Wound treatment plans are frequently ineffective because of a widespread failure to identify wound etiology accurately. One study found that up to 30% of all wounds lack a differential diagnosis,1 and this poses a real barrier to administering effective treatments. Furthermore, recent advances in the understanding of wounds, including the use of growth factors and bioengineered tissue and the ability to grow cells in vitro, present new opportunities to provide more effective treatment. Wound bed preparation that incorporates the TIME framework (tissue management, Infection or inflammation, moisture imbalance, and edge of wound) into the A, B, C, D, E wound bed preparation care cycle can significantly increase the ability to perform the following accurately2:
Selecting the proper treatment hinges on the ability to assess all of the components of the TIME framework accurately. The relationship between observed conditions and the appropriate treatment is discussed in greater depth here.
The observed presence of necrotic, slough, or otherwise-compromised tissue must be treated by removing the affected tissue through debridement; this includes any non-viable tissue that may be yellow, gray, blue, brown, or black; tissue that has a soft, boggy, or slimy consistency; and tissue that forms a hard, leathery eschar. Various methods of debridement are available for the removal of unhealthy tissue when there is an adequate arterial supply.3 When tissue is sloughy, autolytic, enzymatic, mechanical, or biological debridement may all be considered. Limited sharp debridement is often enough because slough is usually superficial; when it is more adherent, enzymatic preparations may offer a better alternative.4 Debridement should always continue until healthy tissue is reached. Depending on the needs of the patient, debridement may be episodic or continuous.5
Infection or Inflammation
The diagnosis of infection can be difficult because the wound may be anywhere along the wound infection continuum. Bioburden must be controlled to promote healing and maximize the efficacy of therapeutic treatments such as bioengineered skin or growth factors.4 Tissue biopsies can help to determine the composition of the bioburden. Treatment for infection can include oral or intravenous antibiotics or topical antimicrobials. Persistent inflammation can indicate the presence of systemic inflammatory disease in chronic wounds such as diabetic foot ulcers. The presence of an inflammatory disease may be confirmed through blood tests, a biopsy, or a specialist consultation.5
Keeping wounds moist accelerates re-epithelization; however, a proper moisture balance must be maintained because excess moisture can contribute to maceration of the wound. It should also be noted that the role of moisture is different for acute and chronic wounds. Acute wounds have fluid that stimulates the in vitro proliferation of fibroblasts, keratinocytes, and endothelial cells. Exudate contents from chronic wounds, conversely, can block cellular proliferation and angiogenesis. Fluid from chronic wounds also contains matrix metalloproteinases (MMPs), which can aid the healing process, although excessive MMP activity will inhibit healing.6 Achieving moisture balance and avoiding desiccation or maceration can involve several strategies. If the wound is dry, it should be treated through rehydration by selecting the proper dressings that can achieve the ideal moisture balance. If the wound has excessive edema or exudate, the moisture balance can also be restored by selecting the appropriate absorptive dressings.5 Dressings should be changed regularly to ensure that the proper moisture balance is being maintained.3
Edge of Wound Advancement (Epithelial Advancement)
Healing requires re-epithelization for restoration of skin function. However, this re-epithelization can be inhibited for several reasons, including hypoxia, infection, desiccation, dressing trauma, or hyperkeratosis.4 Epithelial non-advancement occurs when the edges of wounds become callused, have dried exudate or accumulated slough, are necrotic, or have the persistent presence of non-viable tissue. The line between viable and non-viable tissue is also frequently a site of infection, particularly if the wound becomes macerated.3 Edge advancement may also be impacted by extrinsic factors, such as repeated trauma, ischemia, or poor metabolic controls, by or intrinsic factors, such as the deficiency of growth factors, abnormal extracellular matrix components with excess protease, and reduced fibroblast activity.3
Treatment to support edge advancement directly targets the identified cause of non-epithelization and can include measures such as additional debridement, skin grafts, biological agents, and adjunctive therapies.5 Standard methods for the preparation of the wound bed will frequently optimize the conditions in a way that promotes healing. However, there are instances in which the wound will fail to heal. This could be indicative of another contributing factor, such as an inappropriate cytokine, growth factor, protease, and reactive oxygen species production by cells within granulation tissue. In these instances, advanced therapies, or even skin grafting, may be necessary.4
Wound bed preparation treatment methods continue to evolve as we learn more about optimizing conditions that promote healing. There is a current proposal to update the TIME framework to TIMERS, which would add two additional components: regeneration or repair of the tissue and social factors. These two factors expand the scope of holistic patient care to encompass additional components that may have an impact on healing. They may also help to better identify where advanced adjunctive therapies should be considered as a part of the standard of care.7 When taken together, treatment plans that account for all factors that may impact a patient’s ability or inability to heal have a much greater likelihood of resulting in positive patient outcomes.
1. Guest JF, Ayoub N, McIlwraith T, et al. Health economic burden that different wound types impose on the UK’s National Health Service. Int Wound J. 2017;14(2):322-330.
2. Moore Z, Dowsett C, Smith G, et al. TIME CDST: an updated tool to address the current challenges in wound care. J Wound Care. 2019;28(3):154-161.
3. Edmonds M, Foster AVM, Vowden P. Wound bed preparation for diabetic foot ulcers. In: Calne S, Moffatt C, Flanagan M, et al., eds. Wound Bed Preparation in Practice. European Wound Management Association (EWWA). London, United Kingdmom: MEP Ltd.; 2004.
4. Moffatt C, Morison MJ, Pina E. Wound bed preparation for venous leg ulcers. In: Calne S, Moffatt C, Flanagan M, et al., eds. Wound Bed Preparation in Practice. European Wound Management Association (EWWA). London, United Kingdom: MEP Ltd.; 2004.
5. Schultz GS, Sibbald RG, Falanga V, et al. Wound bed preparation: a systematic approach to wound management. Wound Repair Regen. 2003;11(1):1-28.
6. Falanga V. (Wound bed preparation: science applied to practice. In: Calne S, Moffatt C, Flanagan M, et al., eds. Wound Bed Preparation in Practice. European Wound Management Association (EWWA). London, United Kingdom: MEP Ltd.; 2004.
7. Atkin L, Bucko Z, Conde Montero E, et al. Implementing TIMERS: the race against hard-to-heal wounds. J Wound Care. 2019;23(suppl 3a):S1-S50.
The views and opinions expressed in this blog are solely those of the author, and do not represent the views of WoundSource, HMP Global, its affiliates, or subsidiary companies.