According to a recent high-profile report,1 an estimated 10 million people will die each year from antimicrobial resistance. If left unchecked, the tide of unresolved infections is projected to kill more people than cancer by 2050.1 There is an increasing awareness that approximately 65% of all microbial infections and 85% of all chronic infections are associated with biofilm, a recognized problem for more than 90% of chronic wounds and 6% of acute wounds.2 An analysis of specific disabilities looked at diabetes and diabetic foot complications as a separate category and calculated that as many as 148 million diabetic foot infections are possible if the trend in infections is not interrupted.1,3 Similarly, escalating numbers of infections are occurring among other wound types, such as surgical site infections (~300,000 per year), the third most commonly reported healthcare-associated infections in the United States.4 Clearly, the current approach — using antibiotics to manage wound infection and colonization — is shortsighted and needs to be modified.
THE BIOFILM BAROMETER
After recent recognition that biofilm- and non-biofilm-forming isolates had similar infectious outcomes, the trend in treating biofilm as a category and barrier to healing by itself has refocused the need for aggressive, multimodal care.5 Today, wound treatment principles continue to encourage early infection/biofilm treatment and intervention beginning with local wound bed preparation. Most clinical wound care guidelines currently have directives regarding infection assessment and care designed to remove barriers to wound healing, including stopping the progression of infection to reestablish a natural healing process. Guideline measures blending wound bed preparation with preemptive biofilm care can be exemplified in the TIME (Tissue, Infection/Inflammation, Moisture Balance, Wound Edges) principles of wound care.6 The mnemonic TIME gained popularity more than 15 years ago and encourages clinicians to understand the underlying abnormalities that prevent wounds from healing. Laying the foundation for less linear thinking, we have also learned that a combination of management strategies termed “multimodal wound care” can be an effective tactic to removing barriers to natural wound healing by addressing multiple TIME principles simultaneously.6,7
TIME FOR DEBRIDEMENT
Using the systematic approach encouraged by the TIME principles, clinicians began to test the relationship between wound bed preparation with other products, soon realizing that a combinational approach to care improves wound healing and patient outcomes. This concept has been demonstrated by combining the benefit of sharp debridement with enzymes.8 The interplay of cellular and molecular activities continues to inform and spark innovation, especially for biofilm interventions.9 Contemporary wound care stresses wound treatments that provide multiple actions. Conceptually, stacking synergistic clinical therapies, such as debridement, with topical biofilm management as an approach to wound management is clearly needed.
In a groundbreaking study, Piaggesi et al demonstrated the dramatic effectiveness of excisional debridement.10 Another recent landmark study from Georgetown University has expanded this concept by examining the effectiveness of clinic-based excisional debridement on wound bed bacteria.9 Sharp debridement often is performed serially in the outpatient setting and is considered a “gold standard” component in the care of chronic wounds; however, after evaluating the change in bacterial amounts with sharp
debridement in a clinical setting, the study found that clinic-based excisional
debridement did little to impact the bacterial confluence in the wound bed.9
According to another article published in August of this year, indications for clinic debridement in general, is the removal of devitalized tissue such as necrotic tissue, slough, bioburden, biofilm, and apoptotic cells.11 Clearly, excisional debridement is needed, but based on the findings from the Georgetown University study,11 clinic-based debridement is insufficient as a standalone method to remove bacterial bioburden or biofilm. Another study from 2016 demonstrated a residual bacterial bioburden post-debridement of 102 or less, even in the presence of ultrasonic debridement using hypochlorous acid. This sounds impressive until one realizes that debridement stimulates remaining bacteria and fractionated biofilm segments to reform mature biofilm faster than the original biofilm, often in as little as 15 minutes, with firmly attached aggregates in 24 hours.12,13
Because biofilm and bioburden do not cover the entire wound but are known to exist in separate, nonvisible microcolonies, methods to remove or reduce the level of biofilm should be considered in multiple steps along the wound healing continuum. Application of current research should entice clinicians to consider new information in the context of established wound principles, including TIME, and to think in terms of pre- and post-debridement multimodal therapies. Clinicians recognize that debridement is needed, but they also must be cognizant that it only opens a time-dependent window to treat biofilm.14 An optimized TIME model of debridement plus biofilm treatment promotes an increased biological awareness of wound healing. Incorporating debridement with TIME principles helps anticipate what is happening in the wound bed and offset barriers to healing with early intervention principles such as combining frequent sharp debridement with fast-acting antimicrobial therapy, managing wound exudate, and adjusting wound edges to promote epithelization.6-8 Using this notion of preemptive pre- and post-debridement therapies to impact the formation and virulence of biofilm or downstream infections is an ideal optimization of the TIME model and one that is supported through research and clinical practice.6-12 n
Elliot T. Walters, MD, is a diabetic limb salvage research fellow at the Center for Wound Healing at MedStar Georgetown University Hospital, Washington, D.C.
Patricia Stevenson is a wound care clinician in the Tulsa, OK, area and a clinical consultant at Next Science, Jacksonville, FL.
1. O’Neill J. Antimicrobial resistance: tackling a crisis for the health and wealth of nations. London, UK: Review on Antimicrobial Resistance. 2014. Accessed online: http://bit.ly/2PNPkHt.
2. Petrova O, Sauer K. Sticky situations: key components that control bacterial surface attachment. J Bacteriol. 2012;194(10):2413-25.
3. Lazzarini PA, Pacella RE, Armstrong DG, van Netten JJ. Diabetes-related lower-extremity complications are a leading cause of the global burden of disability. Diabet Med. 2018. [Epub ahead of print]
4. Loyola University Health System. Surgical site infections are the most common and costly of hospital infections: guidelines for preventing surgical site infections are updated. Science Daily. Accessed online: www.sciencedaily.com/releases/2017/01/170119161551.htm.
5. Barsoumian AE, Mende K, Sanchez CJ, et al. Clinical infectious outcomes associated with biofilm-related bacterial infections: a retrospective chart review. BMC Infect Dis. 2015;15:223.
6. Falanga V. Wound bed preparation and the role of enzymes: a case for multiple actions of therapeutic agents. Wounds. 2002;2;14(2):47-57.
7. Schultz G, Barillo D, 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.
8. Percival SL, McCarty SM, Lipsky B. Biofilm and wounds: an overview of the evidence. Adv Wound Care. 2015;4(7):373-81.
9. Kim PJ, Attinger CE, Bigham T, et al. Clinic-based debridement of chronic ulcers has minimal impact on bacteria. Wounds. 2018;30(5):114-19.
10. Piaggesi A, Schipani E, Campi F, et al. Conservative surgical approach versus non-surgical management for diabetic neuropathic foot ulcers: a randomized trial. Diabetic Med. 1998;15(5):412-7.
11. Manna B, Morrison CA. Wound Debridement. In: StatPearls. Treasure Island, FL: StatPearls Publishing; 2018.
12. Hiebert JM, Robson MC. The immediate and delayed post-debridement effects on tissue bacterial wound counts of hypochlorous acid versus saline irrigation in chronic wounds. Eplasty. 2016;16:e32.
13. Attinger C, Wolcott RD. Clinically addressing biofilm in chronic wounds. Adv Wound Care. 2012;1(3):127-32.
14. Wolcott RD, Rumbauch KP, James G, et al. Biofilm maturity studies indicate sharp debridement opens a time-dependent therapeutic window. J Wound Care. 2010;19(8):320-8.