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Wound Healing Strategies and Management

Wound Chronicity

For wound healing to occur a complex well-defined cascade of events must take place between the body’s natural host processes. When this cascade of events is disturbed a wound can fall into a state of non-healing or chronicity (Mihai, Preda, Lungu, Gestal, Popa, & Holban, 2018). In clinical practice, chronic wounds such as pressure ulcers, vascular ulcers, and neuropathic wounds behave differently and may be extremely slow to heal. A chronic wound by definition is a wound that has failed to progress through the “normal” healing process or are not responsive to management in a timely manner (Bohn, Schultz, Liden, Designe, Lullove, Zilberman, Regan, Ostler, Edwards, Arvanitis, & Hartman, 2017). Most wounds greater than 30 days are considered chronic wounds and examples include pressure ulcers, traumatic wounds and lower extremity wounds. Contributing factors include poor circulation, ongoing pressure, systemic illness, age, repeated trauma, inadequate or inappropriate treatments, increased bacterial load, excessive proteases such as MMP’s, elastase, inflammatory byproducts such as cytokines that may prolong the inflammatory processes and contribute to senescent, aberrant or quiescent cells. The wound healing phases (hemostasis, inflammatory, proliferative, and maturation) overlap but when the wound essentially gets “stuck” in the inflammatory phase and this “chronic state” develops it can last from weeks to years. Regulation of the inflammatory phase is handled by the immune system. The innate immune cells including neutrophils, monocytes, and macrophages become altered and persist in the wound increasing inflammation which inhibits wound closure (Murray, West, & McGuiness, 2018).

Wound Bed Preparation & the Impact on Chronicity

Over the past decade, the research analyzing the cellular, biochemical, and molecular components of acute and chronic wounds has significantly expanded the knowledge base related to the complexities of normal wound healing, the pathophysiologic mechanisms of chronic wounds and has aided in the development of treatment options to correct or control the underlying pathology (Rahim, Saleha, Zhu, Huo, Basit, & Luiz, 2017). One of those approaches is the T.I.M.E. pneumonic that embraces the wound bed preparation model.  By spelling the word time, T. I. M. E., clinicians can go through the assessment process to keep the wound progressing, take a chronic or delayed wound and get it moving forward again, or keep a wound that will most likely not heal and prevent it from worsening (Ousey, Rogers, & Rippon, 2016). The T.I.M.E. wound management framework is a practical evidence-based approach especially for healthcare practitioners, when conducting wound assessments, identifying barriers to healing, and developing a comprehensive plan of care. It is also a reminder to treat the whole patient, not just the hole in the patient.  Getting chronic wounds back on track is the focus of the “E” of the pneumonic which stands for keeping the wound edge healthy and the progression of epithelial cells across the surface of the wound. Examples of modalities that assist with getting chronic wounds back on track are electrical stimulation, utilization of collagen dressings, growth factor therapy, and negative pressure wound therapy.

Electrical Stimulation

An article by Zhou, Ma, & Brogan (2015) discusses how direct electrical current flow exists in wounds and is constant until the wound re-epithelializes completely. This electrical field guides cell migration across the wound and also stimulates nerve sprouting. When this activity is disrupted healing stalls. The use of electrical stimulation therapy can aid in the restoration of this electrical field and stimulate vascular endothelial growth factor(VEGF) production by endothelial cells and osteoblasts. The authors also noted that electrical stimulation can also stimulate an increase in VEGF in patients with chronic ulcers and shorten the healing time. The percentage of wound closure is significantly higher in wounds treated with electrical stimulation compared to non-treated wounds respectively (Wang, Zhang, & Rouabhia, 2016).

Collagen Dressings

Using collagen dressings in stalled wounds aids in stimulating tissue growth. This is accomplished by helping the migration of cells including fibroblasts and keratinocytes in the wound. Collagen is a protein and encourages all phases of wound management including debridement, angiogenesis, and reepithelialization as it provides a natural scaffold or base for the growth of new tissue. They also act as a diversion for and chemically bind to matrix metalloproteinases (MMPs) which can impede wound healing thus leaving the body’s natural collagen available for wound healing (Morgan, 2018). Collagen dressings are indicated to boost the healing of partial and full thickness wounds including pressure injuries, foot ulcers, venous ulcers, minor burns, skin grafts and donor sites, and chronic wounds needing to be “jump-started” by reducing mediators of inflammation (Advanced Tissue, 2014). The only contraindications for collagen dressing use are third-degree burns, wounds that have formed eschar, or known allergies to bovine, porcine, or avian derived products. Collagen is available in many formats including sheets, pads, gels, powders and pastes and can be combined with other additives such as alginates and antimicrobials.

Growth Factors

Growth factors are substances secreted by the body to stimulate the growth and proliferation of cells responsible for wound healing. Growth factors therefore increase the number of wound healing cells thereby facilitating faster wound healing. It takes multiple cell types and numerous growth factors and cytokines to achieve the complex process of wound healing. In recent years the use of growth factor therapy has increased due to its efficacy in the clinical management of non-healing wounds such as pressure injuries, venous ulcers, and diabetic foot ulcers to name a few. Currently there are four growth factors and cytokines being used to aid wound healing including platelet derived growth factor (PDGF), vascular endothelial growth factor (VEGF), granulocyte-macrophage colony stimulating factor (GM-CSF), and basic fibroblast growth factor (bFGF).  When wounds fall into a non-healing state studies show that these growth factors have become deregulated causing impaired healing. However as a result of genetic engineering and biologic technology advancements the potential for the use of exogenous growth factors and cytokines may present as a possible solution to the problem of non-healing wounds (Barrientos, Brem, Stojadinovic, & Tomic-Canic, 2014).

PDGF or platelet derived growth factor is important to all phases of wound healing. It is released from  platelets upon injury and present in wound fluid. It helps initiate the inflammatory phase and enhances fibroblast proliferation in the proliferative phase which produces the extracellular matrix and granulation tissue formation.  In chronic wounds PDGF is decreased because of the impact of proteolytic environment of the chronic wound. This is the basis for the addition of recombinant human PDGF to chronic wounds to speed up wound closure (Barrientos, Brem, Stojadinovic, & Tomic-Canic, 2014).

Fibroblast growth factor or FGF is produced by keratinocytes, fobroblasts, endothelial cells, smooth muscle cells, chondrocytes, and mast cells (Barrientos, Brem, Stojadinovic, & Tomic-Canic, 2014).FGF is integral to wound healing as it plays a key role in granulation tissue formation, re-epithelialization, and remodeling. Its ability to aid in extracellular matrix formation increases keratinocyte mobility promoting the migration of fibroblasts. Studies have shown that recombinant human bFGF topically applied to pressure injuries increased angiogenesis and had better healing than those treated with recombinant human granulocyte macrophage colony stimulating factor or GM-CSF.

Key to angiogenesis is vascular endothelial growth factor or VEGF due to its early stimulation of endothelial cell migration and proliferation. This is very important to individuals with pure vascularity such as those with ischemic diabetic limbs. In addition to its topical use in patients with diabetes and ischemic extremities the intramuscular gene transfer of VEGF to individuals with ischemic ulcers or rest pain secondary to peripheral vascular disease demonstrated a significant decrease in rest pain (Barrientos, Brem, Stojadinovic, & Tomic-Canic, 2014).

Negative Pressure Wound Therapy

The emergence of negative pressure wound therapy or NPWT over the last few decades has essentially been a game changer in wound healing. These devices are commonly used in the treatment of pressure injuries, open abdominal wounds, sternal wounds, traumatic wounds, diabetic foot infections, second-degree burns and skin graft recipient sites. Negative pressure wound therapy is contraindicated in wounds with malignant tumor present, untreated fistulas, and untreated osteomyelitis (Huang, Leavitt, Bayer, & Orgill, 2014). Extreme caution should be exercised when used near vascular structures like large blood vessels or near the heart since erosion can occur resulting in hemorrhage.  A fistula can result from use near visceral organs due to erosion as well.

Negative pressure wound therapy is accomplished by using an airtight wound dressing attached to a pump to create a negative pressure environment in the wound. This promotes healing and aids in managing exudate in acute, chronic, and burn wounds. Variations of the therapy are being used to control edema, treat incisional wounds, and for the instillation of irrigation fluids and antibiotics (Huang, Leavitt, Bayer, & Orgill, 2014).  Variations in the type of contact material may allow for variations in the intended use and a customized outcome. For instance NPWT can be combined with other wound care products such as dermal scaffolds or allogenic or xenogenic materials and procedures to improve healing.

Conclusion

Getting back to basics and following the principles of wound care is important to quality outcomes. If a wound has not shown significant signs of improvement and fails to achieve sufficient healing within 4 weeks of treatment reassessment of the patient and a review of underlying factors must be considered. Following wound bed preparation principles is imperative to overcoming the factors and various pathologies that contribute to wound chronicity. Adopting and implementing advanced wound therapies is essential to taking a wound from a chronic state and getting it back on track to healing.

 

 

 

 

 

 

References

Advanced Tissue (2014). Advantages of using collagen in wound care. Retrieved from https://www.advancedtissue.com/advantages-using-collagen-wound-care/

Barrientos, S., Brem, H., Stojadinovic, O., & Tomic-Canic, M. (2014). Clinical application of growth factors and cytokines in wound healing. Wound Repair and Regeneration, 22(5), 569-578. doi:  10.1111/wrr.12205. Retrieved from

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4812574/

Bohn, G.A., Schultz, G.S., Liden, B.A., Designe, M.N., Lullove, E.J., Zilberman, I., Regan, M.B., Ostler, M., Edwards, K., Arvanitis, G.M., & Hartman, J.F. (2017). Proactive and early aggressive wound management: A shift in strategy developed by a consensus panel examining the current science, prevention, and management of acute and chronic wounds. Wounds, 29(11), S37-S42.

Huang, C., Leavitt, T., Bayer, L.R., & Orgill, D.P. (2014).  Effect of negative pressure wound therapy on wound healing. Current Problems in Surgery, 51(7), 301-331. doi: https://doi.org/10.1067/j.cpsurg.2014.04.001. Retrieved from

https://www.currprobsurg.com/article/S0011-3840(14)00084-7/fulltext

Mihai, M. M., Preda, M., Lungu, I., Gestal, M.C., Popa, M.I., & Holban, A.M. (2018). Nanocoatings for chronic wound repair – modulation of microbial colonization and biofilm formation. International Journal of Molecular Sciences, 19, (4), 1179-1199. Retrieved from http://www.mdpi.com/1422-0067/19/4/1179/htm

Morgan, N. (2018). What you need to know about collagen wound dressings. Wound Care Advisor. Retrieved from https://woundcareadvisor.com/what-you-need-to-know-about-collagen-wound-dressings/

Murray, R.Z., West, Z.E., & McGuiness, W. (2018). The multi factorial formation of chronic wounds. Wound Practice & Research: Journal of the Australian Wound Management Association, 26(1), 38-46. Retrieved from https://search.informit.com.au/documentSummary;dn=559466353034176;res=IELHEA

Ousey, K., Rogers, A.A., Rippon, M.G. (2016). Hydro-responsive wound dressings simplify T.I.M.E. wound management framework. British Journal of Community Nursing, 21(12), 29-39. Retrieved from https://doi.org/10.12968/bjcn.2016.21.Sup12.S39

Rahim, K., Saleha, S., Zhu, S., Huo, L., Basit, A., & Luiz, O. (2017). Bacterial contribution in chronicity of wounds. Microbial Ecology, 73(3), 710-721. Retrieved from https://link.springer.com/article/10.1007/s00248-016-0867-9

Zhou, K., Ma, Y., & Brogan, M.S. (2015). Chronic and non-healing wounds: The story of vascular endothelial growth factor. Science Direct: Medical Hypothesis. Retrieved from http://dx.doi.org/10.1016/j.mehy.2015.06.017

Wang, Y., Zhang, Z., & Rouabhia, M. (2016). Pulsed electrical stimulation benefits wound healing by activating skin fibroblasts through the TGFβ1/ERK/NF-kB axis. Researchgate, 1-10. doi: 10.1016/j.bbagen.2016.03.023. Retrieved from

July Practice Accelerator: Wound Bed Preparation Month White Paper: Clinical Concepts: The TIME Model of Wound Bed Preparation: A framework overview of the TIME model of wound bed preparation (tissue, infection/inflammation, moisture balance and edge of wound) including definitions and clinical strategy points.

#1 A review of chronic wound tissue types, and interventions to support wounds on a healing path based on the TIME principles of wound bed preparation.

Restoring the Wound Base: The Role of Tissue Management

Successful utilization of the TIME Model for wound management requires a working knowledge of chronic wound tissue types. Also 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.

Chronic wound tissue types

Viable

This describes vascular tissue with dynamic biologic activity.

Epithelium: This should be dry to touch and can appear white or light pink, it is comprised 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 either pale (poor perfusion), or dark red/ruddy (vascular congestion/stasis) or “bubbly”/friable (bleeds with very gentle contact), it is technically considered non-viable, as it will not support migrating epithelial cells. should this go under nonviable tissue or stay here?

Subcutaneous: This layer will typically appear as shiny yellow lumps (subcutaneous fat), as it is rincipally composed of adipose tissue and the plexus of blood vessels that supply the subdermal perfusion to the dermis.

Muscle: Muscle tissue appears dark red/burgundy with parallel striations and, when visible, the shiny and smooth fascial covering contribute 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/capillaries and veins): Most vascular structures large enough to see appear tubular in nature. Arteries are generally deeper in tissue, will visibly pulsate, and be deep red. Veins are more superficial, may appear purple/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.  Too much detail?

Nonviable

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 present with an stringy or fibrinous texture. Slough can be grey, 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 will be white and soft, it is technically considered nonviable tissue, as when the epithelium or granulation tissue is overhydrated due to prolonged exposure to excess moisture and proteases from chronic wound fluid, it loses its cellular structure.

Other: Structures such as necrotic tendon can be dark yellow or brown, and necrotic bone can be dull tan or grey.

Suture or graft….Too much detail?

Interventions based on the TIME model

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 nonviable tissue and stalled wound edges is the cornerstone of wound bed preparation. There are multiple debridement modalities, some of which are selective for nonviable tissue and some which are nonselective (viable tissue is removed as well, e.g. mechanical debridement with gauze sponges): Sharp (conservative or excisional/surgical), Mechanical, Autolytic, Enzymatic/Chemical, and Biologic.

Topical therapies: Dressings and other topical treatments including grafts and application of growth factors should be complimentary 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/Compression: These are both crucial modalities in the treatment plan for wounds with potential for vascular compromise and subsequent tissue death due to prolonged pressure or tissue edema resulting in poor perfusion. (added 6/3—Compression of edematous limbs can also decrease exudate, assisting with moisture management)

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 in order to support the growth of new tissue. Progression through the phases of Contamination, Colonization, Critical Colonization, Infection, and Sepsis can be stopped by debriding nonviable tissue, improving host factors such as nutrition, optimizing disease state (blood glucose and immunosuppression), selecting an ppropriate antimicrobial dressing, and prescribing targeted antibiotic therapy from sensitivities provided from quantitative tissue biopsy of healthy-appearing tissue.

Nutrition: Despite all other interventions being implemented and an otherwise impeccable treatment plan execution, wounds may lack the ability to form viable tissue secondary to 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 auto-destruction) and disorders of coagulopathy (excessive bleeding due to deficiency of coagulation factors) in patients with wounds may require atraumatic dressings. This can present a problem if the wound is excessively moist, as most nonadherent primary dressing layers also retain moisture.

…closing information needed?

 

#2 The pathophysiology of chronic wounds with discussion on the role of bioburden management and key mechanisms to manage wound infection

Controlling Bacterial Burden in Chronic Wounds

Bioburden in chronic wounds can be a principal contributor to inflammation, clinical wound infection, and further delayed wound healing. Clinically diagnosing infection in chronic wounds can be problematic, as most individuals susceptible to developing chronic wounds are subject to physiologic states which often blunt typical infectious responses in various ways. These responses include pain, erythema, febrile state, leukocytosis, edema and increased wound exudate, wound odor etc. For example, a patient with neuropathic ulcer and diabetes mellitus may not report pain, fever, or present with leukocytosis, but will have increased edema and wound exudate. A patient with an ischemic ulcer of PAD may report pain, erythema, fever and leukocytosis, but not have perfusion sufficient to produce edema or increased wound exudate. Understanding how to concurrently manage factors that can contribute to infection, assess for symptoms of wound infection, and implement interventions to prevent such infection is imperative. –sounds weird and I cant figure out what im trying to say lol

Each letter in the pneumonic of the TIME model represents a factor that contributes to the pathophysiology of the chronic wound. Let’s review how each factor contributes to wound bioburden (the problem) and the associated interventions that can assist with managing bioburden and addressing infection (the solution).

 

Tissue

Problem

Nonviable tissue must be eradicated while growth of healthy tissue is supported. Nonviable tissue is a breeding ground for bacteria, and its presence causes production of proinflammatory cytokines that damage proliferative cells such as fibroblasts and growth factors such as vascular endothelial growth factor (VEGF), which are responsible for collagen and vascular tissue formation respectively.

Solution

Debride nonviable tissue as needed and episodically to return wound to acute status.

Optimize nutrition to support healthy collagen growth.

Infection/Inflammation

Problem

Wounds become chronic due to perpetuation of inflammatory states due to a multitude of factors, including host factors (immunosuppression, malnutrition) and extrinsic factors such as bacterial burden and topical therapies. Depending on a combination of these factors and how they are managed at a given time in treatment, wounds can progress in both directions along the spectrum from contamination, colonization, critical colonization, infection, and sepsis.

Solution

Use topical therapies with protease inhibitors to decrease degradation of healthy tissue.

Administer systemic anti-inflammatories as appropriate.

Use topical antimicrobials judiciously in presence of clinical symptoms in response to wound bioburden; do not use as monotherapy when clinical infection is suspected, as true wound infections are near impossible to eradicate in this manner.

Obtain a culture should using literature validated processes such as qualitative tissue biopsy of healthy appearing tissue; if this is not possible, swab of wound exudate using a procedure such as the Levine technique is recommended.

Administer targeted antibiotic therapy using sensitivities from qualitative tissue biopsy; this is the gold standard for treating wound infection.

Treat with oral or IV antibiotics as required depending on severity and type of infection; collaborate with Infectious Disease professionals as needed for complicated infections.

Consider atypical wound etiology and workup/refer as necessary if wounds do not respond to treatment as expected.

Moisture

Problem

Moisture in excess causes maceration, which as we have noted previously is nonviable tissue; this perpetuates the cycle of nonviable tissue and its contribution to presence of bioburden. Also, lack of moisture delays or prevents epithelialization, as wound bed dehydration hampers keratinocyte migration

Solution

Apply topical therapies appropriate for managing the dynamic environment of wounds, such as hydrating dressings for lowly exudating wounds or specialty absorptive for wounds with copious exudate.

Control edema with NPWT and/or extremity compression to manage wound exudate and excessive moisture in edematous limbs with wounds.

*Clinicians should note that sharp increase in wound exudate may be an early indicator of impending infection.

Edge

Problem

Epithelialization in full thickness wounds beings when healthy granulation tissue is available for migrating keratinocytes and ends when keratinocytes from opposing wound edges meet. This phenomenon is known as contact inhibition. Unfortunately, this process also occurs when wound edges become stalled due to undermining or rolled wound edges (epibole) where epithelial cells meet and cellular signaling causes the body to “think” the edge wound is closed, but migration occurred in a shelf-like formation versus bridging across the wound bed. This can happen when there is insufficient viable tissue to support eplithialization, which is why reduction of bioburden to decrease subsequent tissue necrosis is crucial.

Solution

Surgical excision of the nonviable wound edge is recommended if the wound is not progressing despite addressing the remaining parts of the TIME model.

Even in the presence of viable tissue and appropriate treatment plan, stalled wound edges contribute to chronicity of the chronic wound, further increasing the likelihood of progression through the spectrum from contamination to infection.

Managing bioburden can prevent perpetuation of chronic inflammation related to presence of pathogens and subsequent wound infection. Implementing interventions to reduce bioburden is key to progression through the inflammatory phase into the proliferative phase of wound healing. For a summary of interventions complimentary to the TIME Model for Wound Bed Preparation, please review the previous practice accelerator installment.

 

 

Acute and Chronic Wounds – E-Book

By Ruth Bryant, Denise Nix

TIME model pdf, smith/nephew

Wound bed preparation in practice”

By EWMA

Wound Bed Preparation and the T.I.M.E. Model

First things first, before embarking on the journey of wound bed preparation the goals for wound care should be carefully considered. A realistic look at the goals and expectations from the perspective of the patient as well as the wound care team is the first step in developing and implementing the appropriate plan of care. Is the wound healable? This requires that the individual’s body can support the phases of wound healing in an expected time frame. Treatment should be aggressive to prevent any delay the healing process and result in the stalling of wound healing or the wound falling into a state of chronicity. Is maintenance the goal? If so then efforts should focus on keeping the wound from deteriorating by providing comprehensive wound care. Is hospice or palliative care the goal? If the wound is not expected to heal and the individual’s body can’t support the phases of wound healing within an expected time frame, then comfort measures are more important than a cure (Powers, Higham, Broussard, & Phillips, 2016). All parties should be on the same page with goals and objectives so in partnership they are working toward the best outcome for the individual.

T.I.M.E. Wound Management Model

T.I.M.E. is a pneumonic that embraces the wound bed preparation model.  By spelling the word time, T. I. M. E., the clinician can go through the assessment process to keep the wound progressing, take a chronic or delayed wound and get it moving forward again, or keep a wound that will most likely not heal and prevent it from worsening (Ousey, Rogers, & Rippon, 2016).  The “T” stands for tissue management, or removal of nonviable tissue, foreign material or debris from the wound bed. This can be accomplished by appropriate cleansing and debridement.  The “I” stands for management of inflammation and infection. The “M” stands for management of moisture imbalance including keeping the wound bed moist, preventing desiccation, or for management of too much moisture. The “E” stands for keeping the wound edge healthy and the progression of epithelial cells across the surface of the wound. The T.I.M.E. wound management framework is a practical approach especially for healthcare practitioners, when conducting wound assessments, identifying barriers to healing, and developing a comprehensive plan of care. It is also a reminder to treat the whole patient, not just the hole in the patient.

 

Cleansing

Appropriate cleansing is a vital part of wound bed preparation and involves the use of proper technique, appropriate and adequate amounts of solution and the correct equipment for completion of the procedure (McLain & Moore, 2015). Wound cleansing should be done prior to any dressing change and before any assessment.  Wound cleansing removes surface contaminants such as bioburden, debris and toxins from the wound bed (Sibbald, Elliott, Ayello, & Somayaji, 2016). There are several ways that this can be accomplished such as with a clean technique versus a sterile procedure.  The clinician should use enough fluid volume to remove any wound contaminates. The procedure should provide adequate cleansing while minimizing any chemical or mechanical (such as scrubbing) trauma, but aggressive enough to remove any foreign items so that wound infection can be prevented or wound healing be supported. Commercially available wound cleansing agents use surfactants which help to reduce surface tension and release debris from the wound bed. Some commercial cleansers have ingredients in them to help reduce surface bacteria and debris such as benzethonium chloride, polyhexamethylene biguanide or hypochlorous acid. Skin cleansers and soaps should only be used on intact skin, as they are not intended for use in the wound bed. Ingredients such as povidone-iodine, chlorhexidine, hydrogen peroxide, and acetic acid have been shown to interfere with fibroblast formation and epithelial growth.  Wound cleansing can be done with several solutions such as normal saline.  Solutions should be delivered with an irrigation pressure of 4 to 15 pounds per square inch (P. S. I.).  This level of P.S.I. can be delivered using a 35 milliliter syringe with a 19 gauge needle or angiocatheter attached, this will deliver approximately 8 P.S.I. Many commercial wound cleansers also deliver the appropriate P.S.I, usually with a trigger sprayer set on a stream setting, it is recommended to follow the manufacturer’s guidelines.  Saline “bullets” do not provide sufficient P. S. I. for adequate cleansing of the debris from the wound bed, nor is their enough volume to adequately irrigate.

T = Tissue and Debridement

The importance of debridement is to remove the necrotic tissue, such as eschar and slough; senescent or aberrent cells that although they cannot be seen, may harbor bacteria, increase the risk of infection, delay the healing process, impair macrophage function and physically splint the wound open (Ousey, Rogers, & Rippon, 2016).  Additionally, any foreign material that inhibits healing such as toxins, microbes, biofilms, bacteria, yeast or viruses, also substances such as dressing residue, animal hair or dander, suture material or any other types of debris should be removed. Until the wound bed is prepared and debrided the wound bed is not fully visible and appropriate assessment is not possible.  Also when debridement of a wound is contemplated a number of considerations must be taken into account including the condition of the patient, the cost of the products, the therapeutic effectiveness, the efficiency of the procedure, and resources available.  There are also many ways to debride a wound including sharp surgical and conservative sharp debridement, as well as mechanical, enzymatic, biological, and autolytic debridement. Matching the appropriate method to the patient’s overall needs is essential to achieving the best outcome.

I = Inflammation and Infection Control

Inflammation is a component of the healing process and it is important to remember that all wounds are contaminated with microorganisms.  These low levels of bacteria can actually stimulate wounds to repair themselves.  It is when the organisms abundantly increase in the wound bed that they delay the inflammatory phase of wound healing and can severely retard or prevent wound repair (Sibbald, Elliott, Ayello, & Somayaji, 2016). Understanding the difference in inflammation and infection is important since they can present very similarly with erythema, warmth, pain, and edema. To this point it is also very helpful to differentiate between contamination, colonization, and infection.

Wound contamination is the presence of nonreplicating bacteria.   The host controls the environment, healing is not impaired by these bacteria. When wound bed preparation is not achieved and wound management is not effective, then bacteria will begin to replicate.   If there is an increase in the number of bacteria, depending on the virulence of those bacteria, this process can begin to overwhelm the host. The concept of critical colonization was invented to describe the idea that bacteria might play a role in non-healing wounds that do not have any obvious signs and symptoms of infection.  In reality, this concept likely describes the presence of a biofilm.  When a wound is infected it now has the presence of replicating bacteria that are invading the tissue whether superficially or deep penetration.  Again the host response will show a local reaction or a systemic reaction and infection is a clinical diagnosis based on signs and symptoms not just the presence of bacteria or the number of bacteria in the wound (Spinchler, Hurwitz, Armstrong, & Lipsky, 2015).

M = Moisture Management

Although it can be a challenge it is important to have and maintain moisture balance in a wound bed, to enable cells such as fibroblasts and keratinocytes, along with growth factors and cytokines, to move across the wound bed. Too much moisture can lead to periwound maceration and skin breakdown, while too little moisture can impair cellular activities and desiccation promotes necrotic tissue formation, which results in poor wound healing.  Early studies on blisters showed that maintaining a moist wound healing environment provided continuous autolytic debridement, promotion of granulation tissue formation, faster healing, and less scarring, pain, and bioburden (Kahn, 2017).

A moist wound environment is maintained primarily by appropriate dressings, with occlusive, semi-occlusive, absorptive, hydrating and hemostatic characteristics, depending on the surface exudate and the need for moisture balance in the wound bed. Transparent films, hydrogels, hydrocolloids, foams, alginates and gelling fibers and superabsorbent polymers will aid in maintaining the delicate balance needed for a moist wound healing environment (Dabiri, Damstetter, & Phillips, 2016).

Transparent films are used for dry to moist wounds, they provide a waterproof, bacterial barrier, they are 100% adhesive, so why they are not recommended for skin tears, they are not occlusive as they have the ability to transfer moisture vapor.  They are indicated for prevention or as a primary or secondary dressing. These dressings can be left in place up to seven days. They come with and without antimicrobial features, and the moisture level is appropriate if the drainage stays within the confines of the dressing.

Hydrogels are water based products that come in amorphous, or sheets versions.  One of the features of hydrogel dressings is their ability to donate moisture to a relatively dry wound.  The gel sheets may have features that allow them to either donate or absorb varying degrees of moisture.  These dressings can contain different ingredients including antimicrobial silver, are indicated for either partial or full thickness wounds, and are excellent for use when gentle adhesion is required. Depending on the viscosity of the gel, they can be worn for up to seven days.

Hydrocolloid dressings are indicated for dry to moderately draining wounds and are 100% adhesive.  They provide a waterproof bacterial barrier, come in occlusive or semi-occlusive dressings, and are indicated for prevention on at risk areas, partial thickness, or shallow full thickness wounds.  These dressings can be left in place for up to seven days, however they should be used with caution in immunocompromised patients or on those at risk for skin tears.

Foam dressings are designed for use with minimal to heavily draining partial or full thickness wounds, or as a preventative measure on high risk areas for pressure or shear. These dressings are available with and without antimicrobial properties and may help to prevent hypergranulation tissue formation. Foam dressings can be left in place up to seven days or changed sooner based on “strike through” or visible saturation. They can be used alone as a primary dressing or as a secondary dressing in combination with alginates, gelling fibers, or other primary dressing types. This may enhance wear time and decrease the necessity for more frequent dressing changes.

Alginates and gelling fibers are non-woven, non-adhesive pads, ribbons and ropes composed of natural polysaccharide fibers derived from seaweed, carboxymethylcellulose, and chitosans . They are designed to manage moderate to heavy drainage.  These dressings form a moist gel through a process of ion exchange. They also come with or without antimicrobial properties and can be left in place for up to seven days.   Frequency of dressing change is determined by strike through on the secondary dressing, and if used in combination with foams the wear time may be increased. Alginates and gelling fibers are indicated for all types of partial and full thickness wounds including surgical wounds.  However if there is concern about retrieving the dressing from a cavity, tunnel, or dead space do no place in the wound bed. Alginates should not be used with hydrogels.

Another option for addressing moisture balance is the super absorbent polymer dressing category recommended for moderate to heavily draining wounds.  They are multi-layer non-adherent wound covers combined with highly absorptive polymers that act as a super absorbent core. These polymers lock away exudate by converting it into a gel. By locking excess moisture away from the wound bed it helps to protect the periwound skin from maceration.  Some versions of absorbent dressings vertically wick the fluid through the dressing into the outer dressing. They are indicated for all types of partial and full thickness wounds and may be worn for up to seven days.

E = Edge

After providing and addressing appropriate wound bed preparation, including debridement, infection, inflammation and moisture balance, and wound repair and healing is stalled with no progress made within 2 to 4 weeks, advanced topical treatments may be considered when the epithelium fails to migrate. Several edge-environment topical treatments and therapies support the addition of missing components to include collagen, growth factors, fibroblasts, epithelial cells or matrix components. Biomaterials and wound healing agents, such as collagen and growth factors, target specific defects in the chronic wound environment. Considerable evidence indicates that collagen-based dressings may be capable of stimulating healing by manipulating wound biochemistry. Collagen dressings are available as gels, particles, powders and sheets derived from animal sources (Yun, Samad, & Milica, 2017).
T.I.M.E Helps Heal Wounds

Understanding the importance of appropriate wound bed preparation is a key component in achieving positive wound outcomes.  T.I.M.E should be understood, not just as an acronym but as guidance to best practice in wound management.  Utilizing each component clinicians are able to choose the appropriate products and therapies to yield the best and most cost effective outcome based on the goals and objectives agreed upon by the patient and healthcare provider alike.

References

Dabiri, G., Damstetter, E., & Phillips, T. (2016). Choosing a wound dressing based on common wound characteristicsAdvances in Wound Care, 5(1), 32-41. Retrieved from https://doi.org/10.1089/wound.2014.0586

Kahn, S. (2017). Highlights from the advanced wound healing stream at the LINK Congress. British Journal of Nursing, 26(20), 34-35. Retrieved from https://www.magonlinelibrary.com/doi/abs/10.12968/bjon.2017.26.Sup20.S34?journalCode=bjon

McLain, N.E.M., Moore, Z.E.H. (2015). Wound cleansing for treating venous leg ulcers.  Cochrane Database of Systematic Reviews, 4(1). Art. No.: CD011675. DOI: 10.1002/14651858.CD011675. Retrieved from http://cochranelibrary-wiley.com/enhanced/exportCitation/doi/10.1002/14651858.CD011675

Ousey, K., Rogers, A.A., Rippon, M.G. (2016). Hydro-responsive wound dressings simplify T.I.M.E. wound management framework. British Journal of Community Nursing, 21(12), 29-39. Retrieved from https://doi.org/10.12968/bjcn.2016.21.Sup12.S39

Powers, J.G., Higham, C., Broussard, K., & Phillips, T. (2016). Wound healing and treating wounds: Chronic wound care and management.  Journal of the American Academy of Dermatology, 74(4), 607-625. Retrieved from https://www.jaad.org/article/S0190-9622(15)02183-0/pdf

Sibbald, R.G., Elliott, J.A., Ayello, E.A., & Somayaji, R. (2016). Optimizing the moisture management tightrope with wound bed preparation. Wound Healing Southern Africa, 9(1), 9-15. Retrieved https://journals.co.za/content/mp_whsa/9/1/EJC190662

Spinchler, A., Hurwitz, B.L., Armstrong, D.G., & Lipsky, B.A. (2015). Microbiology of diabetic foot infections: from Louis Pasteur to ‘crime scene investigation’. BioMed Central, 13(2), 1-13. Retrieved from https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-014-0232-0

Yun, X., Samad, A., & Milica, R. (2017). Biochemical and biophysical cues in matrix design for chronic and diabetic wound treatment. Tissue Engineering Part B: Reviews, 23(1), 9-26. Retrieved from https://www.liebertpub.com/toc/teb/23/1

The TIME Model of Wound Bed Preparation

 

Introduction

 

Effective wound bed preparation is a cornerstone of modern wound care, helping to promote rapid healing and minimize the risk of complications such as infection. This makes it extremely important that health care professionals follow wound bed preparation best practices. [1] [2] However, in a fast paced clinical environment, it can be difficult to identify wound needs and implement the most effective wound care plan. In order to ensure that wound bed conditions are optimized to encourage healing, it is important that health care professionals have an effective framework to make decisions and ensure they are adhering to best practices.

The TIME Model of Wound Bed Preparation

The TIME model of wound bed preparation was developed to give clinicians a framework to assess and manage wounds more effectively. It allows health care professionals to better understand patient wounds and implement a plan for wound bed preparation based on modern best practices. This can help improve outcomes for patients by allowing health care professionals to address all critical components of wound care in a systematic way. [2]

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The Importance of Wound Bed Preparation

Wound bed preparation can play a critical role in the care of both chronic and acute wounds. Taking steps to manage tissue, control infection, reduce inflammation and create an optimally moist healing environment will help promote rapid wound healing and reduce the risk of complications. [2]

 

What is Wound Bed Preparation?

Wounds healing relies on many interworking processes and can be impeded by even small imbalances. Traditional wound care has attempted to address each of these potential problems individually without attempting to treat the wound as an organized system.

Wound bed preparation is a holistic and structured approach to wound care. It emphasizes the importance of creating an optimal healing environment by eliminating potential obstacles to healing. It recognizes that each wound will have unique needs, but that there are commonalities that can help improve the effectiveness of external treatments or the body’s own natural healing processes. [2]

 

The Benefits of Wound Bed Preparation

Although originally developed to help augment advanced therapies for chronic wounds, wound bed preparation can provide benefits for nearly all wounds. By minimizing the presence of pathogens, optimizing moisture, controlling exudate and managing tissue, wound bed preparation can improve healing rates and minimize the risk of infection.

In order for health care professionals to most effectively care for wounded patients, it is critical that they understand the underlying causes of delayed wound healing and take steps to promote the body’s wound healing process. This can help ensure that wounds heal quickly and with lower risk of complication. [1]  [2]

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The TIME Model of Wound Bed Preparation

 

The TIME model is a tool for health care professionals that allows them to rapidly implement a wound bed preparation plan. The goal of the TIME model is to create the optimal wound healing environment for each wound. This means ensuring that the wound bed is stable and well-vascularized and that exudate is managed. To this end, the TIME Model provides a structured framework to help health care professionals more effectively apply best practices to the needs of the individual wound. [1] [2]

The Four Principles of TIME Wound Bed Preparation

 

The TIME acronym is derived from its four primary components: Tissue management, infection or inflamation, moisture balance and edge of wound. Assessing and managing each of these elements is critical to comprehensive wound care.

Tissue Management

Nonviable tissue can impede healing and obstruct inspection of the underlying wound. This makes it important that all necrotic tissue, devitalized tissue and bacteria be removed from the wound area. This helps ensure the wound has a healthy base for healing and restores the functionality of extracellular matrix proteins. [2]

The first step to tissue management is thorough debridement of the wound area. This can be accomplished with mechanical, surgical, autolytic or biological methods, depending on the condition of the wound and patient. In cases where a patient’s life or health may be threatened, surgical debridement is often advised, as it is the fastest means of removing necrotic tissue. [1] [2]

Infection and Inflammation Control

 

Bacterial colonies can impede wound healing and threaten the health of the patient. It is important for wound bed preparation to manage bacterial levels in order to prevent infection, improve patient comfort and reduce the risk of complication. Health care professionals should examine patients for signs of bacterial colonization such as tissue damage, odour, fever, inflammation and exudate.

If infection is suspected, wounds should be cleaned with an antiseptic solution and treated with an antimicrobial dressing. This can help reduce the bacterial load in the wound area. It is also important to regularly debride the wound area to reduce the presence of biofilms which may be resistant to topical antibiotics. [2]

Moisture Balance

 

Wound moisture is a critical component of the wound healing process. A moist wound environment can promote rapid healing, aid cellular activities and prevent eschar formation. However excessive moisture can cause maceration of the wound area and impede healing. It is important that healthcare professionals assess and actively manage the wound’s moisture balance in order to improve patient outcomes. [1]

A key component of maintaining the optimal moisture balance in the wound is exudate management. Exudate is produced by the body to aid wound healing. However, in many cases the wound will produce too much or too little exudate, creating suboptimal conditions. Dry wounds should be treated with an occlusive or semi-occlusive dressing to help create a moist environment. Excessively moist wounds should be treated with a dressing that absorbs and traps exudate, such as a foam dressing. [2]

Edge Management

 

In a properly healing wound, the epidermal margins should contract, reducing the size of the wound. If this process is not occuring or occurring too slowly, it is important for healthcare professionals to attempt to identify potential problems that may be preventing the wound from healing. In many cases, these causes may be related to other elements of the TIME model. Dry or excessively moist wound edges, infection, necrotic tissue and biofilms can all prevent  the epidermal margin from migrating. Performing regular assessments of the wound area and the advancement of wound edges can help identify these issues early on. [2]

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Conclusion

 

Wound management practices have advanced significantly in recent years. It is critical that all health care professionals caring for wounded patients understand new best practices for wound bed preparation and implement them in their work. The TIME model provides an effective foundation for wound bed preparation and chronic wound care. It allows health care professionals to focus on the four most important components of wound healing while taking a comprehensive view of the wound and providing an effective foundation for rapid healing. This will help ensure that obstacles to healing are removed and that patients have the best possible outcomes.

 

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References:

[1] Falanga V (2000) Classifications for wound bed preparation and stimulation of chronic wounds. Wound Repair Regen 8: 347–52

[2] Halim, A. S., T. L. Khoo, and A. Z. Mat Saad. “Wound Bed Preparation from a Clinical Perspective.” Indian Journal of Plastic Surgery : Official Publication of the Association of Plastic Surgeons of India 45.2 (2012): 193–202. PMC. Web. 22 May 2018.

Quiz

  1. The presence of which substance contributes to the chronicity of wounds? low protease levels, proliferation of fibroblasts, low bioburden, (proinflammatory cytokines)
  2.  Which dressing can stimulate tissue growth in chronic wounds and comes in several forms including powders, gels, and sheets? Hydrogel, foam, alginate, (collagen)
  3. Electrical stimulation therapy for chronic wounds causes increase in production which of the following?  proteases, leukocytes, keratinocytes (VEGF)
  4. During wound assessment, a small, non-pulsatile, smooth tubular structure which is purple/blue in color is noted arising from the subcutaneous fat. Which should be documented? Artery, suture, drain (vein).
  5. Macerated tissue is devitalized and is appropriate to debride or remove. (true) false
  6. Which of the following tissues is poorly vascularized and relies on surrounding vascular supply and tissue for perfusion? Granulation, muscle, bone (tendon)
  7. Which of the following values is appropriate for wound cleansing, i.e. adequate for removal of debris but safe for viable tissue? 3, 18, 25, (12)
  8. Which of the following substances is non-cytotoxic and may be safely used as a wound cleansing solution? Chlorhexidine, acetic acid, iodine (normal saline)
  9. A hydrocolloid dressing is most appropriate for which of the following wounds: a wound with unstable eschar, a full thickness granulating wound with large exudate, an unstageable pressure ulcer, (partial thickness pressure ulcer).
  10. Which primary dressing is most appropriate for wounds with large exudate? Hydrocolloid, hydrogel, transparent film (foam).
  11. NPWT is an appropriate advanced wound healing modality for which of the following wounds? Diabetic foot ulcer with confirmed osteomyelitis in which antibiotic therapy has not started, abdominal wound healing by secondary intention with a potential unexplored enterocutaneous fistula, an atypical wound of undiagnosed etiology pending pathology results, a full thickness wound with significant depth and high exudate levels
  12. Which of the following is considered a contraindication to topical application of growth factors? Immunocompromised state, full thickness wound, ischemic wound, malignancy
  13. Which of the following methods is considered the gold standard for obtaining tissue for culture from a chronic wound? Swab of exudate wound surface immediately after dressing removal, excision of devitalized tissue from wound bed, collecting debrided tissue from curette for specimen (excision of healthy-appearing tissue after wound is cleansed)


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