Successful utilization of the TIME model for wound bed preparation requires a working knowledge of chronic wound tissue types. In addition, building on this foundational knowledge is the development of accurate wound assessment skills. These components combined will assist the clinician in implementing the appropriate interventions for each wound.
The term "viable" describes vascular tissue with dynamic biological activity.
Epithelium: This should be dry to touch and can appear white or light pink; it is composed of restratified keratinocytes arising from the basement membrane of the dermis.
Granulation: This appears light pink to red and should be moist with a bumpy texture. Capillaries give granulation tissue its characteristic color, and collagen made from fibroblasts provides structural support. If granulation tissue is pale (poor perfusion), dark red or ruddy (vascular congestion or stasis), or "bubbly" or friable (bleeds with very gentle contact), it is technically considered non-viable because it will not support migrating epithelial cells.
Subcutaneous: This layer typically appears as shiny yellow lumps (subcutaneous fat) because it is principally composed of adipose tissue and the plexus of blood vessels that supply the subdermal perfusion to the dermis.
Muscle: Muscle tissue appears dark red or burgundy with parallel striations, and when visible, the shiny and smooth fascial covering contributes to muscle’s characteristic appearance. Muscle may contract when probed with an instrument if it is in proximity to a nerve.
Bone: Viable bone is typically bright white and shiny and will bleed readily if cancellous (inner layer) bone is disturbed.
Tendon: Healthy tendon has a moist, shiny, light yellow appearance and exhibits movement with flexion or extension of the nearby associated joint. Tendon is poorly vascularized and relies on surrounding tissue for perfusion, so it is extremely important that it be kept moist and protected.
Vasculature (arteries or capillaries and veins): Most vascular structures large enough to see appear tubular. Arteries are generally deeper in tissue, visibly pulsate, and are deep red. Veins are more superficial, may appear purple or blue, and generally do not pulsate. Depending on wound type, if arteries are exposed, they may also contain visible suture (sometimes blue or white) if the patient has undergone certain procedures such as a free muscle flap.
Non-viable tissue is also referred to as necrotic or devitalized. These are terms describing avascular tissue that has lost normal cellular structure and physical properties required of living tissue.
Slough: This tissue can be either moist or dry and may have a stringy or fibrinous texture. Slough can be gray, white, yellow, tan, green (from Pseudomonas), blue, or brown (from dressing coloration). It can be adherent or non-adherent to surrounding tissue. Eschar: This is typically black or brown and can be stable (dry) without exudate or unstable (moist, boggy) with exudate.
Maceration: This can be in the wound bed or the periwound and is white and soft. It is technically considered non-viable tissue because when the epithelium or granulation tissue is overhydrated by prolonged exposure to excess moisture and proteases from chronic wound fluid, it loses its cellular structure.1
Tissue structures: Distinct tissue structures that have become devitalized such as muscle, tendon, cartilage, and bone can be present in the wound bed with varying appearances. Tendon can become a dull, boggy yellow with darker yellow or brown or black streaks. Cartilage may appear dull yellow or white with a desiccated and waxy texture; bone generally turns dull tan or gray and becomes dry, and at late stages it will easily crumble when probed.2
Grafting material: Foreign materials such as allografts, xenografts, mesh, suture, and drains can also be present in the wound bed. These are important to assess and document in addition to native tissue. Many biological grafts appear yellowish or white, and some may appear in the wound bed as yellow slough, even days after placement; it is extremely important to communicate or even write on a dressing when a graft is in place because some grafts are mistaken for non-viable tissue and are excisionally debrided.
Sutures: There are numerous types of suture, but those typically found in wounds can be divided into absorbable (purple or white braided [Vicryl], purple [PDS], clear or yellow [chromic gut]) or permanent (black [nylon], or blue [Prolene]).
Drainage devices: Drains often used include Penrose (tubular light yellow latex, ¼" up to 2"+), silicone (flat or round, usually with bulb attached to end, commonly referred to as Jackson-Pratt drains, 15 or 19Fr), latex Foley catheters (12-22Fr+), or red rubber catheters (14 or 16Fr).
Goals of treatment are based on wound tissue type. Each facet of treatment is aimed to address specific phases of the wound healing process.
Debridement: Elimination of non-viable tissue and stalled wound edges is the cornerstone of wound bed preparation. There are multiple debridement modalities, some of which are selective for non-viable tissue, and some of which are non-selective (viable tissue is removed as well, e.g., mechanical debridement with gauze sponges): sharp (conservative or excisional/surgical), mechanical, autolytic, enzymatic or chemical, and biological.
Topical therapies: Dressings and other topical treatments including grafts and application of growth factors should be complementary to the dynamic nature of the wound bed. Examples include managing moisture with absorptive dressings for higher exudate levels, applying hydrogel to dry wounds, or applying grafts and growth factors to wounds deficient in viable cells required for progression to the proliferative phase of wound healing (fibroblasts, keratinocytes, glycosaminoglycans, etc.).
Offloading and compression: These are both crucial modalities in the treatment plan for wounds with potential for vascular compromise and subsequent tissue death secondary to prolonged pressure or tissue edema resulting in poor perfusion.
Blood glucose: Elevated blood glucose causes dysfunction of cells and cytokines requisite for wound healing and impairs the body’s ability to defend itself from pathogens.
Bacterial burden: Bacterial or microbial presence at any level in the wound must be addressed to support the growth of new tissue. Progression through the phases of contamination, colonization, critical colonization, infection, and sepsis can be stopped by debriding non-viable tissue, improving host factors such as nutrition, optimizing disease states (blood glucose and immunosuppression), selecting an appropriate antimicrobial dressing, and prescribing targeted antibiotic therapy from sensitivities provided from quantitative tissue biopsy of healthy-appearing tissue.
Nutrition: Despite all other interventions implemented and otherwise impeccable treatment plan execution, wounds may lack the ability to form viable tissue secondary to a lack of available serum protein or other nutrients such as vitamin C and zinc required for collagen synthesis.
Unique conditions: Some states such as pathergy (tissue injury from debridement causes further tissue autodestruction) and disorders of coagulopathy (excessive bleeding from deficiency of coagulation factors) in patients with wounds may require atraumatic dressings. This can present a problem if the wound is excessively moist because most non-adherent primary dressing layers also retain moisture.
A strong knowledge of tissues types that may be present in chronic wounds and thorough assessment of the wound and patient will guide clinicians in determining appropriate interventions to optimize the wound healing environment by using a holistic framework such as the TIME wound bed preparation model.
1. European Wound Management Association (EWMA). Position Document: Wound Bed Preparation in Practice. London: MEP Ltd; 2004. Available at: http://ewma.org/fileadmin/user_upload/EWMA.org/Position_documents_2002-…. Accessed June 8, 2018.
2. Bryant RA, Nix DP. Acute & Chronic Wounds: Current Management Concepts, 5th ed. St. Louis, MO: Elsevier Health Sciences; 2015.
3. Leaper DJ, Schultz G, Carville K, Fletcher J, Swanson T, Drake R. Extending the TIME concept: what have we learned in the past 10 years? Int Wound J. 2012;9 Suppl 2:1-19.
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.