By Cindy Broadus, RN, BSHA, LNHA, CHCRM, CLNC, CLNI, WCC, DWC, OMS
At one time or another, all wound care professionals encounter a chronic wound, defined as a wound that fails to heal in an orderly and timely manner. Globally, about 67 million people (1% to 5% of the world’s population) suffer chronic wounds. In the United States, chronic wounds affect 6.5 million people and cost more than $25 billion annually to treat.
The normal healing process is complex and can contribute to wound chronicity, which causes delayed healing. Local and systemic factors that can impede wound healing include lack of growth factors, a prolonged inflammatory response, abnormal matrix metalloproteinases, desiccation or decreased perfusion of the wound bed, wound hypoxia, infection or increased bacteria, aged cells, necrotic tissue, excessive or sustained pressure at the wound site, poor nutritional status, and certain medical conditions.
Autolysis, a natural process that occurs during wound healing, requires a moist vascular environment and a functioning immune system. During the inflammatory stage, neutrophils and macrophages digest and remove devitalized tissue debris. In chronic wounds, the autolysis process becomes overwhelmed by high levels of endotoxins released from damaged tissue and use of other debriedement methods are necessary.
Managing chronic wounds requires a holistic and comprehensive approach that considers all factors that can affect wound healing. Debridement remains a standard of care. Fundamental to proper wound healing, it can be done by surgical or nonsurgical methods. Debridement is integral to transforming the hostile environment of a chronic wound to a receptive environment that promotes healing. This article gives an overview of debridement techniques.
Why debridement is crucial to healing
Debridement refers to removal of dead, devitalized, or contaminated tissue or foreign material from a wound to reduce the number of microbes, toxins, and other substances that inhibit healing. Wound care clinicians must strive to achieve a stable, well-vascularized wound bed with minimal exudates. Presence of necrotic or compromised tissue is common in chronic nonhealing wounds. Devitalized tissue provides a growth medium for bacteria, increasing the infection risk. Also, it exudes endotoxins that inhibit migration of fibroblasts and keratinocytes to the wound. Necrotic tissue prevents formation of granulation tissue, wound contraction, and epithelialization.
While all components of wound bed preparation are crucial to an optimal wound-healing environment, both historical and current research indicates that removing exudates and devitalized tissue is essential. Many wounds with underlying pathologies that are untreatable or hard to treat require repeated debridement. (See Wound bed preparation by clicking the PDF icon above.)
Debridement methods can be selective or nonselective. Selective methods remove only devitalized tissue. Nonselective methods don’t differentiate between viable and nonviable tissue.
Debridement methods
Five major debridement methods exist, collectively known as BEAMS—an acronym made up of the first letters of each method. Selective methods include Biological/Biosurgical, Enzymatic, and Autolytic debridement. Nonselective methods include Mechanical and Sharp debridement. (See Choosing the right debridement method by clicking the PDF icon above.)
In some cases, more than one debridement method may be appropriate. In others, no method may be appropriate. For instance, stable eschar (eschar that’s dry, adherent, and intact with no erythema or fluctuance) on the heels serves as a natural covering and shouldn’t be removed. Another example is when healing isn’t an option, as when decreased blood flow from arterial insufficiency delays or impedes wound healing.
Biological/biosurgical debridement
Also known as maggot debridement, larval therapy, or larvae therapy, this method uses medicinal maggots to remove nonviable tissue. Sterile maggots are applied to the wound and covered by a dressing, which remains in place 1 to 3 days. Maggots have three actions:
View: a video for teaching patients about how maggot therapy works
- They debride the wound by liquefying and digesting necrotic tissue.
- They disinfect by killing and consuming bacteria.
- They stimulate wound healing by promoting fibroblast growth.
Rapid and selective, biological debridement has proven effective in debriding chronic wounds and aiding limb salvage.
Enzymatic debridement
Enzymatic debridement involves application of collagenase ointment, which doesn’t harm healthy tissue. Fast acting and highly selective, it involves once-daily application of Santyl, a prescription product with no generic equivalent. This collagenase ointment works from the bottom up by selectively degrading (dissolving) collagen anchored to the wound. It breaks down only denatured collagen, leaving other proteins unaffected. Also, it doesn’t harm the collagen needed to form a scaffold, which is crucial for healing during the second phase of the wound healing cascade.
Enzymatic debridement is faster than autolytic debridement but more conservative than sharps surgical debridement. While Santyl is the only enzymatic debriding ointment available, other topical agents, such as Iodosorb, Oakin, and Mesalt, can promote debridement in the wound bed as well.
Autolytic debridement
A natural physiologic process, autolytic debridement uses the body’s own enzymes to soften and break down necrotic tissue. White blood cells and enzymes enter the wound site during the inflammatory phase of healing, liquefying necrotic tissue. All wounds go through autolytic debridement to some extent. Products that support a moist wound environment can enhance this type of debridement.
Autolytic debridement is slow, selective, painless, and noninvasive. However, it’s not used for infected wounds and isn’t the best choice for wounds with a large amount of necrotic tissue.
Mechanical debridement
Mechanical debridement uses an external force great enough to separate or break the adhesive forces of necrotic tissue. This nonselective method, which can be painful, may involve a whirlpool, wet-to-dry dressings, scrubbing, and irrigation. Contraindications include epithelializing wounds and granulating wounds.
View: a video of administering low-pressure irrigation, a type of mechanical debridement
Sharp debridement
Sharp debridement refers to removal of necrotic devitalized tissue by sharp instruments, such as scalpels, scissors, lasers, curettes, or forceps. Nonselective, this method is the fastest debridement method. It can be either surgical or conservative.
- Surgical debridement is a major procedure performed by a surgeon, another physician, or a podiatrist. It involves complete debridement and transforms a chronic wound to an acute wound. It produces rapid results but sacrifices some viable tissue. Pain control during and after the procedure is important and can be accomplished with analgesics. (See Sharp debridement by clicking the PDF icon above.)
- Conservative debridement is done at the bedside by a trained clinical practitioner (such as a therapist or nurse, if the state practice act allows) or a physician. This minor procedure, which involves use of scalpels, scissors, or curettes, removes only devitalized tissue. It may require several sessions.
One type doesn’t fit all
Not all patients with necrotic wounds are candidates for every debridement method. To choose the most appropriate method, clinicians must understand the need for debridement and the available options. Keep in mind that in many cases, debridement isn’t a one-time intervention but must be repeated until healthy granulation tissue appears. Be sure to reassess the patient and wound regularly to ensure the best care.
Selected references
Benbow M. Available options for debridement. Independent Nurse. June 6, 2011. www.independentnurse.co.uk/cgi-bin/go.pl/library/articlehtml.cgi?
uid=84294;type=Clinical. Accessed February 27, 2013.
European Wound Management Association. Wound Bed Preparation in Practice: Position Document. 2004. www.smith-nephew.com/global/assets/en/documents/
wbp_english.pdf. Accessed February 27, 2013.
Harris RJ. The nursing practice of conservative sharp wound debridement: promotion, education and proficiency. Wound Care Canada. 2009;7(1):22-30. http://cawc.net/images/uploads/wcc/harris.pdf. Accessed February 27, 2013.
Hess CT. Checklist for factors affecting wound healing. Adv Skin Wound Care. 2011;24(4):192.
Hess CT. Clinical Guide to Skin and Wound Care. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012.
Moore M, Jensen P. Assessing the role and impact of enzymatic debridement. Podiatry Today. 2004;17(7). www.podiatrytoday.com/article/2785?page=1. Accessed February 27, 2013.
Payne WG, Salas RE, Ko F, Naidu DK, Donate G, et al. Enzymatic debriding agents are safe in wounds with high bacterial bioburdens and stimulate healing. Eplasty. 2008;7;8:e17.
Sardina D. Wound bed preparation. In: Skin and wound management course workbook. Lake Geneva, WI: Wound Care Education Institute; August 2010;5:42-58.
Sen CK, Gordillo GM, Roy S, Kirsner R, Lambert L, et al. Human skin wounds: a major and snowballing threat to public health and the economy. Wound Repair Regen. 2009;17(6):763-71.
Singhal A, Reis ED, Kerstein MD. Options for nonsurgical debridement of necrotic wounds. Adv Skin Wound Care. 2001;14(2):96-100.
Cindy Broadus is a clinical instructor at the Wound Care Education Institute in Plainfield, Illinois.
This article is very helpful in educating me about the debridement procedure and why I should have my vascular doctor handle my chronic, stasis ulcer wound. He has suggested this remedy, but I was unsure because I did not have enough information about it. Thank you for enlightening me.
Well I guess i’m one tough lady. 7 years chronic necrosis. I have bechets disease. Here is what I have noticed. Where is the blood. Meaning in these lesions there is blood that drains. However you can sense a dryness. Now the necrosis process already started way before. Probably at the base of the lesion. This entire process is continuous meaning constantly changing and never ending. Whenvi first started getting this it was hard lumps all over. Rock hard and sizeable. The material inside had to be broken down and an open lesion left which hundreds of peices of necrosis could come out of one. So I had all these lesions all over in the beginning no necrosis. I went to a dermatologist that treated these with steroid injections. 2 x a week about 40 injections. Then one night after dinner started screaming. Emergency room found out I had MRSA PHEONOMPENIA. 30 DAYS IN HOSPITAL Then another 8. Kidneys shut down. No more injections. Predisone 10 a day 5 x 2. . Then the Necrosis started its been 7 to 8 long years. Agonizing years. Still continuing. The only thing that has made a difference is chemo. I believe I have removed over 100k or more peices of necrosis including granuals which are the worst. Its like pulling glass rocks sticks rose branchesc from inside your body out. You scream yell cry breath hard sweat its worst then having a baby over and over again. You have to wonder how come no heart attack by now. Its amazing im still alive