Wound Bed Preparation

Without a healthy wound bed, most wound care products are ineffective. In order to create a healthy wound bed, there are five steps required. The first three steps in wound bed preparation are the restoration of the bacterial balance, the elimination of nonviable tissue, and providing a moist environment/maintaining moisture balance.

 

The fourth step is what we are going to focus on right now–the correction of cellular dysfunction. (The final step is the restoration of biochemical balance, which we will discuss in the final post in this series.)

 

Cells play a key role in wound healing

Cells play a key role in angiogenesis (new blood vessel formation), as well as adhesion, migration, proliferation, and capillary bed formation. Keratinocytes are key cells involved in restoring the epidermal skin layer. In chronic wounds, these keratinocytes don’t lose their nuclei, thus they are incapable of normal cellular migration over the wound bed. (On the flip side, sometimes hyperproliferation of keratinocytes occurs, which is when the cells reproduce rampantly, resulting in a thick layer of cells at the wound margin.)

 

What happens to the wound environment in chronic wounds?

 

In chronic wounds, the environment is typically proinflammatory and full of high levels of cytokines and matrix metalloproteinases. In addition, this proinflammatory environment is lacking the tissue inhibitors of metalloproteinases. This out-of-balance state impairs the normal progression of wound healing and closure.

 

Chronic wounds are slow to heal, thanks to cells that become senescent (think lazy, old, unresponsive, unable to divide). When cells are senescent, they are also unresponsive to cytokines (protein messengers) and growth factors. Because these cells are unresponsive, chronic wounds are often inflamed, slow to close, and secrete excessive wound fluid, all of which in turn results in cellular senescence. When wound edge migration is slow or nonexistent, it stops the normal programmed cellular death within fibroblasts and keratinocytes. In other words, it’s a vicious cycle.

 

Systemic factors often exacerbate chronic wounds

Often, chronic wounds are exacerbated by underlying patient physiological issues, including diabetes, vascular insufficiency, ischemia, and nutritional deficiencies. When cells are unresponsive, the use of topical growth factors is often unsuccessful, as the underlying cellular dysfunction is what needs to be addressed.

 

The extracellular matrix plays a role in wound healing

The extracellular matrix (ECM), a structure that surrounds and supports cells, contains specialized proteins and molecular signals that are used to control the cell’s shape, migration, proliferation, differentiation, and overall survival.

 

Collagen is a component of the ECM, because it’s an important connective protein and structural component within cells. Collagen helps with clotting factors, promoting granulation and epithelialization, and forming a stronger tissue base for remodeling. Collagen is also a key component in products used for wound healing, as it assists in cell differentiation, cell behavior, cell migration, proliferation, and synthesis of a number of proteins, including collagen itself.

 

Wound dressings can promote healing in chronic wounds

Recent research has indicated the use of collagen can stimulate proliferation, migration, and the synthesis of new proteins in a chronic wound, and that adding collagen (or specifically configured denatured collagen) to wound dressings can target the nonadvancing wound edge and help promote wound closure.

 

Such a dressing should absorb exudate, be non-adherent to the wound bed, act as a depot for cells and proteins that help in wound closure, and contain topical antibacterial agents to maintain bacterial balance. To learn more about advanced wound products that can assist in wound bed preperation, consider taking one of the courses offered by WoundEducators.com

 

Register today and begin an exciting career as a certified wound specialist.

 

Sources

Elizabeth A. Ayello, PhD, RN, ACNS-BC, ETN, FAPWCA, FAAN (2009). The TIME Principles of Wound Bed Preparation. Retrieved April 15 from www.woundcarejournal.com.

 

Frank DiCosmo, PhD (2009). Edge Effect: The Role of Collagen in Wound Healing. Retrieved April 17 from www.woundcarejournal.com.

 

Chuck Gokoo, MD, CMO CWS, FACCWSa (2009). A Primer on Wound Bed Preparation. Journal of the American College of Certified Wound Specialists. 1, 35–39.

 

Kathryn Vowden RGN, DPSN(TV) & Peter Vowden MD, FRCS (2002). Wound Bed Preparation. Retrieved April 14 from www.worldwidewounds.com.

 

As previously discussed, a healthy wound bed lays the foundation for wound care product effectiveness. The first two steps in wound bed preparation are the restoration of the bacterial balance, and the elimination of nonviable tissue.

 The third step is providing a moist environment and maintaining moisture balance. (The fourth and fifth steps are the correction of cellular dysfunction, and the restoration of biochemical balance, respectively, which we will discuss in the next two posts.)

 

How does a moist wound bed facilitate healing?

A moist wound bed facilitates healing in many ways.  Studies show that a moist wound heals three to five times faster than a dry wound. There are many reasons for this: First, by preventing scab or crust formation over the wound bed, a moist wound environment eliminates the energy and time that would have been required for the body to breakdown these materials.  Keratinocyte travel time and distance across the wound surface are greatly reduced, as the cells are able to literally swim across the moist wound bed rather than burrow down beneath the dry tissue. A moist environment also traps enzymes within the wound bed, facilitating autolytic debridement. And lastly, a moist wound environment preserves growth factors within the wound fluid, and increases fibroblast proliferation and collagen synthesis.

Why is it important to maintain moisture balance?

It is important to maintain the proper moisture balance within a wound because, while a moist wound bed facilitates healing, a wound that is too wet can actually delay healing. For example, if a wound is too wet, the wound fluid will not only pool on the wound surface, but also flow onto the intact periwound causing maceration.  Excessive moisture may stop the healing process, slowing down or even blocking the proliferation of key cells in the wound healing process such as keratinocytes, fibroblasts and endothelial cells. If left unchecked, exudate can damage the surrounding healthy skin, as well as play host to bacteria.

How can wound moisture be managed?

Wound moisture can be managed directly with the use of absorbent dressings (the wound and surrounding skin should be kept moist but not saturated, and the use of absorptive dressings that have the ability to wick up and lock in moisture to prevent periwound maceration are best), compression and/or elevation, and Topical Negative Pressure (via devises such as the VAC - Vacuum Assisted Closure).

Indirectly, exudate can be managed via the control of infection or bacterial load, control of edema by systemic therapy, and use of immunosuppression or steroids to control inflammatory exudate from wounds (such as pyoderma gangrenousum, vasculitic or rheumatoid ulcers).

Why is dressing selection so important?

A moist wound environment enhances wound healing, so the dressing you select must assist with obtaining and maintaining this type of environment. This process begins with understanding the major dressing categories and indications and contraindications for each. 

To learn more about evidence based wound management and dressing selection register for our exiting and interactive wound management training program at www.woundeducators.com .

Sources
Elizabeth A. Ayello, PhD, RN, ACNS-BC, ETN, FAPWCA, FAAN (2009). The TIME Principles of Wound Bed Preparation. Retrieved April 15 from www.woundcarejournal.com.

Mark Chariker, MD (2009). Moisture Balance: Exploring Options in Negative Pressure Wound Therapy. Retrieved April 16 from www.woundcarejournal.com.

Chuck Gokoo, MD, CMO CWS, FACCWSa (2009). A Primer on Wound Bed Preparation. Journal of the American College of Certified Wound Specialists. 1, 35–39.

Betsy Meyers (2007). Wound Management; Principles and Practice. Upper Saddle River, Prentice Hall, PA.

Kathryn Vowden RGN, DPSN(TV) & Peter Vowden MD, FRCS (2002). Wound Bed Preparation. Retrieved April 14 from www.worldwidewounds.com.

We’ve already discussed the importance of a healthy wound bed, which lays the foundation for wound care product effectiveness. And we’ve covered the first step in wound bed preparation, otherwise known as the restoration of the bacterial balance. 

 

The next step in wound bed preparation is the elimination of nonviable tissue, a process known as wound debridement.

 

Why is debridement necessary?

Nonviable tissue is often necrotic and includes both eschar (dried-out tissue, forming a thick, leathery texture) and slough (yellow and fibrinous necrotic tissue). Removal of necrotic tissue, also known as debridement, is necessary in order to address the bioburden levels in the wound bed, stimulate growth factor activity, and eliminate senescent cells and hyperproliferative nonmigratory tissue. When addressed correctly, the former two help in healing, while the latter, when not addressed, impairs healing. The goal of debridement is to remove necrotic tissue while preserving the healthy tissue. Necrotic tissue can accumulate continually, a process that in turn requires continuous debridement.

Debridement methods

Debridement, which is technically the process of removing devitalized tissue and foreign material from a wound, can be achieved with a variety of techniques, including autolytic, biosurgery, enzymatic, mechanical, and surgical. Autolytic debridement gets rid of nonviable tissue by promoting the activities of phagocytic cells and endogenous enzymes. Biological/biosurgical debridement relies on the use of inoculating larvae that feed on the necrotic tissue in the wound. Enzymatic debridement uses exogenous agents such as proteolyic enzymes to digest necrotic tissue. Mechanical debridement utilizes gauze, which is allowed to dry on the wound and then removed (with the dead tissue adhered to the material). Hydrotherapy is also a type of mechanical debridement. Surgical debridement is just how it sounds, removing the necrotic tissue with a sharp instrument, or via ultrasound or hydrosurgery.

Determining the best debridement method

The type of debridement used depends on the patient’s overall condition and their individual treatment plan, as well as the size and position of the wound, wound etiology, the wound bed tissue involved, and moisture levels. Also taken into account are the patient’s pain tolerance, and the time available for the procedure. With chronic wounds, debridement is often conducted over a number of weeks and requires more than one method.

 

Wound care management is undergoing rapid changes in which new information becomes available constantly. At wound educators.com, we are committed to providing you with the latest, most up-to-date evidence-based knowledge available.

If you are interested in becoming a certified wound care specialist, visit www.woundeducators.com to learn how easy it is to take your career to the next level.

 

Elizabeth A. Ayello, PhD, RN, ACNS-BC, ETN, FAPWCA, FAAN (2009). The TIME Principles of Wound Bed Preparation. Retrieved April 15 from www.woundcarejournal.com.

 

Chuck Gokoo, MD, CMO CWS, FACCWSa (2009). A Primer on Wound Bed Preparation. Journal of the American College of Certified Wound Specialists. 1, 35–39.

 

Cathy Thomas Hess, BSN, RN, CWOCN (2008). Meeting the Goal: Wound Bed Preparation. Advances in Skin & Wound Care (www.woundcarejournal.com). Vol 21, No. 7, Page 344.

 

Kathryn Vowden RGN, DPSN(TV) & Peter Vowden MD, FRCS (2002). Wound Bed Preparation. Retrieved April 14 from www.worldwidewounds.com.

Without a healthy wound bed, wound care products aren’t effective. But before such products can do their job, the wound bed must be prepared. The goal is a well vascularised, stable wound bed.

In order to achieve that, bacterial balance must be restored. Wounds already contain many organisms, but it is up to the clinician to recognize when a wound has become infected by assessing the wound bed and periwound tissue. (Wound bed preparation also requires the elimination of nonviable tissue, providing a moist environment and maintaining moisture balance, correction of cellular dysfunction, and restoration of biochemical balance, all of which we will discuss in the next four posts.) 

What variables affect the bacterial burden of a wound?

Four variables affect the bacterial burden of a wound: the amount of necrotic tissue, the number of microorganisms present, the bacterial virulence, and the host resistance. Host resistance is often the culprit, and can occur with conditions such as vascular disease, edema, and diabetes, as well as lifestyle issues including alcohol abuse, poor nutritional status, smoking, and immunosuppression/use of steroid medications. 

What are the local signs of infection?

Local signs of infection often include redness, warmth, edema, induration, and pain. These signs are also seen during the inflammatory and proliferative phase of wound healing, which can make it difficult to determine if the wound is infected. When any of these signs, in addition to purulent drainage, foul odor, discolored or friable granulation tissue, or tissue breakdown, are seen together, it is safe to say that bacterial infection at the wound site should be ruled out. 

How is infection determined?

 Clinical infection is determined by bacteria load; a load greater than 100,000 bacteria per gram of tissue or milliliter of fluid indicates the presence of infection. Infection is determined via tissue or punch biopsy, or with a swab culture using the Levine method. The Levine method involves rotating a swab culture over a 1-cm2 area of the wound with sufficient pressure to extract fluid from within the wound tissue. The swab must be taken after the wound is cleaned with normal saline and taken from viable tissue (bacteria growing in the tissue), not from dead or devitalized tissue.

How is wound infection treated?

When infection is present, treatment can include topical and adjunctive therapies to reduce the bacterial load, contain the exudate, and improve the wound’s granulation tissue. Oral or intravenous antibiotics may also be used to decrease the bacterial load. Because topical antimicrobials can lead to resistance and treatments must be applied frequently, antimicrobial wound dressings such as those containing silver and cadexemor iodine are a good option to manage wound bioburden.

 

If you are interested in learning more about wound care, or wish to become certified as a wound care specialist, visit us online at woundeducators.com to explore your options. 

 

Sources:

Chuck Gokoo, MD, CMO CWS, FACCWSa (2009). A Primer on Wound Bed Preparation. Journal of the American College of Certified Wound Specialists. 1, 35–39.

 

Cathy Thomas Hess, BSN, RN, CWOCN (2008). Meeting the Goal: Wound Bed Preparation. Advances in Skin & Wound Care (www.woundcarejournal.com). Vol 21, No. 7, Page 344.

 

Harriett Loehne, PT, DPT, CWS, FACCWS (2009). Managing Bacterial Burden with Silver Dressings. Wound Care Journal (www.woundcarejournal.com).

 

Kathryn Vowden RGN, DPSN(TV) & Peter Vowden MD, FRCS (2002). Wound Bed Preparation. Retrieved April 14 from www.worldwidewounds.com.