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Pearls for Practice: Advancing the Science of Wound Bed Preparation for Chronic Wounds

  Wound healing is the result of dynamic interactive processes that begin at the moment of wounding and involve soluble mediators, many cell types, and extracellular matrices.1 When a wound proceeds through an orderly and timely reparative process and results in a sustained restoration of anatomic and functional integrity, it has been labeled an acute wound.2 Conversely, a chronic wound is one that has failed to proceed through an orderly and timely process to produce anatomic and functional integrity or has proceeded through the repair process without establishing a sustained anatomic and functional result. Therefore, it is important to understand the various events involved in wound healing in order to select the most appropriate wound treatment.3   Wound bed preparation is the management of a wound in order to accelerate endogenous healing or to facilitate the effectiveness of other therapeutic measures.3 The concept of wound bed preparation has evolved to provide a systematic approach to removing the barriers to natural wound healing and enhancing the effects of wound therapies.4 Dowsett and Ayello5 applied the acronym TIME — tissue (nonviable or deficient), infection/inflammation, moisture (imbalance), and edge (nonadvancing or undermined) — as a simple way to assess the wound and the state of wound bed preparation. Spruce6 suggested in a series of cases that the hydroconductive dressing Drawtex (SteadMed Medical LLC, Ft. Worth, TX), could be used effectively within the wound bed preparation framework.

  To be effective in wound bed preparation, a product would have to facilitate debridement of necrotic tissue and debris, decrease excessive wound exudate, decrease the tissue bacterial level, remove deleterious chemical mediators, and set the stage for acceleration of endogenous healing or wound closure by wound approximation, skin graft, or pedicle flap. Recently, data have been reported demonstrating that using Drawtex for wound treatment can accomplish each of the requirements for effective wound bed preparation.7

  Removal of necrotic tissue, debris, and slough from the wound is the first step of wound bed preparation. This can be accomplished in multiple ways including surgical, enzymatic, mechanical, biological, and autolytic debridement.8 Dressings act by providing either mechanical or autolytic debridement or a combination of the two. Wolvos9 demonstrated the ability of Drawtex to remove necrotic debris and slough from chronic wounds using digital wound bed analyses (iCLR technology, powered by Elixr, Imago Care Ltd, England). The average area of necrotic tissue, debris, and slough removed in a series of patients was 36% in 1 week, 52% by week 2, and 77% in 3 weeks. In a series of eight patients with Buruli ulcers of the lower extremity, Treadwell and Macdonald10 reported removal of necrotic tissue with the use of Drawtex dressings and compression.

  Excessive exudate impedes healing and must be decreased for effective wound bed preparation. Wolvos9 reported that Drawtex can remove up to 150 cc/hour of wound exudate. Wolcott and Cox11 reported the advantages of the exudate removal by hydroconductive dressings were several-fold. Not only was the fluid removed, but also nutrients in the exudate that facilitate biofilm production are drawn off. Concomitant with the exudate removal, periwound maceration decreased.

  A high tissue bacterial bioburden has been associated with a failure of wound healing.12 The level of tissue bacterial bioburden that inhibits healing has been shown in multiple studies12,13 to be >105 or at least 1 × 106 bacteria per gram of tissue. Such high levels of tissue bacteria can be present without clinical signs of infection and when present can deleteriously affect wound healing.14 Attempts to control the tissue bacterial bioburden have been difficult. Systemically administered antibiotics do not effectively decrease the level of bacteria in a chronic granulating wound15; topical antimicrobials or antiseptics have been used, but many have cytotoxic effects on the wound.16

  Drawtex can effectively draw bacteria from wound tissue into its fibers. Ortiz et al17 demonstrated both in in vitro and in vivo models that Drawtex can draw methicillin-resistant Staphylococcus aureus (MRSA) from either an inoculated broth or an experimental burn wound eschar. Ochs et al18 reported similar results in patients with chronic wounds; tissue biopsy bacterial counts decreased from 106 to 102 CFUs per gram of tissue while at the same time the bacterial counts in the Drawtex dressings increased up to 104 CFUs.

  Chronic wounds have excessive inflammation, increased pro-inflammatory cytokines, increased proteases such as matrix metallo-proteinases (MMPs), and decreased growth factors.19-21 Removing or decreasing the deleterious cytokines is an important aspect of wound bed preparation. Wendelken et al22 demonstrated that Drawtex could draw MMP-9 from chronic wounds and transport the cytokine for a distance up to 7 cm from the wound. Such an effective transport away from the wound allows the wound to proceed to healing without the deterrent of MMP-9. Ochs et al18 showed that both MMP-9 and MMP-1 were drawn out of chronic wounds dressed with Drawtex. They showed a decrease in tissue levels of the MMPs and a concomitant rise in the MMPs in the Drawtex dressings used to treat the wounds.

  Although exact correlations with each aspect of wound bed preparation and spontaneous wound healing or wound closure by surgical means are difficult to document, data are available regarding the ability of a wound to heal once the bacterial bioburden is controlled. Establishing bacterial balance in a chronic wound by decreasing the tissue bacterial level to 105 or fewer CFUs per gram of tissue has been demonstrated to accelerate healing by secondary intention.23 Similarly, wound closure by wound approximation, skin grafting, or pedicle flap has been demonstrated to be successful only when bacterial counts were at 105 or fewer CFUs per gram of tissue.24-26 The fact that Drawtex has been demonstrated to decrease the wound bacterial bioburden suggests its ability to improve wound bed preparation should result in improved healing outcomes. The data reviewed here help explain the beneficial effects seen in the healing of wounds treated with this hydroconductive dressing.6,9,10,11,22

 Pearls for Practice is made possible through the support of SteadMed Medical, LLC, Fort Worth, TX (www.steadmed.com). The opinions anmd statements of the clinicians providing Pearls for Practice are specific to the respective authors and not necessarily those of SteadMed Medical, LLC, OWM, or HMP Communications.

This article was not subject to the Ostomy Wound Management peer-review process.

1. Robson MC, Steed DL, Franz MG. Wound healing: biologic features and approaches to maximize healing trajectories. Current Probl Surg. 2001;38(2):61–140.

2. Lazarus GS, Cooper DM, Knighton DR, Margolis DJ. Pecararo RE, Rodeheaver G, et al. Definitions and guidelines for assessment of wounds and evaluation of healing. Arch Dermatol. 1994;130(4):489–493.

3. Schultz GS, Sibbald RG, Falanga V, Ayello EA, Dowsett C, Harding K, et al. Wound bed preparation: a systematic approach to wound management. Wound Repair Regen. 2003;11(suppl 1):S1–S28.

4. Schultz GS, Barillo DJ, Mozingo DW, Chin GA, Wound Bed Advisory Board Members. Wound bed preparation and a brief history of TIME. Int Wound J. 2004;1(1):19–32.

5. Dowsett C, Ayello E. TIME principles of chronic wound bed preparation and treatment. Br J Nurs. 2004;13(15):S16–S23.

6. Spruce P. Preparing the wound to heal using a new hydroconductive dressing. Ostomy Wound Manage. 2012;58(7):8–10.

7. Robson MC. Innovations for wound bed preparation: the role of Drawtex hydroconductive dressings. WOUNDS. 2012;24(9 suppl):2.

8. Franz MG, Robson MC, Steed DL, Barbul A, Brem H, Cooper DM, et al. Guidelines to aid healing of acute wounds by decreasing impediments to healing. Wound Repair Regen. 2008;16(6):723–748.

9. Wolvos T. Analysis of wound bed documentation in advanced wound care using Drawtex, a hydroconductive dressing with LevaFiber Technology. WOUNDS. 2012;24(9 suppl):9–10.

10. Treadwell T, Macdonald J. Buruli ulcer: its impact and treatment worldwide. An interval report. WOUNDS. 2012;24(9 suppl):19–20.

11. Wolcott RD, Cox S. The effects of a hydroconductive dressing on wound biofilm. WOUNDS. 2012;24(9 suppl):14–16.

12. Robson MC. Wound infection: a failure of wound healing caused by an imbalance of bacteria. Surg Clin North Am. 1997;77(3):637–650.

13. Heggers JP, Robson MC. Quantitative Bacteriology: Its Role in the Armamentarium of the Surgeon. Boca Raton, FL: CRC Press;1991.

14. Serena T, Robson MC, Cooper DM, Ignatious J. Lack of reliability of clinical/visual assessment of chronic wound infection: the incidence of biopsy-proven infection in venous leg ulcers. WOUNDS. 2006;18:197–202.

15. Robson MC, Edstrom LE, Krizek TJ, Groskin MG. The efficacy of systemic antibiotics in the treatment of granulating wounds. J Surg Res. 1974;16(4):299–306.

16. Hiro ME, Pierpont YN, Ko F, Wright TE, Robson MC, Payne WG. Comparative evaluation of silver-containing antimicrobial dressings on in vitro and in vivo processes of wound healing. ePlasty. 2012;12:409–419.

17. Ortiz RT, Moffatt LT, Robson MC, Jordan MH, Shupp JW. In vivo and in vitro evaluation of the properties of Drawtex Levafiber wound dressing in an infected burn wound model. WOUNDS. 2012; 24(9 suppl):3–5.

18. Ochs D, Uberti MG, Donate GA, Abercrombie M, Mannari RJ, Payne WG. Evaluation of mechanisms of action of a hydroconductive wound dressing, Drawtex, in chronic wounds. WOUNDS. 2012; 24(9 suppl):6–8.

19. Nwomeh BC, Yager DR, Cohen IK. Physiology of the chronic wound. Clin Plast Surg. 1998;25(3):341–356.

20. Tarnuzzer RW, Schultz GS. Biochemical analysis of acute and chronic wound environments. Wound Repair Regen. 1996;4(3):321–325.

21. Mast BA, Schultz GS. Interactions of cytokines, growth factors, and proteases in acute and chronic wounds. Wound Repair Regen.1996;4(4):411–420.

22. Wendelken M, Lichtenstein P, DeGroat K, Alvarez O. Detoxification of venous ulcers with a novel hydroconductive wound dressing that absorbs and transports chronic wound fluid away from the wound. WOUNDS. 2012;24(9 suppl):11–13.

23. Bendy RH, Nuccio PA, Wolfe E, Collins B, Tamburro C, Glass W, et al. Relationship of quantitative wound bacterial counts to healing of decubiti. Effect of topical gentamicin. Antimicrob Agents Chemother. 1964;10:147–152.

24. Robson MC, Lea CE, Dalton JB, Heggers JP. Quantitative bacteriology and delayed wound closure. Surg Forum. 1968;19:501–502.

25. Krizek TJ, Robson MC, Kho E. Bacterial growth and skin graft survival. Surg Forum. 1967;18: 518–519.

26. Murphy RC, Robson MC, Heggers JP, Kadowaki M. The effect of microbial contamination on musculocutaneous and random flaps. J Surg Res. 1986;41(1):75–80.

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