- Email: [email protected]
Débridement of the noninfected wound
Débridement of the noninfected wound Rhonda S. Cornell, DPM,a Andrew J. Meyr, DPM,b John S. Steinberg, DPM,c and Christopher E. Attinger, MD,d Washington, DC; and Philadelphia, Pa The utility of wound débridement has expanded to include the management of all chronic wounds, even in the absence of infection and gross necrosis. Biofilm, metalloproteases on the wound base, and senescent cells at the wound edge irreversibly change the physiology of wound healing and contribute to a pathologic, chronic inflammatory environment. The objective of this review is to provide surgeons with a baseline understanding of the processes of débridement in the noninfected wound. ( J Vasc Surg 2010;52:31S-6S.)
The most general definition of débridement is the process in which all materials incompatible with healing are removed from a wound. This definition has grown broader with time and classically involves the surgical excision of all grossly infected and necrotic tissue. Military surgeons in the 18th and 19th centuries, most notably the Belgian Antione Depage, developed techniques of aggressive excision on the battlefields of Europe to prevent gangrene and save lives.1 We now know, however, that tissue does not have to be actively infected or necrotic to impair the biologic wound healing processes of the body. Effective débridement can be achieved with nonsurgical means in some cases, while the growing utility and importance of serial débridement of chronic wounds is becoming more apparent.2-13 The intended emphasis of this article is to provide a review of the processes of débridement in the noninfected wound. The goals are to (1) focus on the pathophysiology of the target tissue causing wound-healing impairment in the absence of infection, and (2) recommend specific techniques for débridement. INFLAMMATION VS INFECTION Because inflammation is an objective hallmark of both infected and chronic wounds, it can often represent a clinical challenge to determine whether a lower extremity wound is actively infected or simply chronically inflamed. One might easily say that all infection is inflammatory but From the Diabetic Limb Salvage, Department of Plastic Surgery, Georgetown University Medical Center;a Department of Podiatric Surgery, Temple University School of Podiatric Medicine;b Department of Plastic Surgery, Georgetown University School of Medicine, and The Center for Wound Healing, Georgetown University Hospital;c and Division of Wound Healing, Department of Plastic & Orthopedic Surgery, Georgetown University School of Medicine, and The Center for Wound Healing, Georgetown University Hospital.d Competition of interest: none. This article is being co-published in the Journal of Vascular Surgery® and the Journal of the American Podiatric Medical Association. Correspondence: Christopher E. Attinger, MD, Georgetown University Medical Center, Department of Plastic Surgery, 3800 Reservoir Rd, NW, Washington, DC 20007 (e-mail: [email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a competition of interest. 0741-5214/$36.00 Copyright © 2010 by the Society for Vascular Surgery and the American Podiatric Medical Association. doi:10.1016/j.jvs.2010.06.006
that not all inflammation is infectious. Further clouding this issue is the reality that all wounds are expected to have at least some degree of bacterial colonization, even in the absence of active clinical infection. Indeed ⱖ60% of chronic wounds contain biofilm.14 It is important to determine at which point critical colonization has been reached or the level at which the type and quantity of bacteria begin to cause active infection. Although the presence of any bacteria is certain to have at least some effect on the biologic processes of wound healing, specific treatment and surgical interventions should depend on whether critical colonization is present with active infection. These seemingly subtle differences should guide the surgical treatment plan and the target tissues of débridement. Surrounding erythema, swelling, induration, tenderness, and malodor are the expected characteristics of an infected wound. The target tissue for débridement in this situation is the en masse excision of all grossly infected and necrotic tissue. The wound requires exploration to discover any deep pockets, abscesses, or tracking along fascial and tendinous structures. Adjunctive antibiotic therapy is required to help in eradicating the bacteria. On the other hand, a noninfected but chronic wound can still be expected to have a rim of surrounding erythema, even without other local clinical signs of infection. Periwound erythema does not necessarily indicate a cellulitis from an infection source but rather inflammation in response to an open lesion. The target tissue for débridement in this case is somewhat different. Certainly, any necrotic tissue and bacterial colonization should be removed, but equally important is targeting the débridement toward the cells on the wound edge and base that are irreversibly fixed in the inflammatory stage of wound healing. The important distinction here is that in the absence of infection, a wound can be caught in a chronic inflammatory phase, despite bacteria having been controlled with topical and systemic antibiotics. Débridement is required to convert the chronic wound bed into an acute wound. Another situation is where a wound may have the clinical appearance of local infection and periwound cellulitis, but the erythema is due to ischemic rubor. Here, all local signs of infection disappear with simple elevation of the limb. In this case, the target tissue for intervention is not local but involves systemic revascularization. These three situations of periwound erythema around a wound have a similar presenta31S
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tion yet demonstrate three different interventions in terms of surgical target tissue. Surgeons working with the lower extremity must develop a sharp clinical acumen to determine the difference between an infected wound and one that is merely chronically inflamed. It is important to appreciate that most of our laboratory and advanced imaging diagnostic tools provide clinicians with general information about inflammation and not specifically infection. These are indirect markers that should guide clinical judgment. Lower extremity wound infection is primarily a clinical diagnosis, and experience is required to make the correct diagnosis. ACUTE VS CHRONIC WOUND HEALING Chronic inflammation is an important consideration not just in the clinical presentation of a wound but also in terms of the pathophysiology of wound development. Acute wounds should proceed quickly and uneventfully through the normal stages of the healing processes: inflammation, proliferation, and maturation.15 These stages represent normal physiology after a linear pathway. There is a distinct start point represented by wound formation and a clear end point marked by wound closure. Unfortunately for chronic wounds, the progression along this linear pathway is arrested, and one sees the pathophysiology of a chronic cycle without a clear end point of wound closure. A chronic wound is usually arrested in the inflammatory stage and cannot progress further. Infection is not required for a wound to become fixed in the inflammatory stage, although it could be a contributing factor. Abnormal metalloproteases produced by necrotic tissue, foreign material, and bacteria impede the body’s attempt to heal by overwhelming the building blocks— chemotactant factors, growth factors, mitogens—needed for normal wound healing. This hostile environment enables bacteria to proliferate and could lead to critical colonization. This environment further inhibits healing by producing destructive enzymes and consuming the local resources— oxygen, nutrition, and building blocks—necessary for healing. Further, there are two significant changes to the cells of a chronic wound, specifically those on the wound base and edge, which are affected by this pathophysiology even in the absence of infection. The presence of senescent cells and biofilm irreversibly impair acute wound healing. Fibroblasts, one of the normal building blocks of an acute wound, have demonstrated phenotypically and irreversibly altered differences in the setting of chronic wounds.16 From a mitotic standpoint, these cells are less active and have decreased ability to perform the DNA replication required for proliferation.17 They also produce abnormal proteolytic enzymes and metalloproteases that contribute to the chronic wound environment.18-20 And similar to the critical contamination concept when considering bacteria, there may be a “critical number” of senescent cells within a wound that make healing unlikely regardless of intervention.21,22 In addition, the role of bacterial biofilms in chronic wound development has become increasingly apparent in
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recent years. According to a study that used scanning electron microscopy, 60% of chronic wounds contained a biofilm compared with only 6% of acute wounds.14 A biofilm is a polymicrobial sessile community of phenotypically-altered microorganisms that develop on the surface of chronic wounds, requiring only the presence of bacteria and not critical colonization.23,24 These bacterial cells bind to each other and the wound base, producing an extrapolymetric substance varying in depth from a single cell layer to a thick community of cells. Quorum sensing describes the process through which the cells are phenotypically altered and able to operate with down-regulated cellular activity and at a lower metabolic level.25,26 The embedded nature and altered metabolic state of the biofilm represent an effective barrier to traditional forms of intervention, including topical treatments and antibiotic therapy. The biofilm and senescent cells on the wound base and periphery comprise the primary target tissues for surgical intervention of the noninfected wound. One may equate the excision of these cells from a noninfected wound as the equivalent of the excision of most if not all of the bacteria from an infected wound. SURGICAL DÉBRIDEMENT TECHNIQUES The use of atraumatic surgical techniques should be maximized when performing débridement to avoid damaging the underlying healthy tissue. One should also attempt to leave behind as much viable tissue as possible, because these remnants will form the building blocks for subsequent healing in vascular in-growth and the delivery of growth factors and nutrients. Traumatic techniques that will cause untoward damage to otherwise healthy and biologic tissue include the charring of tissue with electrocautery and tying off large clumps of tissue with suture. Although both may be necessary to a lesser degree to achieve adequate hemostasis, their use should be avoided as much as possible and topical hemostatic agents and pressure should be used instead. The specific tools of débridement will also have an effect on the underlying viable tissue. Whether in the office or operating room, sterile surgical instruments are recommended over the use of disposable suture removal kits. The latter are usually dull and may crush and damage the remaining skin edge and underlying tissue. The basic tools of débridement include blades, forceps, scissors, curettes, and rongeurs (Fig 1). Only the tissue that is being excised should be grasped with the forceps, and #10 or #20 blades are used to sequentially slice off thin layers of tissue. These blades should be changed frequently because they can dull quickly. Sharpedged curettes are useful for removing the proteinaceous coagulum that accumulates on top of both fresh and chronic granulation tissue. Rongeurs are useful for removing hard-to-reach soft tissue and for débriding or biopsying bone. An air-driven or electrical sagittal saw can serially remove thin layers of bone until normal cortex and marrow is reached. Cutting burrs and rasps permit fine débridement of the bone surface until the telltale punctate bleeding at
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Fig 1. The basic tools of débridement include rongeurs, curettes, scissors, forceps, and surgical blades.
the freshened bone surface is visible. If serial débridement is planned, it is important to keep tissues moist to prevent dessication between débridements. This holds particularly true for subcutaneous tissue, fascia, and tendons. It is important to pay attention to the colors of the wound bed during débridement. Wounds should be débrided until all grey and black substances have been removed, and only red (muscle), white (tendon, bone, fascia), and/or yellow (subcutaneous fat) tissues remain. Examples of this can be seen in Figs 2-4, and 6. One useful débridement technique is to paint methylene blue over the entire wound bed before débridement to help the surgeon ensure complete, thorough débridement of the wound (Figs 4-6). The blue staining binds irreversibly to the superficial cells of the wound base as well as any exposed crevices or tracks. This technique helps ensure that no exposed or contaminated tissue is left in the wound bed. By removing all of the blue-stained tissue, it is easier to ensure that the entire wound surface is débrided and that colonized cells on the wound surface are removed. Those basic principles hold true for the débridement of both infected and noninfected wounds, but special consideration must be paid to noninfected wounds. Because of the senescent cells around the wound edge, it may be necessary to excise a 2- to 3-mm rim around the periphery of the wound. Senescent cells can have the appearance of an epithelial rim and may very well bleed with superficial débridement. They have been found several millimeters away from the edge of chronic venous leg ulcers even though the tissue appears healthy.27 Although it may seem overly aggressive to remove a rim of apparently normalappearing tissue from a noninfected wound, it is necessary
Fig 2. Chronic wound before débridement. Note the colors of the wound bed. All fibrotic grey and necrotic black tissue must be totally removed to achieve effective débridement.
to remove the senescent cells to recreate an acute wound so that the wound healing cascade can get a fresh start (Figs 5 and 6). The biofilm that develops on the wound base may also have the appearance of granular and viable tissue. It is important to remember that this is essentially an invisible “layer” formed by an extracellular matrix that binds to the wound base, whether dermis, fascia, muscle, tendon, or bone. Because the biofilm binds irreversibly, it is necessary to aggressively débride the wound base with blades, curettes, burrs, and/or electrical blades. It may not be enough to curette deeper, relatively avascular tissues such as tendons and bone.28 For this reason, the authors have recently adopted the use of a hydrosurgical débrider that uses a water jet with up to 15,000 psi to débride these tissues (Fig 3, 6). The Venturi effect caused by this high-pressure water jet evacuates the débrided tissue into the stream of water, thus separating it from underlying tissue. This type of hydrosurgical débridement has been shown to more effectively and efficiently reduce bacteria and biofilm.29 It also removes unwanted tissue and debris with greater precision than with a scalpel by cutting less than a millimeter at a time, therefore minimizing peripheral tissue damage and reducing the removal of healthy tissue.
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Fig 5. Methylene blue has been painted on the entire wound bed intraoperatively. The wound periphery is also outlined with a marking pen to demonstrate senescent cells at the wound edge that need to be removed.
Fig 3. Chronic wound during débridement. Hydrosurgical débridement of the wound bed is performed to remove all nonviable tissue. Note the difference in wound colors compared with the predébridement picture (Fig 2). Only granulation tissue (red), tendon, bone, and fascia (white), and subcutaneous fat (yellow) tissue remains.
Fig 6. Venous stasis wound during débridement. Débridement is performed until all markings are removed, effectively turning the chronic wound into an acute wound. Note the red, white, and yellow wound colors compared with Fig 4.
Fig 4. Chronic, noninfected venous stasis wound. Note the clinical appearance and colors of this chronic wound before débridement.
ISCHEMIC WOUNDS The presence of peripheral vascular disease and chronic limb ischemia deserves special mention, as noninfected
wounds have slightly more flexibility in the timing of a débridement. In the presence of active infection, a wound should be débrided immediately regardless of the need for revascularization. However, if a wound or dry gangrene is present without clinical signs of infection, then revascularization should be performed first. The blood supply to a wound should be optimized before débridement to ensure that potentially viable tissue is not unnecessarily removed. This can be achieved by waiting 4 to 8 days after an open bypass or 3 to 4 weeks after endovascular surgery before performing any definitive débridement on a noninfected wound.30 The difference between viable and nonviable tissue becomes markedly clouded in the presence of ischemia, even without the presence of infection. If dry gangrene is present in a vascularized limb, closely observe for evidence of new tissue growth underneath the
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eschar. If there is purulence or no evidence of new tissue growth, then the wound should be débrided. However, if there is evidence of new tissue growth, then the wound may be observed until the eschar falls off or until signs of infection necessitate débridement. NONSURGICAL DÉBRIDEMENT TECHNIQUES Not all patients are surgical candidates, and not all wounds need to go directly to the operating room for immediate débridement. Several nonsurgical débridement techniques may be used in these situations. Wet-to-dry dressings, where the saline-moistened gauze is allowed to dry on the wound and then is physically ripped off, were a standard mechanical débridement technique. Although this nonselective form of débridement effectively removes dead tissue, it can harm the viable tissue left behind and can be painful in the sensate patient. Therefore, newer techniques, such as topical enzymatic débriding agents that can digest the collagen in necrotic tissue, are now considered first-line treatments.31-35 Maggot débridement therapy (MDT) had been used for centuries to heal wounds but has only been recently revisited and revised as a form of therapy when surgical intervention is not an option. It has also been found to be surprisingly effective in the presence of resistant strains of bacteria. Medical maggots, most commonly the blowfly species Lucilia sericata, are selective in débriding necrotic, fibrotic tissue while sparing healthy tissue. In addition to the secretion of proteolytic digestive enzymes that dissolve necrotic tissue, L sericata has also been shown to secrete various cytokines and tissue growth factors that can increase local tissue oxygenation.36 It has therefore been proposed that MDT not only débrides and disinfects wounds but also promotes healing. Studies have demonstrated that MDT is a cost-effective, efficient method in débridement of ulcerations in nonsurgical patients with relatively very few side effects.36-38 However, aside from débridement of venous wounds, Dumville et al39 found that MDT did not increase healing rates and was associated with significantly more pain in the patients receiving MDT compared with hydrogel. Débridement using noncontact low-frequency ultrasound therapy also appears to play a role in débriding and healing chronic ulcers.40-44 This technique creates a combination of cavitation and microstreaming that provides a mechanical energy capable of altering cell membrane activity, and in turn, cellular activity.44 It helps separate necrotic tissue from the underlying bed, kills bacteria, and disrupts biofilm. It also may induce wound healing through a broad range of factors, including leukocyte adhesion, growth factor production, collagen production, increased angiogenesis, increased macrophage responsiveness, increased fibrinolysis, and increased nitric oxide levels.45 One study suggests that ultrasound débridement may disrupt quorum sensing within biofilms, thereby leading to decreased coordinated virulence38; however, further research in this area is needed.
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CONCLUSION Panuncialman and Falanga16,45 have recently reviewed the science of wound bed preparation and underscore the importance of débridement as a critical step in the transition of a chronic wound into an acute wound. They appropriately caution, however, that débridement is just one of the required interventions and that it can be difficult to determine when débridement has achieved its maximum effect. Patients must also be systemically optimized from a metabolic standpoint, with considerations of nutritional status, smoking status, and glycemic control at the forefront. The vasculature must be regulated, both in arterial supply maximization and periwound edema minimization. Other potential causes of wound formation, such as increased areas of pressure in the setting of neuropathy, must also be addressed. Although there are many potential causes for the pathophysiology of wound chronicity in the absence of infection, the irreversible development of senescent cells around the wound edge and biofilm on the wound base should not be overlooked. Wounds that do not progress toward closure at a consistent rate (about a 50% decrease in wound volume in 4 weeks or a 10% to 15% decrease in wound volume per week), should be considered chronic and warrant a change in intervention.46 Débridement, even in the absence of infection, remains a cornerstone of these potential interventions. REFERENCES 1. Broughton G, Janis JE, Attinger CE. A brief history of wound care. Plast Reconstr Surg 2006;117(7 Suppl):6S-11S. 2. Attinger CE, Bulan E, Blume PA. Surgical debridement: the key to successful wound healing and reconstruction. Clin Podiatr Med Surg 2000;17:599-630. 3. Attinger CE, Janes JE, Steinberg JS, Schwartz J, Al-Attar A, Couch K. Clinical approach to wounds: debridement and wound bed preparation including the use of dressings and wound-healing adjuvants. Plast Reconstr Surg 2006;117(7 Suppl):72-109S. 4. Armstrong DG, Lavery LA, Nixon BP, Boulton AJ. It’s not what you put on, but what you take off: techniques for debriding and off-loading the diabetic foot wound. Clin Infect Dis 2004; 39(Suppl 2): S92-9. 5. Cardinal M, Eisenbud DE, Armstrong DG, Zelen C, Driver V, Attinger C, et al. Serial surgical debridement: a retrospective study on clinical outcomes in chronic lower extremity wounds. Wound Repair Regen 2009;17:306-11. 6. Saap LJ, Falanga V. Debridement performance index and its correlation with complete closure of diabetic foot ulcers. Wound Repair Regen 2002;10:354-9. 7. Kumagi SG, Mahoney CR, Fitzgibbons TC, McMullen ST, Connolly TL, Henkel L. Treatment of diabetic (neuropathic) foot ulcers with two-stage debridement and closure. Foot Ankle Int 1998;19:160-5. 8. Williams D, Enoch S, Miller D, Harris K, Price P, Harding KG. Effect of sharp debridement using curette on recalcitrant nonhealing venous leg ulcers: a concurrently controlled, prospective cohort study. Wound Repair Regen 2005;132:131-7. 9. 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;183:61-4. 10. Brem H, Sheehan P, Rosenberg HJ, Schneider JS, Boulton AJ. Evidence-based protocol for diabetic foot ulcers. Plast Reconstr Surg 2006;117(7 Suppl):193-209S. 11. Piaggesi A, Schipani E, Campi F, Romanelli M, Baccetti F, Arvia C, et al. Conservative surgical approach versus non-surgical management for
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diabetic neuropathic foot ulcers: a randomized trial. Diabet Med 1998;15:4412-7. Dryburgh N, Smith F, Donaldson J, Mitchell M. Debridement for surgical wounds. Cochrane Database Syst Rev 2008:CD006214. Gottrup F. Debridement: another evidence problem in wound healing. Wound Repair Regen 2009;17:294-5. James GA, Swogger E, Wolcott R, Pulcini ED, Secor P, Sestrich J, et al. Biofilms in chronic wounds. Wound Repair Regen 2008;16:37-44. Broughton G 2nd, Janis JE, Attinger CE. The basic science of wound healing. Plast Reconstr Surg 2006;117(7 Suppl):12-34S. Panuncialman J, Falanga V. The science of wound bed preparation. Surg Clin North Am 2009;89:611-26. Clark RA. Oxidative stress and “senescent” fibroblasts in non-healing wounds as potential therapeutic targets. J Invest Dermatol 2008;128: 2361-4. Vande Berg JS, Rose MA, Haywood-Reid PL, Rudolph R, Payne WG, Robson MC. Cultured pressure ulcer fibroblasts show replicative senescence with elevated production of plasmin, plasminogen activator inhibitor-1, and transforming growth factor-beta 1. Wound Repair Regen 2005;13:76-83. Almqvist S, Werthen M, Johansson A, Tornqvist J, Agren MS, Thomsen P. Evaluation of near-senescent human dermal fibroblast cell line and effect of amelgenin. Br J Dermatol 2009;160:1163-71. Mendez MV, Raffetto JD, Phillips T, Menzoian JO, Park HY. The proliferative capacity of neonatal fibroblasts is reduced after exposure to venous ulcer fluid: a potential mechanism for senescence in venous ulcerats. J Vasc Surg 1999;30:734-43. Harding KG, Moore K, Phillips TJ. Wound chronicity and fibroblast senescence—implications for treatment. Int Wound J 2005;2:364-8. Stanley A, Osler T. Senescence and the healing rates of venous ulcers. J Vasc Surg 2001;33:1206-11. Martin JM, Zenilman JM, Lazarus GS. Molecular microbiology: new dimensions for cutaneous biology and wound healing. J Invest Dermatol 2010;130:38-48. Davis SC, Martinez L, Kirsner R. The diabetic foot: the importance of biofilms and wound bed preparation. Curr Diab Rep 2006;6:439-45. Brady RA, Leid JG, Calhoun JH, Costerton W, Shirtliff ME. Osteomyelitis and the role of biofilms in chronic infection. FEMS Immunol Med Microbiol 2008;52:13-22. Costerton W, Veeh R, Shirtliff M, Pasmore M, Post C, Ehrlich G. The application of biofilm science to the study and control of chronic bacterial infections. J Clin Invest 2003;112:1466-77. Brem H, Golink MS, Stojadinovic O, Kodra A, Diegelmann RF, Vukelic S, et al. Primary cultured fibroblasts derived from patient with chronic wounds: a methodology to produce human cells and test putative growth factor therapy such as GMC SF. J Transl Med 2008; 6:75. Kirsner R. Biofilms, bioburden, and senescent cells: role of biofilms in osteomyelitis and wound failure. Presented at the Diabetic Limb Salvage Conference, Washington, DC; Sept 24-26, 2009. Bowling FL, Stickings DS, Edwards-Jones V, Armstrong DG, Armstrong AJ. Hydrodebridement of wounds: effectiveness in reducing
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wound bacterial contamination and potential for air bacterial contamination. J Foot Ankle Res 2009;2:13. Caselli A, Latini V, Lapenna A, Di Carlo S, Pirozzi F, Benvenuto A, et al. Transcutaneous oxygen tension monitoring after successful revascularization in diabetic patients with ischaemic foot ulcers. Diabet Med 2005;22:460-5. Game F. The advantages and disadvantages of non-surgical management of the diabetic foot. Diabetes Met Res Rev 2008;24(Suppl 1): S72-5. Enoch S, Grey JE, Harding KG. ABC of wound healing. Non-surgical and drug treatments. BMJ 2006;332:900-3. Klasen HJ. A review of the nonoperative removal of necrotic tissue from burn wounds. Burns 2000;26:207-22. Davies CE, Turton G, Woolfrey G, Elley R, Taylor M. Exploring debridement options for chronic venous leg ulcers. Br J Nurs 2005;14: 393-7. Singhal A, Reis ED, Kerstein MD. Options for nonsurgical debridement of necrotic wounds. Adv Skin Wound Care 2001;14:96-100. Sherman RA. Maggot therapy for foot and leg wounds. Int J Low Extrem Wounds 2002;1:135-42. Sherman RA, Shapiro CE, Yang RM. Maggot therapy for problematic wounds: uncommon and off-label applications. Adv Skin Wound Care 2007;20:602-10. Tantawi TI, Gohar YM, Kotb MM, Beshara FM, El-Naggar MM. Clinical and microbiological efficiency of MDT in the treatment of diabetic foot ulcers. J Wound Care 2007;16:379-83. Dumville JC, Worthy G, Bland JM, Cullum N, Dowson C, Iglesias C, et al; VenUS II team. Larval therapy for leg ulcers (VenUS II): randomized controlled trial. BMJ 2009;338:b773. Bell AL, Cavorsi J. Noncontact ultrasound therapy for adjunctive treatment of nonhealing wounds: retrospective analysis. Phys Ther 2008;88:1517-24. Ramundo J, Gray M. Is ultrasonic mist therapy effective for debriding chronic wounds? J Wound Ostomy Continence Nurs 2008;35:579-83. Hinchliffe RJ, Valk GD, Apelqvist J, Armstrong DG, Bakker K, Game FL, et al. A systemic review of the effectiveness of interventions to enhance the healing of chronic ulcers of the foot in diabetes. Diabetes Metab Res Rev 2008;24(Suppl 1):S119-44. Ennis WJ, Foremann P, Mozen N, Massey J, Conner-Kerr T, Meneses P. Ultrasound therapy for recalcitrant diabetic foot ulcers: results of a randomized, double-blind, controlled, multicenter study. Ostomy Wound Manage 2005;51:24-39. Ennis WJ, Valdes W, Gainer M, Meneses P. Evaluation of clinical effectiveness of MIST ultrasound therapy for the healing of chronic wounds. Adv Skin Wound Care 2006;19:437-46. Panuncialman J, Falanga V. The science of wound bed preparation. Clin Plast Surg 2007;34:621-32. Sheehan P, Jones P, Giurini JM, Caselli A, Veves A. Percent change in wound area of diabetic foot ulcers over a 4-week period is a robust predictor of complete healing in a 12-week prospective trial. Plast Reconstr Surg 2006;117(7 Suppl):239S-244S.
The most general definition of débridement is the process in which all materials incompatible with healing are removed from a wound. This definition has grown broader with time and classically involves the surgical excision of all grossly infected and necrotic tissue. Military surgeons in the 18th and 19th centuries, most notably the Belgian Antione Depage, developed techniques of aggressive excision on the battlefields of Europe to prevent gangrene and save lives.1 We now know, however, that tissue does not have to be actively infected or necrotic to impair the biologic wound healing processes of the body. Effective débridement can be achieved with nonsurgical means in some cases, while the growing utility and importance of serial débridement of chronic wounds is becoming more apparent.2-13 The intended emphasis of this article is to provide a review of the processes of débridement in the noninfected wound. The goals are to (1) focus on the pathophysiology of the target tissue causing wound-healing impairment in the absence of infection, and (2) recommend specific techniques for débridement. INFLAMMATION VS INFECTION Because inflammation is an objective hallmark of both infected and chronic wounds, it can often represent a clinical challenge to determine whether a lower extremity wound is actively infected or simply chronically inflamed. One might easily say that all infection is inflammatory but From the Diabetic Limb Salvage, Department of Plastic Surgery, Georgetown University Medical Center;a Department of Podiatric Surgery, Temple University School of Podiatric Medicine;b Department of Plastic Surgery, Georgetown University School of Medicine, and The Center for Wound Healing, Georgetown University Hospital;c and Division of Wound Healing, Department of Plastic & Orthopedic Surgery, Georgetown University School of Medicine, and The Center for Wound Healing, Georgetown University Hospital.d Competition of interest: none. This article is being co-published in the Journal of Vascular Surgery® and the Journal of the American Podiatric Medical Association. Correspondence: Christopher E. Attinger, MD, Georgetown University Medical Center, Department of Plastic Surgery, 3800 Reservoir Rd, NW, Washington, DC 20007 (e-mail: [email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a competition of interest. 0741-5214/$36.00 Copyright © 2010 by the Society for Vascular Surgery and the American Podiatric Medical Association. doi:10.1016/j.jvs.2010.06.006
that not all inflammation is infectious. Further clouding this issue is the reality that all wounds are expected to have at least some degree of bacterial colonization, even in the absence of active clinical infection. Indeed ⱖ60% of chronic wounds contain biofilm.14 It is important to determine at which point critical colonization has been reached or the level at which the type and quantity of bacteria begin to cause active infection. Although the presence of any bacteria is certain to have at least some effect on the biologic processes of wound healing, specific treatment and surgical interventions should depend on whether critical colonization is present with active infection. These seemingly subtle differences should guide the surgical treatment plan and the target tissues of débridement. Surrounding erythema, swelling, induration, tenderness, and malodor are the expected characteristics of an infected wound. The target tissue for débridement in this situation is the en masse excision of all grossly infected and necrotic tissue. The wound requires exploration to discover any deep pockets, abscesses, or tracking along fascial and tendinous structures. Adjunctive antibiotic therapy is required to help in eradicating the bacteria. On the other hand, a noninfected but chronic wound can still be expected to have a rim of surrounding erythema, even without other local clinical signs of infection. Periwound erythema does not necessarily indicate a cellulitis from an infection source but rather inflammation in response to an open lesion. The target tissue for débridement in this case is somewhat different. Certainly, any necrotic tissue and bacterial colonization should be removed, but equally important is targeting the débridement toward the cells on the wound edge and base that are irreversibly fixed in the inflammatory stage of wound healing. The important distinction here is that in the absence of infection, a wound can be caught in a chronic inflammatory phase, despite bacteria having been controlled with topical and systemic antibiotics. Débridement is required to convert the chronic wound bed into an acute wound. Another situation is where a wound may have the clinical appearance of local infection and periwound cellulitis, but the erythema is due to ischemic rubor. Here, all local signs of infection disappear with simple elevation of the limb. In this case, the target tissue for intervention is not local but involves systemic revascularization. These three situations of periwound erythema around a wound have a similar presenta31S
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tion yet demonstrate three different interventions in terms of surgical target tissue. Surgeons working with the lower extremity must develop a sharp clinical acumen to determine the difference between an infected wound and one that is merely chronically inflamed. It is important to appreciate that most of our laboratory and advanced imaging diagnostic tools provide clinicians with general information about inflammation and not specifically infection. These are indirect markers that should guide clinical judgment. Lower extremity wound infection is primarily a clinical diagnosis, and experience is required to make the correct diagnosis. ACUTE VS CHRONIC WOUND HEALING Chronic inflammation is an important consideration not just in the clinical presentation of a wound but also in terms of the pathophysiology of wound development. Acute wounds should proceed quickly and uneventfully through the normal stages of the healing processes: inflammation, proliferation, and maturation.15 These stages represent normal physiology after a linear pathway. There is a distinct start point represented by wound formation and a clear end point marked by wound closure. Unfortunately for chronic wounds, the progression along this linear pathway is arrested, and one sees the pathophysiology of a chronic cycle without a clear end point of wound closure. A chronic wound is usually arrested in the inflammatory stage and cannot progress further. Infection is not required for a wound to become fixed in the inflammatory stage, although it could be a contributing factor. Abnormal metalloproteases produced by necrotic tissue, foreign material, and bacteria impede the body’s attempt to heal by overwhelming the building blocks— chemotactant factors, growth factors, mitogens—needed for normal wound healing. This hostile environment enables bacteria to proliferate and could lead to critical colonization. This environment further inhibits healing by producing destructive enzymes and consuming the local resources— oxygen, nutrition, and building blocks—necessary for healing. Further, there are two significant changes to the cells of a chronic wound, specifically those on the wound base and edge, which are affected by this pathophysiology even in the absence of infection. The presence of senescent cells and biofilm irreversibly impair acute wound healing. Fibroblasts, one of the normal building blocks of an acute wound, have demonstrated phenotypically and irreversibly altered differences in the setting of chronic wounds.16 From a mitotic standpoint, these cells are less active and have decreased ability to perform the DNA replication required for proliferation.17 They also produce abnormal proteolytic enzymes and metalloproteases that contribute to the chronic wound environment.18-20 And similar to the critical contamination concept when considering bacteria, there may be a “critical number” of senescent cells within a wound that make healing unlikely regardless of intervention.21,22 In addition, the role of bacterial biofilms in chronic wound development has become increasingly apparent in
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recent years. According to a study that used scanning electron microscopy, 60% of chronic wounds contained a biofilm compared with only 6% of acute wounds.14 A biofilm is a polymicrobial sessile community of phenotypically-altered microorganisms that develop on the surface of chronic wounds, requiring only the presence of bacteria and not critical colonization.23,24 These bacterial cells bind to each other and the wound base, producing an extrapolymetric substance varying in depth from a single cell layer to a thick community of cells. Quorum sensing describes the process through which the cells are phenotypically altered and able to operate with down-regulated cellular activity and at a lower metabolic level.25,26 The embedded nature and altered metabolic state of the biofilm represent an effective barrier to traditional forms of intervention, including topical treatments and antibiotic therapy. The biofilm and senescent cells on the wound base and periphery comprise the primary target tissues for surgical intervention of the noninfected wound. One may equate the excision of these cells from a noninfected wound as the equivalent of the excision of most if not all of the bacteria from an infected wound. SURGICAL DÉBRIDEMENT TECHNIQUES The use of atraumatic surgical techniques should be maximized when performing débridement to avoid damaging the underlying healthy tissue. One should also attempt to leave behind as much viable tissue as possible, because these remnants will form the building blocks for subsequent healing in vascular in-growth and the delivery of growth factors and nutrients. Traumatic techniques that will cause untoward damage to otherwise healthy and biologic tissue include the charring of tissue with electrocautery and tying off large clumps of tissue with suture. Although both may be necessary to a lesser degree to achieve adequate hemostasis, their use should be avoided as much as possible and topical hemostatic agents and pressure should be used instead. The specific tools of débridement will also have an effect on the underlying viable tissue. Whether in the office or operating room, sterile surgical instruments are recommended over the use of disposable suture removal kits. The latter are usually dull and may crush and damage the remaining skin edge and underlying tissue. The basic tools of débridement include blades, forceps, scissors, curettes, and rongeurs (Fig 1). Only the tissue that is being excised should be grasped with the forceps, and #10 or #20 blades are used to sequentially slice off thin layers of tissue. These blades should be changed frequently because they can dull quickly. Sharpedged curettes are useful for removing the proteinaceous coagulum that accumulates on top of both fresh and chronic granulation tissue. Rongeurs are useful for removing hard-to-reach soft tissue and for débriding or biopsying bone. An air-driven or electrical sagittal saw can serially remove thin layers of bone until normal cortex and marrow is reached. Cutting burrs and rasps permit fine débridement of the bone surface until the telltale punctate bleeding at
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Fig 1. The basic tools of débridement include rongeurs, curettes, scissors, forceps, and surgical blades.
the freshened bone surface is visible. If serial débridement is planned, it is important to keep tissues moist to prevent dessication between débridements. This holds particularly true for subcutaneous tissue, fascia, and tendons. It is important to pay attention to the colors of the wound bed during débridement. Wounds should be débrided until all grey and black substances have been removed, and only red (muscle), white (tendon, bone, fascia), and/or yellow (subcutaneous fat) tissues remain. Examples of this can be seen in Figs 2-4, and 6. One useful débridement technique is to paint methylene blue over the entire wound bed before débridement to help the surgeon ensure complete, thorough débridement of the wound (Figs 4-6). The blue staining binds irreversibly to the superficial cells of the wound base as well as any exposed crevices or tracks. This technique helps ensure that no exposed or contaminated tissue is left in the wound bed. By removing all of the blue-stained tissue, it is easier to ensure that the entire wound surface is débrided and that colonized cells on the wound surface are removed. Those basic principles hold true for the débridement of both infected and noninfected wounds, but special consideration must be paid to noninfected wounds. Because of the senescent cells around the wound edge, it may be necessary to excise a 2- to 3-mm rim around the periphery of the wound. Senescent cells can have the appearance of an epithelial rim and may very well bleed with superficial débridement. They have been found several millimeters away from the edge of chronic venous leg ulcers even though the tissue appears healthy.27 Although it may seem overly aggressive to remove a rim of apparently normalappearing tissue from a noninfected wound, it is necessary
Fig 2. Chronic wound before débridement. Note the colors of the wound bed. All fibrotic grey and necrotic black tissue must be totally removed to achieve effective débridement.
to remove the senescent cells to recreate an acute wound so that the wound healing cascade can get a fresh start (Figs 5 and 6). The biofilm that develops on the wound base may also have the appearance of granular and viable tissue. It is important to remember that this is essentially an invisible “layer” formed by an extracellular matrix that binds to the wound base, whether dermis, fascia, muscle, tendon, or bone. Because the biofilm binds irreversibly, it is necessary to aggressively débride the wound base with blades, curettes, burrs, and/or electrical blades. It may not be enough to curette deeper, relatively avascular tissues such as tendons and bone.28 For this reason, the authors have recently adopted the use of a hydrosurgical débrider that uses a water jet with up to 15,000 psi to débride these tissues (Fig 3, 6). The Venturi effect caused by this high-pressure water jet evacuates the débrided tissue into the stream of water, thus separating it from underlying tissue. This type of hydrosurgical débridement has been shown to more effectively and efficiently reduce bacteria and biofilm.29 It also removes unwanted tissue and debris with greater precision than with a scalpel by cutting less than a millimeter at a time, therefore minimizing peripheral tissue damage and reducing the removal of healthy tissue.
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Fig 5. Methylene blue has been painted on the entire wound bed intraoperatively. The wound periphery is also outlined with a marking pen to demonstrate senescent cells at the wound edge that need to be removed.
Fig 3. Chronic wound during débridement. Hydrosurgical débridement of the wound bed is performed to remove all nonviable tissue. Note the difference in wound colors compared with the predébridement picture (Fig 2). Only granulation tissue (red), tendon, bone, and fascia (white), and subcutaneous fat (yellow) tissue remains.
Fig 6. Venous stasis wound during débridement. Débridement is performed until all markings are removed, effectively turning the chronic wound into an acute wound. Note the red, white, and yellow wound colors compared with Fig 4.
Fig 4. Chronic, noninfected venous stasis wound. Note the clinical appearance and colors of this chronic wound before débridement.
ISCHEMIC WOUNDS The presence of peripheral vascular disease and chronic limb ischemia deserves special mention, as noninfected
wounds have slightly more flexibility in the timing of a débridement. In the presence of active infection, a wound should be débrided immediately regardless of the need for revascularization. However, if a wound or dry gangrene is present without clinical signs of infection, then revascularization should be performed first. The blood supply to a wound should be optimized before débridement to ensure that potentially viable tissue is not unnecessarily removed. This can be achieved by waiting 4 to 8 days after an open bypass or 3 to 4 weeks after endovascular surgery before performing any definitive débridement on a noninfected wound.30 The difference between viable and nonviable tissue becomes markedly clouded in the presence of ischemia, even without the presence of infection. If dry gangrene is present in a vascularized limb, closely observe for evidence of new tissue growth underneath the
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eschar. If there is purulence or no evidence of new tissue growth, then the wound should be débrided. However, if there is evidence of new tissue growth, then the wound may be observed until the eschar falls off or until signs of infection necessitate débridement. NONSURGICAL DÉBRIDEMENT TECHNIQUES Not all patients are surgical candidates, and not all wounds need to go directly to the operating room for immediate débridement. Several nonsurgical débridement techniques may be used in these situations. Wet-to-dry dressings, where the saline-moistened gauze is allowed to dry on the wound and then is physically ripped off, were a standard mechanical débridement technique. Although this nonselective form of débridement effectively removes dead tissue, it can harm the viable tissue left behind and can be painful in the sensate patient. Therefore, newer techniques, such as topical enzymatic débriding agents that can digest the collagen in necrotic tissue, are now considered first-line treatments.31-35 Maggot débridement therapy (MDT) had been used for centuries to heal wounds but has only been recently revisited and revised as a form of therapy when surgical intervention is not an option. It has also been found to be surprisingly effective in the presence of resistant strains of bacteria. Medical maggots, most commonly the blowfly species Lucilia sericata, are selective in débriding necrotic, fibrotic tissue while sparing healthy tissue. In addition to the secretion of proteolytic digestive enzymes that dissolve necrotic tissue, L sericata has also been shown to secrete various cytokines and tissue growth factors that can increase local tissue oxygenation.36 It has therefore been proposed that MDT not only débrides and disinfects wounds but also promotes healing. Studies have demonstrated that MDT is a cost-effective, efficient method in débridement of ulcerations in nonsurgical patients with relatively very few side effects.36-38 However, aside from débridement of venous wounds, Dumville et al39 found that MDT did not increase healing rates and was associated with significantly more pain in the patients receiving MDT compared with hydrogel. Débridement using noncontact low-frequency ultrasound therapy also appears to play a role in débriding and healing chronic ulcers.40-44 This technique creates a combination of cavitation and microstreaming that provides a mechanical energy capable of altering cell membrane activity, and in turn, cellular activity.44 It helps separate necrotic tissue from the underlying bed, kills bacteria, and disrupts biofilm. It also may induce wound healing through a broad range of factors, including leukocyte adhesion, growth factor production, collagen production, increased angiogenesis, increased macrophage responsiveness, increased fibrinolysis, and increased nitric oxide levels.45 One study suggests that ultrasound débridement may disrupt quorum sensing within biofilms, thereby leading to decreased coordinated virulence38; however, further research in this area is needed.
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CONCLUSION Panuncialman and Falanga16,45 have recently reviewed the science of wound bed preparation and underscore the importance of débridement as a critical step in the transition of a chronic wound into an acute wound. They appropriately caution, however, that débridement is just one of the required interventions and that it can be difficult to determine when débridement has achieved its maximum effect. Patients must also be systemically optimized from a metabolic standpoint, with considerations of nutritional status, smoking status, and glycemic control at the forefront. The vasculature must be regulated, both in arterial supply maximization and periwound edema minimization. Other potential causes of wound formation, such as increased areas of pressure in the setting of neuropathy, must also be addressed. Although there are many potential causes for the pathophysiology of wound chronicity in the absence of infection, the irreversible development of senescent cells around the wound edge and biofilm on the wound base should not be overlooked. Wounds that do not progress toward closure at a consistent rate (about a 50% decrease in wound volume in 4 weeks or a 10% to 15% decrease in wound volume per week), should be considered chronic and warrant a change in intervention.46 Débridement, even in the absence of infection, remains a cornerstone of these potential interventions. REFERENCES 1. Broughton G, Janis JE, Attinger CE. A brief history of wound care. Plast Reconstr Surg 2006;117(7 Suppl):6S-11S. 2. Attinger CE, Bulan E, Blume PA. Surgical debridement: the key to successful wound healing and reconstruction. Clin Podiatr Med Surg 2000;17:599-630. 3. Attinger CE, Janes JE, Steinberg JS, Schwartz J, Al-Attar A, Couch K. Clinical approach to wounds: debridement and wound bed preparation including the use of dressings and wound-healing adjuvants. Plast Reconstr Surg 2006;117(7 Suppl):72-109S. 4. Armstrong DG, Lavery LA, Nixon BP, Boulton AJ. It’s not what you put on, but what you take off: techniques for debriding and off-loading the diabetic foot wound. Clin Infect Dis 2004; 39(Suppl 2): S92-9. 5. Cardinal M, Eisenbud DE, Armstrong DG, Zelen C, Driver V, Attinger C, et al. Serial surgical debridement: a retrospective study on clinical outcomes in chronic lower extremity wounds. Wound Repair Regen 2009;17:306-11. 6. Saap LJ, Falanga V. Debridement performance index and its correlation with complete closure of diabetic foot ulcers. Wound Repair Regen 2002;10:354-9. 7. Kumagi SG, Mahoney CR, Fitzgibbons TC, McMullen ST, Connolly TL, Henkel L. Treatment of diabetic (neuropathic) foot ulcers with two-stage debridement and closure. Foot Ankle Int 1998;19:160-5. 8. Williams D, Enoch S, Miller D, Harris K, Price P, Harding KG. Effect of sharp debridement using curette on recalcitrant nonhealing venous leg ulcers: a concurrently controlled, prospective cohort study. Wound Repair Regen 2005;132:131-7. 9. 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;183:61-4. 10. Brem H, Sheehan P, Rosenberg HJ, Schneider JS, Boulton AJ. Evidence-based protocol for diabetic foot ulcers. Plast Reconstr Surg 2006;117(7 Suppl):193-209S. 11. Piaggesi A, Schipani E, Campi F, Romanelli M, Baccetti F, Arvia C, et al. Conservative surgical approach versus non-surgical management for
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