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Wound Bed Preparation: What Works Best And When

Recognizing the challenges of wound bed preparation for chronic wounds that are continually evolving, these authors review common debridement techniques, keys to ensuring moisture balance and the importance of addressing wound bioburden. 

Before considering wound bed preparation, it is important to understand the local and systemic factors that play roles in the development of a wound. While that is not the objective of this article, one clearly needs to consider a patient’s vascular, nutritional and neurologic status.1 It goes without saying that clinicians also need to consider the etiology of the wound and its needs, whether it is a diabetic wound secondary to neuropathy, a venous stasis ulcer or any of the other more “common” etiologies that arise as well as those that we may consider “uncommon.”

Local factors such as neuropathy and peripheral vascular disease may require additional attention. When it comes to assessing the patient for neuropathy, one would use a 10 g Semmes-Weinstein monofilament to gauge protective sensation, a 128 Hz tuning fork for vibratory perception and the clinical exam to assess proprioception and reflexes. A subsequent diagnosis of peripheral neuropathy would require proper patient education, including the importance of daily inspection, to try to prevent the development of a wound.2 Wound bed perfusion must be sufficient in order for growth factor migration and wound healing. Appropriate screening for peripheral vascular disease via peripheral pulses, ankle brachial index (ABI) and toe pressures must occur and appropriate referral to a vascular surgeon to optimize blood flow is essential.

Removing pressure from a wound presents a particularly unique challenge in treating chronic wounds. Failure to offload allows for continued mechanical trauma and shearing forces, decreasing the healing potential of wounds.3-6 Clinicians must ensure proper offloading through the use of felted foam dressings, surgical shoes and total contact casts. We need to optimize all of these factors in order to allow for a wound to heal and “prepare” a wound for ultimate closure.7

Normal phases of wound healing in an acute wound consist of the hemostasis, inflammation, proliferation and remodeling phases. Complex interactions occur between growth factors, cell and matrix components that help to move a wound sequentially through each phase of healing. When a wound proceeds through a timely reparative process and results in the restoration of anatomic and functional integrity, we describe it as having undergone normal wound healing. Conversely, in abnormal wound healing, as one sees with chronic wounds, there is a disruption in these phases and wounds stall in the inflammatory phase, delaying or preventing healing.8 There are several factors that keep a chronic wound in a delayed healing state. These factors include repetitive trauma, local tissue ischemia, necrotic tissue, heavy bacterial burden and tissue breakdown.

Diabetic foot ulcerations are characterized by reduced growth factor production as well as decreased or impaired angiogenic response, macrophage function, collagen accumulation, and epidermal barrier function. These factors keep a wound in a chronic inflammatory state. In the chronic wound state, there are an increased number of activated inflammatory cells that secrete the inflammatory cytokines tumor necrosis factor alpha (TNF-a) and interleukin 1-beta (IL1-b), which increase the production of matrix metalloproteinases (MMPs). Excessive activity of MMP 2 and MMP 9 degrades growth factors and their target cell receptors. They also degrade the extracellular matrix, impairing cell migration and connective tissue deposition, preventing the wound from entering the proliferative phase, and continuing the vicious cycle of the chronic wound.9  

Reviewing The Different Forms Of Debridement
Historically, clinicians have relied solely on debridement for wound bed preparation. However, wound bed preparation is based upon the foundation of debridement, moisture balance and establishing and maintaining bacterial balance. The goals of debridement are to remove any foreign body and devitalized tissue. Necrotic tissue often masks signs of local infection so removal of necrotic tissues allows for an accurate visualization and assessment of a wound bed. Local stimulation also increases platelet and endogenous growth factor migration into the wound.  

Through debridement, you remove senescent fibroblasts, leaving younger and more viable cells. By decreasing the bacterial load, you are removing the source of damaging enzymes that inhibit the formation of granulation tissue and reepithelialization. During debridement, one must pay attention to remove any hyperproliferative non-migratory wound edge that slows healing. You must eliminate any undermining and explore any tendon sheath or tunneling that may reveal an infection that may tract proximally and distally. It is important to identify any bone exposure complicated by underlying osteomyelitis, which will require extended systemic antibiotic use or surgical management.

There are four techniques of debridement with appropriate clinical indications for each method.

Surgical debridement is the fastest means. It is the method of choice in life- or limb-threatening infections with necrotic eschar or gangrene. Sharp surgical debridement is often non-selective as one may inadvertently remove healthy tissue as well as necrotic tissue. Ultrasonic debridement can be an alternative to your standard sharp debridement. There are many commercial  devices available and ultrasonic debridement has shown clinical efficacy for the removal of biofilms, preparing a wound bed for a split thickness skin graft and for diabetic foot ulcerations.10,11

Mechanical debridement through the conventional wet to dry dressing has been a technique wound care clinicians have used for decades. By manually removing a dry dressing after it has adhered to the surface of the wound, you remove any adherent fibrous tissue. While this dressing plays a role in minimally sloughy necrotic ulcerations, the wet to dry dressing often causes pain and bleeding to the patient. It can be nonselective and one may inadvertently remove any healing epithelium.

Autolytic debridement uses the body’s own enzymes and moisture to rehydrate, soften and liquefy hard eschar and slough. This is very selective for necrotic tissue and one can augment it with the use of occlusive or semi-occlusive dressings such as hydrogels, hydrocolloids and transparent films.

Enzymatic debridement utilizes chemical enzymes like collagenase and papain-urea to break down necrotic debris. Clinicians often employ enzymatic debridement for non-surgical patients with highly necrotic wounds. With proper application, there is minimal to no damage to healthy tissues.

You must consider the patient’s overall condition and goals for care when selecting the method of debridement. For example, in the presence of an ischemic ulceration, prior to aggressive wound debridement, one must ensure that blood flow has been restored in order to minimize damage to surrounding healthy tissue.

In addition to the aforementioned types of debridement, there are now dressings available that may help prepare a wound for ultimate closure. These dressings and solutions include silver-, honey- or cadexomer iodine-based dressings, hydrogel, Prontosan (B Braun) and collagen dressings. These dressings may not only create a moist wound environment but also interact with wound components to further enhance wound healing. These dressings are in contrast to “passive” dressings, such as wet or moist to dry gauze dressings, that clinicians used in the past and serve more of a protective function.

Pertinent Insights On Maintaining Moisture Balance
Moisture balance is an important aspect of wound bed preparation. In order to attain moisture balance, one should create and maintain a warm, moist bed, and avoid excessive periwound moisture that would cause surrounding skin maceration. Achieving moisture balance is important to enhance the optimal effects of growth factors and cytokines within the wound to stimulate proliferating cells such as keratinocytes, endothelial cells and fibroblasts. Wound exudate production is a normal part of the inflammatory phase of wound healing as increased fluid production can help facilitate the cleansing of a wound surface. The production of serous fluid occurs as a normal response to vasodilation due to inflammatory markers such as bradykinin and serotonin early in the inflammatory phase of wound healing. However, in the chronic wound,  which may be stuck in the inflammatory phase, or infected wounds, the type or amount of wound exudate may change.   

In under-hydrated wounds, a lack of moisture balance causes an inhibition of cellular activity and an eschar will form, preventing the migration of growth factors. If the moisture balance turns toward an overhydrated wound, this causes maceration of tissue edges, which decreases the defensive barrier against microbial invasion. Over-hydrated wounds also have excessive enzymes that break down and damage the extracellular matrix. Increased exudate can be the cause of edema, increased bacterial colonization and breakdown of necrotic tissue.

In particular for venous ulcerations or wounds with significant lower extremity edema, clinicians may employ a combination of compression therapy and limb elevation to facilitate the local reduction of edema. Medical management can also be effective for addressing lower extremity edema. Physicians can significantly reduce lower extremity edema with compression therapy, limb elevation and medical fluid balance.

How To Address Wound Bioburden
Debridement of tissue can help remove the bacterial bioburden that leads to excessive exudate. You must determine the amount of exudate in order to choose a topical dressing capable of absorbing the exudate. As the amount of exudate increases, alginates and foams can be good choices.

A critical factor in preparing the wound bed is considering the nature and extent of the bacterial bioburden to ensure it will not interfere with wound healing. We can describe bioburden as the number of contaminating microbes that compete with normal cells for the available oxygen and nutrients. Assessment of bioburden is based on host resistance, wound characteristics and wound culturing. Bacteria levels of 106 are generally considered to be an infection.12

All chronic wounds exist along a bacterial continuum that ranges from contamination and colonization to critical colonization and infection. Contamination refers to the presence of non-replicating bacteria. It is a normal condition in any chronic wound and will not impair healing. Colonization is the presence of replicating bacteria without a host reaction. It is well accepted that chronic wounds are contaminated and colonized.

Critically colonized wounds are those with a change in the local signs of the wound. These include changes in wound bed color, friable granulation tissue, abnormal odor or an increase in serous exudate. Routine wound debridement is an important adjunct in critically colonized wounds, not only to reduce the bacterial burden but also to reduce biofilm formation, which tends to be more resistant to typical wound care.

The last stage of bacterial bioburden is local and systemic infection, which occurs when bacteria have invaded the tissue, are multiplying and are causing a systemic host reaction and impairing healing. Once an infection is established, all healing potential has halted and a wound is stuck in the inflammatory phase. Fibroblasts in chronically infected wounds are not only reduced in number but have reduced metabolic activity and form weak collagen. Clinical characterization of infection appears as unhealthy granulation tissue, abnormal odor, increased serous exudate, increased pain or change in the color of the wound bed. Systemic signs of infection include fever, chills, tachycardia, nausea, vomiting and changes in mental status. While traditional signs and symptoms of infection are often not present in wound infection, subtle signs such as increasing pain, further wound breakdown and increased drainage may be present.13-14  

It is well accepted that chronic wounds are contaminated and colonized. This led to the guidelines that suggest one should not utilize swab cultures to diagnose wound infection as they detect only the surface bacteria and will not reflect the organisms causing tissue infection.15 Recommendations for preparation of contaminated and colonized wounds include thorough cleansing, debridement, exudate management and consideration of a topical agent. As a rule of thumb, when wounds are present with strictly local signs of infection, then local or topical therapy can be adequate. If there are systemic signs of infection, systemic therapy is indicated.

Recognizing The Impact Of NPWT On Wound Bed Preparation
Lastly, any discussion of wound bed preparation would not be complete without mentioning the role of negative pressure wound therapy (NPWT), which can be an effective adjunct for wound bed preparation and has become a mainstay in wound management. Negative pressure can take a wound that is either acutely infected or colonized, remove excessive fluids and promote a healthy granular bed. Along those lines, NPWT may also stimulate a chronic wound to promote a foundation for healing. Through various mechanisms of action, an effective course can help prepare a wound for delayed primary closure, grafting techniques, skin substitutes or a flap.14

In Conclusion
Wound care is a dynamic and rapidly evolving process. As wound care specialists, we must understand that this is a continuous process that requires an understanding of the patient, the underlying cause of the wound and the wound environment. Appropriate knowledge about wound bed preparation is necessary to allow for appropriate and timely healing of chronic wounds.

Dr. Migonis is a Clinical Fellow in Surgery at Harvard Medical School and a second- year resident at Beth Israel Deaconess Medical Center in Boston.

Dr. Rosenblum is an Assistant Clinical Professor of Surgery at Harvard Medical School and the Associate Chief of the Division of Podiatric Surgery at Beth Israel Deaconess Medical Center in Boston. He is a Fellow of the American College of Foot and Ankle Surgeons.

References

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  2.     Jeffcoate WJ, Harding KG. Diabetic foot ulcers. Lancet. 2003;361(9368):1545–1551
  3.     Cavanagh PR, Ulbrecht JS, Caputo GM. The non-healing diabetic wound: fact or fiction? Ostomy Wound Manage. 1998;44 (suppl):6S-12S.
  4.     Vinik AI. Diagnosis and management of diabetic neuropathy. Clin Geriatr Med. 1999;15(2):293-320.
  5.     Brodsky JW. Evaluation of the diabetic foot. AAOS Instructional Course Lectures. 1999;48:289-303.
  6.     Frykberg RG, Lavery LA, Pham H, et al. Role of neuropathy and high foot pressures in diabetic foot ulceration. Diabetes Care. 1998;21(10):1714-1719
  7.     Schultz GS, Sibbald RG, Falanga V, et al. Wound bed preparation: A systematic approach to wound management. Wound Repair Regen. 2003;11(Suppl 1):S1–28.
  8.     Yagar DR, Zhang LY, Liang HX, et al. Wound fluids from human pressure ulcers contain elevated matrix metalloproteinase levels and activity compared to surgical wound fluids. J Inves Dermatol. 1996;107(6):743-748
  9.     Mast BA, Schultz GS. Interactions of cytokines, growth factors, and proteases in acute and chronic wounds. Wound Rep Regen. 1996;4:411-420.
  10.     Davis SC, Martinez L, Kirsner R. The diabetic foot: the importance of biofilms and wound bed preparation. Curr Diab Rep. 2006;6(6):439-45.
  11.   Stuck R, Schmidt B, Blume P. Point-counterpoint: are bioengineered alternative tissues better than split thickness skin grafts for DFUs? Podiatry Today. 2015; 28(3):54-58..
  12.     Wound Healing Society. Guidelines for the best care of chronic wounds. Wound Repair Regen. 2006;14:647–710
  13.     Gardner SE, Frantz RA, Doebbeling BN. The validity of the clinical signs and symptoms used to identify localized chronic wound infection. Wound Repair Regen. 2001;9(3):178–86
  14.     Borgquist O, Gustafsson L, Ingemansson R, Malmsjo M. Micro- and macromechanical effects on the wound bed of negative pressure wound therapy using gauze and foam. Ann Plast Surg. 2010;64(6):789–93.
  15.     Chakraborti C, Le C, Yanofsky A. Sensitivity of superficial cultures in lower extremity wounds. J Hosp Med. 2010; 5(7):415-20.
  16.     Panuncialman J, Falanga V. The science of wound bed preparation. Clin Plast Surg. 2007;34(4):621–32.
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Alison Migonis, DPM, and Barry Rosenblum, DPM, FACFAS
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