Approximately 2 million people in the United States are living with limb loss, and this figure is expected to double by 2050. Lower-limb amputation accounts for the vast majority of all amputations, and diabetes—specifically, diabetic foot ulcers (DFUs)—is the leading cause of nontraumatic...
by the WoundSource Editors
One of the greatest challenges when dealing with biofilms in chronic wounds is identifying their existence in the first place. The extracellular polymeric substance or EPS on biofilms essentially is an invisible cloak that protects and hides biofilms from both the body's immune system and antimicrobial therapies. This biofilm property keeps the wound from advancing through the phases of wound healing and thus remaining in the inflammatory phase, thereby allowing further proliferation of biofilms. This is a common theme in wounds with biofilms, but other signs and symptoms will depend on the type and degree of functional impairment the host experiences. Types of inflammatory cells seen may be polymorphonuclear neutrophils, leucocytes, or mononuclear cells, but the type will depend on the predominating immune response of the host.
Visual characteristics, although limited, along with clinical and laboratory data, can aid in determining the existence of biofilm in chronic non-healing wounds. Visually, biofilm is shiny and slimy because of the EPS, and it has a tenacious attachment to the wound bed. A full evaluation should include a detailed wound assessment, a clinical history, signs and symptoms of current wound issues, and microscopic evaluation of culture and tissue samples to identify causative microorganisms.1 As a result of this evaluation, as well as a review of the cofactors and comorbidities that may inhibit or delay wound healing, the appropriate interventions for wound bed preparation can be implemented. Additionally, this is also the time for making appropriate referrals to interdisciplinary team members.
Wound Bed Preparation
Wound care requires setting realistic goals and objectives outlined in the plan of care. Is the wound healable? If the answer is yes, then the individual's body should be able to support the phases of wound healing within an expected time frame. Treatment should be aggressive to prevent any delay that could result in a stalled wound or one that has become chronic. Is the goal maintenance or to keep the wound from deteriorating by providing comprehensive wound care? Is the goal palliative treatment? For example, is the patient receiving hospice or palliative care because the body cannot support the wound through the phases of wound healing as a result of comorbidities? If so, then comfort is more important than cure at this point.2
An effective wound bed preparation model includes debridement and wound cleansing, inflammation and infection control, moisture management, support for granulation and epithelialization, and support to help achieve goals and objectives. Wound cleansing should be done with each dressing change and before assessment to remove surface contaminants, bioburden, and debris from the wound bed. This cleansing can be accomplished by either sterile or clean technique, depending on the particular situation. Fluid volume should be in a sufficient amount and at sufficient pounds per square inch (4 to 15 psi) to clean the wound bed adequately without causing trauma to fragile granulation tissue.3 Wounds may be cleansed with normal saline or with commercial cleansing agents that contain gentle surfactants, which reduce surface tension in the wound bed, thereby loosening debris so that it can be gently cleansed away. Some cleansers contain antimicrobial properties that help reduce bioburden in the wound bed. Cleansing agents such as skin cleansers and soaps should be used only on the skin. They are not intended for use in the wound bed because ingredients such as povidone-iodine, chlorhexidine, hydrogen peroxide, and acetic acid have been shown to interfere with fibroblast formation and epithelial growth.
Why is debridement of the wound necessary? The importance of debridement is in removal of biofilm, necrotic tissue, and senescent or aberrant cells, all of which may harbor bacteria, increase the risk of infection, delay the wound healing process, impair macrophage function, and physically splint the wound open.4 Keeping the wound bed clear of these and other substances that inhibit wound healing will aid the wound in progression through the phases of wound healing in an orderly and timely fashion.
Debridement can be achieved by numerous methods, which may include sharp surgical or conservative sharp debridement or mechanical, enzymatic, biologic, or autolytic debridement. Sharp debridement is performed in the operating room. It is the most efficient debridement method to convert a chronic wound to an acute wound. Conservative sharp debridement is done outside the operating room and is not as aggressive a procedure to make a wound acute. It is the removal of clearly identifiable, devitalized tissue to above the level of viable tissue by using sharp instruments, including but not limited to scalpels, scissors, or curettes. Minimal pain and bleeding are expected, and repeated debridement is often needed. Mechanical debridement is a nonselective, physical method of removing viable and nonviable tissue and debris from a wound by using a physical force such as wet-to-dry dressings, wound irrigations, or pulsatile lavage. Enzymatic debridement can be achieved with the use of exogenous proteolytic enzymes. These enzymes work directly on the devitalized tissue or indirectly by dissolving the collagen that attaches the devitalized tissue to the wound bed. They have little or no effect on healthy tissue.
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Biologic debridement is the application of sterile, medical-grade larvae (maggots) into the wound bed. The larvae remove any devitalized tissue, disinfect the wound bed, and thus promote wound healing. Autolytic debridement is a selective process by which endogenous phagocytic cells and proteolytic enzymes break down necrotic tissue. This process occurs in varying degrees in the presence of a moist wound healing environment and is dependent on the patient's having a functioning immune system. Serial debridement may be performed to prevent biofilm reformation. Maintaining a clean wound bed aids in achieving individual specific patient goals and objectives, especially if the plan is to maintain a positive healing trajectory.3
Management of Biofilm
In addition to cleansing and debridement, management of bioburden and decreasing the risk of biofilm formation are important in preventing the wound from becoming chronic or for resuming a positive healing process. Treatment of infection is usually addressed with topical or systemic antibiotic or antimicrobial therapy. Wound bioburden is typically polymicrobial, thus making identification of the causative organism difficult at best. In turn, this increases the difficulty in choosing an antibiotic and the mode of delivery. Adding to this difficulty is the issue that many chronic wounds are poorly perfused, and if systemic blood flow is impaired, then so is systemic antibiotic delivery at a therapeutic level.5 Topical broad-spectrum antiseptic agents and antimicrobial dressings are preferred because of their broad-spectrum activity and effectiveness. For those patients being treated with systemic antibiotics, it is recommended that topical antiseptics and dressings also be used.
Biofilms play a key role in delayed wound healing and infection. The study of biofilms is very recent, yet it has provided a vast amount of knowledge used in the fight against bioburden and infection. This research has led to the emergence of advanced wound care products such as antimicrobial cleansing agents, antimicrobial dressings, and more advanced debridement products and techniques. As research continues to advance in understanding the mechanisms involved in biofilm resistance, new treatment strategies will emerge directed toward substances that compromise biofilm formation and destabilize established biofilms, as well as the development of new antimicrobial agents that decrease the chance of resistance development by the causative organisms.6
1. Høiby N, Bjarnshold T, Moser C, et al. ESCMID guideline for the diagnosis and treatment of biofilm infections 2014. Clin Microbiol Infect. 2015;21(1):1-25.
2. Ayello EA, Courchene N, Sibbald RG. Strategies for optimal patient-centered care. In Krasner DL, Rodeheaver GT, Sibbald RG, Woo KY, eds. Chronic Wound Care 5. Malvern, PA: HMP Communications; 2012:65-76.
3. Baranoski S, Ayello EA. Wound debridement. In Mills JE, ed. Wound Care Essentials: Practice Principles. Philadelphia, PA: Lippincott Williams & Wilkins; 2012:117–26.
4. Frykberg RG, Banks J. Challenges in the treatment of chronic wounds. Adv Wound Care (New Rochelle). 2015;4(9):560-82.
5. Metcalf D, Bowler P, Parsons D. Wound biofilm and therapeutic strategies. In Dhanasekaran D, Thajuddin N, eds. Immunology and microbiology. London, United Kingdom: InTech Open Publishing; 2016:271–98.
6. Del Pozo JL, Rouse MS, Euba G, et al. Prevention of Staphylococcus epidermidis biofilm formation using electrical current. J Appl Biomater Funct Mater. 2014;5;12(2):81-3.
The views and opinions expressed in this blog are solely those of the author, and do not represent the views of WoundSource, Kestrel Health Information, Inc., its affiliates, or subsidiary companies.