practice Regular debridement is the main tool for maintaining a healthy wound bed in most chronic Sharp debridement is the most clinically and cost-effective way of physically removing and suppressing a biofi lm. Continued debridement, as part of a multifaceted treatment strategy, will keep the biofi lm in a weakened state chronic wounds; biofilm; sharp debridement R.D. Wolcott, MD, he concept of a ‘healthy wound’ seems by our laboratory is showing that over 80% of all CWS, Medical Director, contradictory, yet only when the wound chronic wounds evaluated have biofi lm phenotype Southwest Regional bed is vital will the affected tissue progress bacteria and only wounds that are on a positive Wound Care Center, Lubbock, Texas, US; toward dermal regeneration. A ‘healthy’ healing trajectory and are being treated with bio- J.P. Kennedy, RPh, PhD, wound surface is created when biofi lm fi lm-based wound care do not have detectable Assistant Professor for T infection, physiological stress, infl ammation, exu- biofi lm phenotype bacteria (Dowd et al., unpub- Research, South date and necrotic tissue are minimised to such an lished data). University, School of Pharmacy, Savannah, extent that the host, even the compromised host, Our previous papers have explored the ecology, Georgia, US; can dedicate physiological resources toward tissue nature and physiological effects of biofi lm in S.E. Dowd, PhD, regeneration. wounds,15,16 so we will not repeat this here. Director, Research and This can be achieved through debridement, Testing Laboratory of the although how this works is not completely under- Biofi lm-based wound care South Plains and Medical Biofi lm Research stood. Hypotheses include: Biofi lms are a wound management challenge for Institute, Lubbock, ● Removing senescent cells1 four main reasons: Texas, US. ● Balancing bioburden,2 • They are resistant to antibiotics (50 to 1500 Email: sdowd@ 3 17 ● Improving microcirculation fold) pathogenresearch.org ● Normalising the biochemistry.4 • They are highly resistant to biocides (hydrogen Debridement can be achieved through modalities peroxide, acids, bleach)18 such as: • They evade the host immune system (white blood ● Appropriate dressings cells, antibodies, complement)19,20 ● Pulse lavage • They are poorly penetrated by many antibiotics ● Maggot debridement therapy used. 21-24 ● Enzymatic debridement Physical removal and suppression of biofi lm ref- ● Autolytic debridement. ormation is therefore a necessary part of the wound However, these modalities do not work specifi cal- management regimen. Experience and the literature ly on biofi lms, whereas surgical or sharp debride- have demonstrated that debridement is the most ment does and is much quicker.5-9 effective modality to achieve this.25-28 Debridement can also facilitate an opportunity Biofi lm for antibiotic intervention: it physically disrupts the Chronic wounds are mired in a chronic infl amma- biofi lm, which then must reconstitute itself. To do tory state exhibiting markedly elevated pro-infl am- this, the biofi lm has to reattach to the host surface, matory cytokines (interleukin-1, tumour necrosing becoming metabolically active. This increases the factor-alpha, gamma interferon), elevated matrix rate of proliferation and synthesis, in turn increas- metalloproteases (MMP2, MMP8, MMP9) and exces- ing nutrient uptake. This presents a healing window sive neutrophils.10-14 of opportunity for clinicians as biofi lm phenotypes This persistent infl ammatory state may be are much more susceptible to antibiotics and bio- explained as the consequence of biofi lm phenotype cides in the fi rst 24–72 hours (depending on com- bacteria — namely, chronic infection.15 munity species) due to energy and nutrient expend- Although methods to detect and characterise iture in the growth phase and the immaturity of the biofi lm in wounds are only now being developed protective extracellular polymeric substance (EPS) 17,18 and tested for sensitivity, recent unpublished work matrix. 54 JOURNAL OF WOUND CARE VOL 18, NO 2, FEBRUARY 2009 practice Fig 1. Graphical illustration of the effects of biofi lm-based wound care 100 90 80 Healing window (therapeutic balance) 70 60 Wound stall point { 50 40 30 Wound regression (balance is subtherapeutic) 20 10 { 0 0.0 1.0 2.0 3.0 4.0 5.0 6.0 7.0 8.0 9.0 10.0 11.0 12.0 13.0 14.0 15.0 16.0 17.0 18.0 19.0 20.0 21.0 Debridement Debridement Debridement Concurrent biofi lm Tx day day day Debridement only The goal of biofi lm-based wound care is to ensure the therapy maintains its balance within the healing window, as described in the text. It can be assumed from this fi gure that, without concurrent strategy, the frequency of debridement could be increased to keep the wound from falling below the healing stall point. Debridement remains the primary tool for ensuring the wound stays above the stall point Although debridement can remove the vast concurrent strategies to inhibit the reformation of majority of biofi lm phenotype bacteria, complete biofi lm. sterilisation of an active wound is unlikely, even In this illustration, which is based on our clinical with the most vigorous debridement, as bacteria model for wound care, maintenance debridement have been shown to integrate around deep capillar- alone keeps the wound balance in favour of the host ies29 and, based on both in vitro within 24 hours30 (healing) for approximately 43% of the days between and in vivo within 48 hours31 evidence, extensive visits, although the rate of healing immediately biofi lm can reform in wounds very rapidly. post-debridement is more rapid. However, in this To take advantage of the healing wound, advanced scenario, the wound is capable of regressing in 57% and rapid diagnostic methods are required to iden- of the days between visits as the balance shifts back tify the bacteria and their potential antibiotic sus- to favour the biofi lm. When debridement is com- ceptibilities. These diagnostic methods are now bined with multiple concurrent strategies to further being utilised effectively in our clinic.32 inhibit the biofi lm’s recovery, the healing window Thus, a powerful combination of debridement, (clinical opportunity) remains open for 86% of the rapid molecular diagnosis of infecting agents, topi- days between visits; furthermore, the net rate of cal application of treating agents, and systemic anti- healing is also augmented. In this multiple concur- biotics give a multiple concurrent strategy that we rent strategy, only 14% of the days between visits are fi nding to highly benefi cial clinically. are capable of regression. As well as physically removing biofi lm, temporar- While these are not absolute numbers relative to ily disrupting its colony defences and forcing it to every wound, the order and separation of the rates become more susceptible to antibiotics, biocides for single versus multiple concurrent biofi lm strate- and host immunity,17,18 debridement will also pre- gies are in alignment with what we see in the clinic. pare the wound bed by opening all undermining Regardless, the primary intent of Fig 1 is to illustrate and tunnels, removing all devitalised and poorly the strategy of biofi lm-based wound care in a multi- perfused tissue, and shaping the wound topography. faceted approach; this maximises the wound’s heal- The resulting smooth, well-perfused wound bed will ing potential. inhibit biofi lm adhesion. Maintenance debridement prevents re-establishment. Cost-effectiveness However, complete eradication of biofi lm with The premise of this article is that debridement is debridement is not possible. Continued mainte- pivotal to chronic wound healing. It represents a nance debridement is able to keep wound biofi lm in minor portion of the total US wound-care budget: a weakened and susceptible state. Fig 1 is provided $188 million dollars in 2005, less than 0.8% of the in part to illustrate this. Two healing profi les are total amount spent on wounds.33 It has also been shown: demonstrated, both scientifi cally and experiential- • Healing profi le with debridement alone ly, to decrease back-end costs such as antibiotics, ▲ • Healing profi le using debridement with multiple hospitalisation, amputation and death.8,16 In rela- JOURNAL OF WOUND CARE VOL 18, NO 2, FEBRUARY 2009 55 practice tion to the expense of other treatments that have biofi lm phenotype community to continually re- not been proven as broadly effective,34,35 debride- attach to the host, reform its extracellular polymeric ment would appear to be the most cost-effective substance, and increase its metabolic activity for cell option. division, synthesis and colony activity. Each of these factors provides a clinical opportunity as the biofi lm Conclusion is more vulnerable to antibiotics and selective bio- Biofi lm is an important, and until recently, an cides during the recovery phase of the biofi lm post- unrecognised barrier to chronic wound healing. debridement. Debridement as part of a multiple Clinical experience demonstrates that frequent dis- concurrent strategy for wound care is an effective ruption of biofi lm, through debridement, forces the tool for the suppression of biofi lm. ■ References 1 Panuncialman, J., Falanga, V. The 12 Nwomeh, B.C., Liang, H.X., Miller, A.J. et al. Vancomycin 31 Davis, S.C., Ricotti, C., science of wound bed Cohen, I.K., et al. MMP-8 is the penetration into biofi lm covering Cazzaniga, A. et al. Microscopic preparation. Clin Plast Surg 2007; predominant collagenase in infected prostheses and effect on and physiologic evidence for 34: 4, 621-632. healing wounds and nonhealing bacteria. J Infect Dis; 170: 3, biofi lm-associated wound 2 Sibbald, R.G., Woo, K., Ayello, ulcers. J Surg Res 1999; 81: 2, 720-723. colonization in vivo. Wound E.A. Increased bacterial burden 189-195. 23 Nichols, W.W., Evans, M.J., Repair Regen 2008; 16: 1, and infection: the story of 13 Trengove, N.J., Stacey, M,C., Slack, M,P.