wound exudate, particularly that which comes from chronic wounds, has a number of deleterious effects. For example, it was shown that, in contrast with acute wound fluid (14), chronic wound fluid blocks the proliferation and activity of certain cell types, including fibroblasts and keratinocytes (15). Metalloproteinases and other proteases are abundant in chronic wound fluid, and there is evidence that these enzymes can break down extracellular matrix materials as well as growth factors. Therefore, it is surprising that clinicians often talk about proper wound bed preparation without at the same time taking into account wound exudate. It is likely that many clinicians and investigators believe that a good wound bed would not have clinically significant amounts of exudate, but this assumption is probably incorrect. For example, not uncommonly one can achieve what looks like an optimal wound bed while at the same time still having considerable amounts of exudate coming from the wound. This dissociation between wound bed appearance and wound exudate should be recognized because some of the high technology products in use today, whether they be growth factors or bioengineered skin, do not fare well in a wound microenvironment that contains a high amount of exudate. Indeed, a staging system for wound bed preparation which takes into account these two aspects of wound bed preparation, i.e., wound bed appearance and the amount of wound exudate has recently been developed (16). This staging system, shown in Table 3, needs further validation but may be a starting point for judging wound preparedness and for correlating it with the ultimate outcome of complete wound closure.

Optimal ways to deal with wound exudate are evolving. There are direct and indirect ways. Direct ways include the use of compression bandages, or highly absorbent dressings, or mechanical systems (vacuum based). Indirect ways require recognition of what is causing the exudate in the first place. It might be that the wound is heavily colonized with bacteria, which would need correction for the exudate to diminish or to be eliminated. In other cases, a chronic inflammatory process is the cause of the unstable exudative wound. For example, inflammatory ulcers, such as those due to vasculitis, pyoderma gangrenosum, rheumatoid arthritis, may require systemic agents (i.e., prednisone, other immunosuppressive drugs, etc., ) to bring the exudate under control. Overall, it is unlikely that direct ways to control exudate (i.e., absorptive dressings) will be effective used alone when the underlying cause of the exudate has not been addressed.


Technological and laboratory advances in the last two decades have led the way to better and more effective therapeutic approaches. As one uses these new ways of treating difficult to heal wounds, one must also not forget the lessons from the past. Optimization of the wound bed and removal of exudate are ways to improve the efficacy of new therapeutic agents. It is very likely that, over the next several years and because of the need to maximize the efficacy of novel treatment modalities, increased emphasis will be placed on wound bed preparation, which should result in better overall wound care.


  1. Falanga V. Venous ulceration. in Chronic Wound Care: A Clinical Source Book for Health Care Professionals. Editor Diane Krasner and Dean Kane. Health Management Publications, Inc., pp 165-171, 1997.
  2. Steed DL, Donohoe D, Webster MW, et al. Effect of extensive debridement and treatment on the healing of diabetic foot ulcers. J Am Coll Surg 1996; 183:61-64.
  3. Van de Scheur M, Falanga V. Pericapillary fibrin cuffs in venous disease. A reappraisal. Dermatol Surg 23:955-959, 1997.
  4. Fletcher A, Cullum N, Sheldon TA. A systematic review of compression treatment for venous leg ulcers. Br Med J 1997; 315:576-580.
  5. Cullum N, Nelson EA, Fletcher AW, Sheldon TA. Compression bandages and stockings for venous leg ulcers. Cochrane Database Syst Rev 2000; 2:CD000265.
  6. Falanga V, Margolis D, Alvarez O, Auletta M, Maggiacomo F, Altman M, Jensen J, Sabolinski M, Hardin-Young J. Healing of venous ulcers and lack of clinical rejection with an allogeneic cultured human skin equivalent. Arch Dermatol 1998; 134:293-300.
  7. Falanga V, Sabolinski M. A bilayered skin construct (Apligraf) accelerates complete closure of hard-to-heal venous ulcers. Wound Rep Reg 1999; 7:201-207.
  8. Falanga V. Growth Factors. In AThe Foot in Diabetes@. Editors AJM Boulton, H. Connor, and P.R. Cavanough. John Wiley & Sons, UK. 3rd Edition, 2000, pp. 169-178.
  9. Phillips TJ, Gilchrest BA. Clinical application of cultured epithelium. Epithelial Cell Biol 1992; 1:39-46.
  10. Hasan A, Murata H, Falabella A, Ochoa S, Zhou L, Badiavas E, Falanga V. Dermal fibroblasts from venous ulcers are unresponsive to the action of transforming growth factor-ß 1. J Dermatol Sci 1997; 16:59-66.
  11. Falanga V. How to use Apligraf to treat venous ulcers. Skin & Aging 1999; 7:30-36.
  12. Falanga V. Iodine-containing pharmaceuticals: a reappraisal. In Proceedings of the 6th European Conference on Advances in Wound Management. October 1-4, 1996, Amsterdam. Macmillan Magazines Ltd, London, 1997, pp 191-194.
  13. Falanga V. Wound bed preparation for the use of bioengineered skin. Wound Healing Society Meeting, Toronto, Canada, June 6, 2000.
  14. Katz MH, Alvarez AF, Kirsner RS, Eaglstein WH, Falanga V. Human wound fluid from acute wounds stimulates fibroblast and endothelial cell growth. J Am Acad Dermatol 1991; 25:1054-1058.
  • Bucalo B, Eaglstein WH, Falanga V. Inhibition of cell proliferation by chronic wound fluid. Wound Rep Reg 1993; 1:181-186.

    Table 1. Optimal preparation of the wound bed: critical targets and ways to achieve them

    --TARGET-- -------------WAYS TO ACHIEVE TARGET*----------

    + = minimal effect

    ++ = moderate effect

    +++ = maximal effect

    Table 2. Categories of compression therapy and bandages.

    Methods of Compression:

    Graded elastic stockings
    Inelastic paste gauze bandages (traditionally called Unna boot )
    Elastic wraps/bandages
    Pneumatic pumps
    Compression bandages: Applied as as single spiral

    Class 1: retention (i.e., gauze bandage)
    Class 2: support
    Class 3a: light (14-17 mm Hg)
    Class 3b: moderate (18-24 mm Hg)
    Class 3c: high (25-35 mm Hg)
    Class 3d: extra high (up to 60 mm Hg)
    Combination compression systems

    Short stretch inelastic: orthopedic wool, 1-3 rolls of bandage
    Inelastic paste systems: paste bandage, support bandage
    3-layer elastic multi-layer: orthopedic wool, class 3a bandage, tubular bandages
    4-layer elastic multi-layer: orthopedic wool, support, class 3a bandage, cohesive bandage

    Table 3. Staging system for wound preparation.*

    Wound Bed Appearance Score


    A 100% _ _
    B 50-100% + _
    C <50% + _
    D Any amount + +

    Wound Exudate Score

    1. Fully controlled - none or minimal. No absorptive dressings required. If clinically feasible, dressings could stay on for up to a week.

    2. Partially controlled - moderate amount. Dressing changes required every 2 to 3 days.

    3. Uncontrolled - very exudative wound. Absorptive dressings changes required at least daily
    *Staging of the wound is done by combining the score of the wound bed appearance with that of the wound exudate, i.e., A1, B3, etc.
    Staging copyrighted V. Falanga, 2000. Adapted from V. Falanga, Wound Healing Society Meeting, Toronto, June 6, 2000

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