By the WoundSource Editors
The wound healing cascade is a complex process that follows a strict sequence of molecular events. The complex series of events depend on one another and must take place in a timely and orderly fashion within the body’s natural host processes. The phases of acute wound healing, in order, are hemostasis, inflammatory, proliferative, and maturation. If the cascade of events is interrupted, the acute wound status then develops into a non-healing or chronic status.1 Wound stalling occurs in the inflammatory and proliferative stages of healing.2 In chronic wounds, there appears to be an overproduction of matrix molecules resulting from underlying cellular dysfunction and dysregulation.3 Non-viable or devitalized tissue lengthens the inflammatory phase of healing and increases risk of infection.
In regard to wound science, the abnormal parameters of molecular, cellular, and microbial environments of chronic wounds have been discovered through the years. Non-viable tissue contains a defective matrix and cell debris that impair healing. Debridement methods help restore the base of the wound and functional extracellular matrix proteins. Prolonged inflammation increases cytokines and protease activity while decreasing growth factor activity. Wound bed preparation helps to offset these bacterial imbalances. Excessive exudate causes desiccation or maceration. Wound bed preparation restores an optimal moist environment while enhancing epithelial cell migration. Epithelial migration stalls when non-responsive wound cells, extracellular matrix, and protease activity are abnormal. Wound bed preparation encourages migrating keratinocytes and wound cells while restoring proteases.
Wound Bed Preparation: TIME and DIME
To assess or evaluate a wound properly, you must first be able to visualize the wound bed tissue level. When non-viable or devitalized tissue is present, it slows healing and increases the risk of infection. Biofilm is also another culprit in stalled wound healing. Research has shown biofilm to be present in 78.2% of chronic wounds.4 Developed biofilms harbor physical and metabolic defenses. These defenses enable the biofilm to resist antimicrobials that usually alienate planktonic cells and include resistance to host defenses, biocides, antibiotics, and ultraviolet light. Sequential sharp debridement of wounds disrupts biofilm growth and inhibitory factors and can promote faster healing. It is difficult to predict the outcome because we still do not know the depth needed to remove the entire biofilm colony.5,6
In 2003, the concept of wound bed preparation and the mnemonics TIME and DIME were created. TIME has also been used in acute wound healing. TIME stands for tissue, infection/inflammation, moisture balance, and edge of wound/epithelial cell migration. DIME stands for debridement, infection/inflammation, moisture balance, and edge of wound/epithelial cell migration. Wound bed preparation has been shown to be a major advance in resolving or addressing non-healing or chronic wounds. Wound bed preparation education to clinicians is key to identifying barriers and managing and accelerating healing of non-healing chronic wounds.1 Factors in impeded wound healing include tissue necrosis, hypoxia, bioburden, corrupt matrix, and senescent cells within the wound bed.7
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Non-viable or devitalized tissue slows down the wound healing process and also increases the risk of infection and sepsis. Dead tissue or foreign material is a vehicle for bacterial growth. The goal of debridement is to make the wound acute again and thereby to expedite healing in an orderly fashion.5,6
All wounds contain different levels of bacteria that range from confined superficial levels to deep levels. There are several systemic and local factors that increase the risk of wound infection. Local factors can include large wounds, deep wounds, wound chronicity, anatomical location, poor tissue perfusion, and the presence of non-viable tissue. Systemic factors can include smoking, malnutrition, vascular disease, diabetes, and the use of corticosteroids or immunosuppressants.8
Principles and Types of Debridement
Debridement is used for many reasons within wound bed preparation. The primary goal of wound debridement is to restore the wound’s environment and optimize healing. Debridement is used to remove dead, necrotic, or foreign material from within the wound, and to disrupt biofilm and inhibitory factors. However, it is difficult to predict the outcome due to not knowing the precise depth needed in levels of debridement to remove the biofilm. Biofilm colonies can be deeply embedded into the wound. Removing biofilm may involve combining different methods of debridement.
Of the five debridement methods, autolytic debridement is the least aggressive method, whereas surgical debridement is the most aggressive. Debridement methods can be used alone or together. Clinicians must remember that current standard care guidelines recommend that stable, intact (dry, adherent, intact without erythema or fluctuance) eschar on the heels should not be removed. If the eschar becomes unstable (wet, draining loose, boggy, edematous, red), it should be debrided according to the clinic or facility protocol. Autoimmune, pyoderma gangrenosum, and calciphylaxis wounds should not be surgically debrided.9
Combining debridement methods has been found to be an advantage in managing complex wounds and different pathological tissues since 2006.10 One common method of combining debridement techniques is using enzymatic debridement first to liquefy the tissue and then following with sharp debridement. Combining debridement methods in this way can ensure that you are removing as much dead tissue from the wound as possible and helping to promote wound healing.
Accurate and thorough wound assessments are key. Wound bed preparation using the TIME or DIME framework increases good healing outcomes. Using debridement methods that complement the wound healing process is most effective in optimizing healing rates. Using a structured wound bed preparation approach can empower and serve as an educational tool for clinicians.
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2. Ennis WJ. Menses P. Wound healing at the local level: the stunned wound. Ostomy Wound Manag. 2000;46(1A Suppl):39S–48S.
3. Falanga V. Wound bed preparation and the role of enzymes: a case for multiple actions of therapeutic agents. Wounds. 2000;4(2):47–57.
4. Malone M, Bjarnsholt T, McBain AJ, et al. The prevalence of biofilms in chronic wounds: a systemic review and metanalysis of published data. J Wound Care. 2017;26(1):20–5.
5. Leaper D. Sharp technique for wound debridement. World Wide Wounds. 2002. Available at: http://www.worldwidewounds.com/2002/december/Leaper/Sharp-Debridement.html. Accessed April 11, 2019.
6. ABC of wound healing wound assessment. BMJ. 2006;332:285.
7. Wolcott RD, Kennedy JP, Dowd SE. Regular debridement is the main tool for maintaining a healthy wound bed in most chronic wounds. J Wound Care. 2009;18(2):54–6.
8. Dowsett C, Newton H. Wound bed preparation: TIME in practice. Wounds UK. https://www.bbraun.com/content/dam/catalog/bbraun/bbraunProductCatalog/S.... Accessed April 15, 2019.
9. Suzuki K, Cowan L. Current concepts in wound debridement. Podiatry Today. 2009;22(7):40–8. https://www.podiatrytoday.com/current-concepts-in-wound-debridement. Accessed April 2, 2019.
10. Liu WL, Jiang YL, Wang YQ, Li YX, Liu YX. Combined debridement in chronic wounds: a literature review. Chin Nurs Res. 2017;4(1):5–8. Available at: https://www.sciencedirect.com/science/article/pii/S2095771817300063. Accessed April 15, 2019.
1. Panuncialman J, Falanga V. The science of wound bed preparation. Surg Clin North Am. 2009;89(3):611–26.
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