This article featured in Lower Extremity Review by the always superb Cary Groner
All photos by Cary Groner, courtesy of the Southern Arizona Limb Salvage Alliance.
There are few high-quality studies and no randomized controlled trials documenting its effectiveness, but debridement—from surgical to larval—remains a mainstay of diabetic ulcer care in many practices, and new twists on conventional techniques continue to evolve.
By Cary Groner
Diabetic foot ulcers present clinicians with a host of daunting challenges. Roughly 170 million people worldwide have diabetes and, of those, 15% will develop a foot ulcer at some point.1,2 Yet, despite the array of methodologies available to heal such wounds, the outcomes of one of the most fundamental practices—debridement—have never been studied closely in randomized clinical trials.
Many physicians wish debridement protocols were bolstered by better research. The rationale for the practice appears so sensible that no one is seriously suggesting it be abandoned pending better evidence; clinicians, however, would prefer to be able to back up their opinions with stronger documentation, particularly when choosing among approaches.
The rationale for surgical debridement—the longtime standard of care—is simple enough: to convert a chronic, nonhealing wound into an acute wound that stands a better chance of healing.3 A scalpel is used to remove nonvital tissue and other contaminants from the bed and edge of the wound; this may include hyperkeratotic epidermis and necrotic dermal tissue, debris, and bacteria.
And, despite the lack of robust outcome studies, research has established the biological and molecular basis for debridement fairly well. For example, studies have shown that at the edges of chronic wounds, skin cells known as keratinocytes and fibroblasts exhibit a pathogenic phenotype that slows their migratory capacity and limits their ability to heal the wound.3 They form what is essentially callus, in other words, and debridement aims to clear away such cells so that those more receptive to healing signals and topical agents can proliferate, migrate, and respond to treatment.
Robert Kirsner, MD, PhD, doesn’t deny that debridement seems to offer benefits. Kirsner, who is professor, vice chairman, Stiefel Laboratories chair, and chief of dermatology at the University of Miami Hospital and the associated Miller School of Medicine, would simply like to see better evidence of outcomes.
“There has never been a randomized controlled trial of debridement,” he said, “and I think it behooves the wound care community to understand, first: Does debridement work? Second, how frequently should it be done? Third, what measures of quality should be used?”
Although a handful of clinical trials are routinely cited as evidence of the efficacy of debridement, in a 2010 paper Kirsner and several of his colleagues cast a skeptical eye on them.4 For example, a 1996 paper by Steed et al studied 118 patients treated either with placebo or a topical recombinant growth factor.5 They found that patients treated at wound centers that practiced more frequent debridement healed better than others and called debridement a “vital adjunct in the care of patients with chronic diabetic foot ulcers.”
But as Kirsner and his colleagues pointed out, the Steed paper was a post-hoc analysis of a trial in which debridement was studied secondarily. Among other issues, they noted, wound care centers that debrided more frequently may simply have provided better overall care independent of debridement.
Kirsner similarly questioned the arguments for debridement made in the other studies examined in his paper.6-9 Although most clinicians agree that they’d like better evidence, they’re also realistic about the chances of getting it.
“I think there is not more evidence because it is always a secondary or tertiary question in clinical studies of wound healing,” said David Armstrong, DPM, MD, PhD, professor of surgery and director of the Southern Arizona Limb Salvage Alliance (SALSA) at the University of Arizona College of Medicine in Tucson. “If it’s an industry-sponsored study, it’s almost never the study’s first concern unless what you’re studying is a debridement technology. Or, if it’s a federally sponsored study, the question is so far removed from a laboratory that we end up with mediocre or indirect evidence. I think there have been Herculean efforts made to glean data from other sources, and, if we were able to put that kind of effort into designing a large-scale study with appropriate funding, we could do well. But there are huge gaps in funding in this area.”
Getting on with it
Given that state of affairs, most clinicians do what Armstrong does—use their best judgment as to what methods of debridement seem appropriate for which patients.
“There’s an old adage,” he said. “It’s not what you put on a wound that heals it; it’s what you take off.”
To Armstrong and many others, this means appropriate debridement of nonviable tissue.
“When you do that in noninfected wounds with appropriate blood flow, the majority should heal. Whether that’s predictable or not depends largely on other circumstances, such as infection and ischemia,” he said.
Several of Armstrong’s papers support his views. In a study published in the Archives of Surgery in 2000, for example, he reported that a significantly higher proportion of patients with foot ulcers healed when treated with a foot compression device to reduce edema rather than a nonfunctioning placebo device (75% vs 51%)—and that debridement was an important adjunct to this approach.10 He has also written, “Debridement, when systematically performed, may be as important as offloading in reducing the prevalence of chronic inflammatory by-products in a wound and thus in converting a chronic wound into an acute one.”11 For that matter, the 2012 Infectious Disease Society of America clinical practice guidelines for the diagnosis and treatment of diabetic foot infections, of which Armstrong was a coauthor, noted, “Most diabetic foot infections require some surgical intervention, ranging from minor [debridement] to major.”12
Kirsner himself is an advocate, as it happens.
“Twenty years ago, if we said debridement, it meant removing nonviable or necrotic tissue from the base of a wound,” he said. “Now we envision it as something more. It might mean removing cells from the base of the wound that are not as reactive to stimuli, taking out biofilms or other bacterial burden, or removing cells from the edge that have become nonmigratory and hyperproliferative.”
Stephanie Wu, DPM, MSc, notes that as tools and techniques have expanded, debridement has become a catch-all term that may refer to a number of approaches.
“Traditionally, people have believed that sharp debridement, done using instruments, is the best, but they haven’t really looked at it, or at how aggressive you should be,” said Wu, who is associate dean of research and director of CLEAR [the Center for Lower Extremity Ambulatory Research], and an associate professor of stem cell and regenerative medicine, at Rosalind Franklin University in Chicago, as well as an associate professor of surgery and applied biomechanics at the university’s William Scholl College of Podiatric Medicine. “Should you just take out a little bit, or a huge border? There’s very little evidence to guide those decisions.”
In an article currently in press, Wu discusses causes of wound chronicity and approaches to debridement.13As noted above, cells in the wound base and periphery undergo changes that impair their ability to participate in the healing process. Beyond that, however, the environment and inflammatory response of a chronic wound differ from those in an acute wound; changes in protease regulation, cytokine release, fibroblast morphology, and extracellular matrix composition may impair healing and macrophage function.
Given the complexity of this deleterious biochemical cascade, it becomes especially important to identify the reasons a wound has become stagnant—whether related to peripheral vascular disease, malnutrition, infection, or other pathologies. Debridement nevertheless remains a mainstay of treatment, Wu believes, regardless of how it is approached.
“There are a number of ways to debride—for example, mechanical, ultrasonic, enzymatic, autolytic, and biological,” she told LER. “Sharp or surgical debridement is the gold standard and probably the fastest, but is it best for everyone? Not necessarily; it depends on the patient’s condition. If the patient doesn’t have adequate vascular flow, for example, you have to think twice before you do that.”
In her article, Wu described several innovative debridement methods of which clinicians should be aware before they reach for the scalpel.
For example, pulsed, nonthermal, low-frequency ultrasound enhances inflammatory response and tissue repair; the pressure wave increases cell permeability, stimulates signal transduction pathways, facilitates leukocyte adhesion, and produces growth factors. One study found it comparable to sharp debridement in terms of efficacy and tolerability.14 Others have reported that it increases the healing rate of recalcitrant foot ulcers.15-17
Another approach is hydrosurgery, which cuts tissue using a stream of pressurized water or saline solution—it’s sometimes known as a “water knife”—and has been found effective in both animal and human studies.18-20 Some researchers have raised concerns about collateral soft-tissue damage,21 but others suggest that appropriate lowering of the pressure can diminish this problem.22
Another new debridement technique involves applying a special polyester fiber pad to the wound. The clinician applies circular pressure to the pad, which is designed to trap and remove exudates, slough, hyperkeratotic tissue, and debris. The pad is then pulled off, bringing the contaminants with it. One study reported that the product was 93.4% effective for debridement and caused little or no discomfort.23
Certain approaches to debridement are used more rarely, according to experts. Autolytic debridement essentially involves keeping the wound covered and moist, and letting the body’s scavengers—e.g., mast cells—absorb exudate and other wound by-products.
“We’ll sometimes use that with hospice patients, as a maintenance debridement, or in those with inadequate blood flow,” said Wu. “But it takes a long time.”
A lot of these decisions come down to the medical status of the patient, agreed John Steinberg, DPM, an associate professor in the Department of Plastic Surgery at the Georgetown University School of Medicine in Washington, DC.
Figure 1. David Armstrong, DPM, MD, PhD, applies Santyl collagenase cream to the ulcer of a patient. (Photos by Cary Groner, courtesy of the Southern Arizona Limb Salvage Alliance.)
“If a patient is critically ill, or elderly to the point that it isn’t safe to administer anesthesia, then that rules out sharp debridement in the operating room and the hydrosurgical systems; anything that might cause pain is off the table,” Steinberg said. “Most of the nonsurgical debridement methods are slow, but in palliative care patients, time isn’t necessarily the greatest concern.”
In other cases, clinicians may find value in either enzymatic or biological debridement.
“We almost never use autolytic debridement, but we’ll use chemical [enzymatic] debridement occasionally,” David Armstrong said. “We apply a collagenase cream; it’s an exogenous protease that breaks up collagen, and you can then wipe off or flush out the slough afterward. It’s a gentle debridement in someone who may not tolerate constant interoperative surgical debridements.”
Many clinicians consider biological debridement a more effective approach, but that means contending with the “ick” factor—because “biological” in this case is a polite term for maggots. Patients, not surprisingly, are sometimes repelled by the idea of their open wound roiling with the larvae of green bottle flies. But medical maggots are sterilized with radiation so they can’t progress to the pupae stage, and they’re specialists at breaking down and digesting only necrotic tissue, leaving healthy tissue intact.22
“The difference between surgeons and maggots is that we try to debride what we think is necrotic tissue, but we don’t really know,” said Wu. “The maggots are better surgeons than we are—they can truly distinguish necrotic tissue.”
According to Wu, the maggots have enzymes in their saliva that are particularly suited to breaking down necrotic and tough fibrotic tissue.
“When you scrape fibrotic tissue, it sounds like you’re dragging a spoon across cement,” she said. “The maggots loosen the tissue by crawling around in the wound; they spit out their saliva, bite into the tissue, and slurp it up.”
The helpful crawlers’ saliva also carries antimicrobial enzymes, and their gut enzymes further break down dead tissue and destroy bacteria.
“It doesn’t matter what kind of bacteria it is,” said Wu. “To them, it’s food.”
In her experience, patients treated with maggots can go longer without antibiotics than those who received sharp debridement alone, and research bears this out.24
Figure 2. Biological debridement utilizes medical maggots that break down and digest only necrotic tissue, leaving healthy tissue intact. (Photos by Cary Groner, courtesy of the Southern Arizona Limb Salvage Alliance.)
Other studies support larval therapy. An Israeli paper recently published in the Journal of Wound Care, for example, reported that 82% of patients with chronic wounds enjoyed complete debridement by maggots, while 17% had partial debridement and in only 1% was the approach ineffective (total n=435).25 A 2007 literature review found that maggot debridement was safe and effective,26 and a 2005 paper reported that though eight of 20 nondiabetic patients reported more pain during maggot therapy than before therapy, diabetic patients experienced the same pain levels before and during the therapy.27 A 2002 study in Diabetes Carefound that in 18 patients at a Veterans Affairs center, maggot therapy was more effective than conventional care, leading to more thoroughly debrided wounds, faster growth of granulation tissue, and quicker wound healing.28 A Cochrane review also concluded that maggots reduced wound area better than hydrogel.29
A recent innovation, so far used mainly in Europe, aims to contain both the “ick” factor and its cause by keeping the maggots in a permeable bag instead of giving them direct access to the wound. Wu nevertheless favors the free-range approach.
“Containing them doesn’t work as well,” she said. “The maggots can’t crawl around in the wound, so you’re just relying on their saliva to break down the tissue, and it limits how much they can do. People have also tried to extract their enzymes, but it doesn’t appear to be as good, either. You need the maggots; otherwise it’s like killing the goose that laid the golden egg.”
Some products and procedures are proving to be useful adjuncts to debridement—particularly biogels, artificial skin products, and negative pressure wound therapy (NPWT, also known as vacuum assisted closure, or VAC).
“Bioengineered skin equivalents need that base,” Wu said. “It’s crucial to debride before you use these products; otherwise, the grafts won’t do as well.”
Robert Kirsner agreed, with a caveat.
“There isn’t great evidence to support this yet, but the idea is that a better prepared wound will allow advanced products to work more effectively,” he said. “These products often release growth factors or cytokines, and those could get caught up in the debris of the wound if it wasn’t debrided first.”
NPWT is popular with clinicians. This approach, when used after debridement in a well-vascularized bed, draws the edges of the wound together, removes infectious material, and helps healthy granulated tissue form. It’s been shown to be particularly useful on deep complicated nonhealing wounds.22
Figure 3. Adam Isaac, DPM, a fellow at SALSA, applies Dermagraft to a debrided diabetic foot ulcer. (Photo by Cary Groner, courtesy of the Southern Arizona Limb Salvage Alliance.)
“VAC is becoming one of the most important tools available in wound care,” said Michael Pinzur, MD, a professor of orthopedic surgery and rehabilitation at Loyola University Medical Center in Maywood, IL. “But it requires that you have a clean wound when you apply it.”
Research results have been positive. For example, a 16-week randomized trial in patients with complex diabetic foot wounds reported that subjects in the VAC arm (n = 77) healed faster than controls (n = 85), who received standard moist wound care. Another large multicenter trial found that NPWT patients had faster healing, lower amputation rates, and shorter lengths of hospital stay than controls.30 Other studies have shown that VAC had beneficial effects on wound volume, depth, and healing, particularly in cardiovascular and diabetic patients.31,32,33
But again, as the clinicians interviewed by LER emphasized, all of these benefits depend on excellent debridement first.
Recent investigations into biofilms—biochemical barriers composed of an extrapolysaccharide matrix within the wound bed that shield bacteria from the attacks of the immune system and exogenous antibiotics3—may give debridement a new role, experts say.
“This is the hottest research going on now in the wound environment,” said Michael Pinzur. “There is a bond between bacteria and certain proteins that prevent the body from getting rid of the bacteria. Ideally we’ll be able to get rid of biofilms using detergents, but we’ll still have to get dead and infected tissue out of the way.”
“We are using more PCR [polymerase chain reaction] culture technology now, and diagnosing more biofilm,” confirmed John Steinberg. “The concern is that if you debride a wound but leave just a small fragment of that biofilm behind, it reforms a matrix in a matter of hours.”
This may be particularly important with new technologies. In a paper published this June, Steinberg and a colleague wrote that “advanced wound healing modalities…require optimal wound bed preparation with specific consideration of biofilm reduction before their application.”34
“Biofilm may be our Higgs boson,” said David Armstrong. “It’s elusive, it’s critically important, and only now are we getting better at detecting it.”
Figure 4. Isaac uses a scalpel to debride a diabetic foot ulcer. (Photo by Cary Groner, courtesy of the Southern Arizona Limb Salvage Alliance.)
Armstrong said that awareness of biofilms may ultimately lead clinicians to a more holistic appraisal of wound bed ecology that treats wounds as the complicated neighborhoods they are.
“We now believe that certain kinds of surgical debridement probably eradicate, for a period of time, a certain neighborhood—like dropping a bomb,” he said. “But unless we keep it clean, that neighborhood is going to regrow, and in the future we need to get better at repopulating it in the right way.”
Armstrong drew an analogy to current methods of urban combat—the idea of “clear and hold.”
“Right now, all we’re doing is clearing, using debridement,” he said. “We’re not holding, and we’re not winning hearts and minds in that wound. I think one day we may be adding [beneficial] bacteria back to wounds—installing our own puppet government, as it were. This is what we’re dealing with every day in the clinic: little war zones.”
Cary Groner is a freelance writer in the San Francisco Bay Area.
1. Wild S, Roglic G, Green A, et al. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care 2004;27(5):1047-1053.
2. Consensus Development Conference on Diabetic Foot Wound Care: 7-8 April 1999, Boston, Massachusetts. American Diabetes Association. Diabetes Care 1999;22(8):1354-1360.
3. Gordon KA, Lebrun EA, Tomic-Canic M, Kirsner RS. The role of surgical debridement in healing of diabetic foot ulcers. Skinmed 2012;10(1):24-26.
4. Lebrun E, Tomic-Canic M, Kirsner RS. The role of surgical debridement in healing of diabetic foot ulcers. Wound Repair Regen 2010;18(5):433-438.
5. Steed DL, Donohoe D, Webster MW, Lindsley L. Effect of extensive debridement and treatment on the healing of diabetic foot ulcers. Diabetic Ulcer Study Group. J Am Coll Surg 1996;183(1):61-64.
6. Piaggesi A, Schipani E, Campi F, et al. Conservative surgical approach versus nonsurgical management for diabetic neuropathic foot ulcers: a randomized trial. Diabet Med 1998;15(5):412-417.
7. Piaggesi A, Vicava P, Rizzo L, et al. Semiquantitative analysis of the histopathological features of the neuropathic foot ulcer: effects of pressure relief. Diabetes Care 2003;26(11):3123-3128.
8. Saap LJ, Falanga V. Debridement performance index and its correlation with complete closure of diabetic foot ulcers. Wound Repair Regen 2002;10(6):354-359.
9. Cardinal M, Eisenbud DE, Armstrong DG, et al. Serial surgical debridement: a retrospective study on clinical outcomes in chronic lower extremity wounds. Wound Repair Regen 2009;17(3):306-311.
10. Armstrong DG, Nguyen HC. Improvement in healing with aggressive edema reduction after debridement of foot infection in persons with diabetes. Arch Surg 2000;135(12):1405-1409.
11. Armstrong DG, Lavery LA, Vazquez JR, et al. How and why to surgically debride neuropathic diabetic foot wounds. J Am Podiatr Med Assoc 2002;92(7):402-404.
12. Lipsky BA, Berendt AR, Cornia PB, et al. 2012 Infectious Diseases Society of America clinical practice guideline for the diagnosis and treatment of diabetic foot infections. Clin Infect Dis 2012;54(12):e132-e173.
13. Wu S. Debridement and the current state of play. Podiatry Management. In press.
14. Herberger K, Franzke N, Blome C, et al. Efficacy, tolerability and patient benefit of the ultrasound-assisted wound treatment versus surgical debridement: a randomized clinical study. Dermatology 2011;222(3):244-249.
15. Ennis WJ, Foremann P, Mozen N, et al. Ultrasound therapy for recalcitrant diabetic foot ulcers: results of a randomized, double-blind, controlled, multicenter study. Ostomy Wound Manage 2005;51(8):24-39.
16. Tan J, Abisi S, Smith A, Burnand KG. A painless method of ultrasonically assisted debridement of chronic leg ulcers: a pilot study. Eur J Vasc Endovasc Surg 2007;33(2):234-238.
17. Voigt J, Wendelken M, Driver V, Alvarez OM. Low-frequency ultrasound as an adjunct therapy for chronic wound healing: a systematic review of the literature and meta-analysis of eight randomized controlled trials. Int J Low Extrem Wounds 2011;10(4):190-199.
18. Caputo WJ, Beggs DJ, DeFede JL, et al. A prospective randomized controlled clinical trial comparing hydrosurgery debridement with conventional surgical debridement and lower extremity ulcers. Int Wound J 2008;5(2):288-294.
19. Granick MS, Posnett J, Jacoby M, et al. Efficacy and cost-effectiveness of a high-powered parallel waterjet for wound debridement. Wound Repair Regen 2006;14(4):394-397.
20. McCardle JE. Versajet hydroscalpel: treatment of diabetic foot ulceration. Br J Nurs 2006;15(15):S12-S17.
21. Boyd JI 3rd, Wongworawat MD. High-pressure pulsatile lavage causes soft tissue damage. Clin Orthop Relat Res 2004;(427):13-17.
22. Andros G, Armstrong DG, Attinger CE, et al. Consensus statement on negative pressure wound therapy (V.A.C. Therapy) for the management of diabetic foot wounds. Ostomy Wound Manage 2006;(Suppl):1-32.
23. Bahr S, Mustafi N, Piatkowski A, et al. Clinical efficacy of a new monofilament fibre-containing wound debridement product. J Wound Care 2011;20(5):242-248.
24. Armstrong DG, Salas P, Short B, et al. Maggot therapy in “lower-extremity hospice” wound care: fewer amputations and more antibiotic-free days. J Am Podiatr Med Assoc 2005;95(3):254-257.
25. Gilead L, Mumcuoglu KY, Ingber A. The use of maggot debridement therapy in the treatment of chronic wounds and hospitalized in ambulatory patients. J Wound Care 2012;21(2):78-85.
26. Chan DC, Fong DH, Leung JY, et al. Maggot debridement therapy in chronic wound care. Hong Kong Med J 2007;13(5):382-386.
27. Steenvoorde P, Budding T, Oskam J. Determining pain levels in patients treated with maggot debridement therapy. J Wound Care 2005;14(10):485-488.
28. Sherman RA. Maggot therapy for treating diabetic foot ulcers unresponsive to conventional therapy. Diabetes Care 2003;26(2):446-451.
29. Edwards J, Stapley S. Debridement of diabetic foot ulcers. Cochrane Database Sys Rev 2010;(1):CD003556.
30. Blume PA, Walters J, Payne W, et al. Comparison of negative pressure wound therapy using vacuum-assisted closure with advanced moist wound therapy in the treatment of diabetic foot ulcers: a multi-center randomized controlled trial. Diabetes Care 2008;31(4):631-636.
31. Eginton MT, Brown KR, Seabrook GR, et al. A prospective randomized evaluation of negative-pressure wound dressings for diabetic foot wounds. Ann Vasc Surg 2003;17(6):645-649.
32. Braakenburg A, Obdeijn MC, Feitz R, et al. The clinical efficacy and cost-effectiveness of the vacuum-assisted closure technique in the management of acute and chronic wounds: a randomized controlled trial. Plast Reconstr Surg 2006;118(2):390-397.
33. Armstrong DG, Lavery LA, Abu-Rumman P, et al. Outcomes of subatsmospheric pressure dressing therapy on wounds of the diabetic foot. Ostomy Wound Manage 2002;48(4):64-68.
34. Kim PJ, Steinberg JS. Wound care: biofilm and its impact on the latest treatment modalities for ulcerations of the diabetic foot. Semin Vasc Surg 2012;25(2):70-74.