Wound Bed Preparation: The Science Behind the Removal of Barriers to Healing

Stuart Enoch, MBBS, MRCSEd, MRCS (Eng), Keith Harding, MB ChB, MRCGP, FRCS

Disclosures

Wounds. 2003;15(7) 

In This Article

Treating Infected Wounds

It is important that treatment is initiated as soon as bacteria have been identified as a reason for the impaired healing of a chronic wound. Treating infected wounds will help to reduce the bacterial burden and hence remove one of the barriers to healing. There are a number of means by which bacterial burden can be reduced, which include the use of antibiotics and antiseptics. Though antibiotic therapy is useful to treat infected wounds and helps to prevent infection spreading in the soft tissues beyond the wound (e.g., cellulitis and ascending lymphangitis), repeated use in patients with chronic wounds could lead to the development of bacterial resistance. Therefore, great caution needs to be exerted in the use of antibiotics, and they should be avoided as a first-line management.[107]

The resolution of microbial imbalance with slow-release antiseptics is regaining recognition as an important adjunct to antibiotic treatment.[38] The use of antiseptic agents may be essential for effective wound bed preparation, since inadequate removal of bacteria delays wound healing.[108] In contrast to antibiotics that have a specific mode of action, antiseptics target bacteria at the cell membrane, cytoplasmic organelle, and nucleic acid level. These multitarget antibacterial effects mean that bacterial resistance is unlikely. Commonly applied antiseptics include slow-release antimicrobials, such as cadexomer iodine.[109] Cadexomer iodine is a slow-release antimicrobial capable of absorbing excess wound exudate while providing a sustained level of iodine in the wound bed.[110,111] Evaluation of its benefits have indicated that it is well tolerated and accelerates the healing of chronic leg ulcers.[112,113,114,115,116,117,118] Cadexomer iodine has also demonstrated efficacy in vivo against Staphylococcus aureus and methicillin-resistant Staphylococcus aureus (MRSA).[119,120]

There is some concern and controversy with antiseptic use on wounds because of its cytotoxic effect on cells involved in wound healing (fibroblasts, keratinocytes, and leukocytes) in vitro.[121,122] This effect appears to be concentration dependent, as several antiseptics in low concentrations are not cytotoxic, besides retaining their antibacterial activity.[123] In addition, there is insufficient evidence at present to show that antiseptics have a deleterious effect on healing. On the contrary, nine clinical trials (in humans) comparing the effects of cadexomer iodine with other forms of treatments on chronic ulcers have shown enhanced healing along with decreased pus, debris, pain, and erythema with the use of cadexomer iodine. No negative effect on healing with cadexomer iodine was observed in these trials.[124]

Nanocrystalline silver dressings are a new variety of antimicrobial barrier dressings that may help reduce infection in partial- and full-thickness wounds. These are comprised of a silver-coated, high-density. polyethylene mesh with an absorptive gauze core, which slowly releases silver into the dressing and maintains an effective antimicrobial barrier for up to seven days. Nanocrystalline silver has been shown to be effective against a broad spectrum of bacterial strains in vitro, including MRSA and vancomycin-resistant Enterococcus.[125]

Noble metals like silver have been in use since the middle of the last century in the treatment of both acute and chronic wounds. They have been shown to be effective in combating antibiotic-resistant strains in colonized wounds.[126] Bishop, et al.,[127] investigated the effect of silver sulfadiazine (AgSD) cream in a prospective, randomized, controlled trial of 86 patients with chronic venous ulcers. They found a statistically significant reduction in their size using one-percent AgSD compared to tripeptide copper complex 0.4-percent cream or the placebo. Similarly, Kucan, et al.,[128]observed rapid healing and significant reduction in the bacterial counts of chronic pressure ulcers (reduced to 105 or less per gram of tissue within the three-week test period) using one-percent AgSD compared to povidone-iodine and physiological saline. These studies would probably not meet today's standards required to convincingly demonstrate efficacy. However, more recently, Mi, et al.,[129] demonstrated long-term inhibition of the growth of Pseudomonas aeruginosa and Staphylococcus aureus at an infected wound site using AgSD incorporated in a bilayer chitosan wound dressing.

Debridement of necrotic tissue is another means by which bacterial burden can be reduced to optimize wound healing and enhance wound closure. Research has demonstrated that the presence of necrotic tissue in the wound bed is associated with wound infection,[92,130,131] and its removal works on several levels to reduce bacterial burden. Firstly, debridement enhances local host defense mechanisms and prevents active infection by reducing the amount of devascularized tissue and removing foreign bodies.[45,46] Secondly, by activating the release of growth factors and tissue cytokines, debridement helps to promote the formation of well vascularized granulation tissue.

The diagnosis of infection in a chronic wound is a complex clinical skill, but the most important indicators of infection are both local and systemic host characteristics. Wound bed preparation as a clinical strategy helps clinicians address the issues of increased bacterial burden and remove this barrier to healing using advanced antibacterial agents and debridement.

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