Skip to main content
Features

Assessing Current Options For Debriding Diabetic Foot Ulcers

Debridement is a vital component of successful treatment for diabetic foot ulcers (DFUs). Accordingly, these authors review various available debridement methods and share insights from the literature to help navigate the appropriate treatment pathway for each case.

Foot ulceration is a major complication that affects approximately 15 percent of patients with diabetes.1,2 Debridement, or the removal of nonviable tissue, is an essential aspect of ulcer treatment and considered to be a standard of care.3 Studies show that more frequent debridements are associated with increased wound healing rates.2,4 One can achieve proper debridement in a variety of ways and each technique has its own indications, risks and benefits. Accordingly, let us take a closer look at the most recent and relevant literature related to current debridement techniques, including surgical, hydrosurgical, ultrasonic, enzymatic, biological, mechanical, autolytic and laser debridement.

Sharp, or surgical, debridement is a longstanding treatment of choice in wound care (see top photo above).5 Clinicians often combine adjunctive debridement therapies with sharp debridement. In a randomized controlled study comparing surgical and non-surgical care for diabetic foot ulcerations (DFUs), Piaggesi and colleagues concluded that sharp debridement was a more effective treatment for DFUs, resulting in higher patient satisfaction, lower patient discomfort, less time to healing, lower complications and significantly fewer infections.5 

The process of sharp debridement converts chronic, non-healing ulcerations into acute wounds.6 Histologically, neutrophils and macrophages that are recruited to the site of the acute trauma secrete growth factors to stimulate wound healing and wound bed perfusion, and increase phagocytosis of bacteria and non-viable wound tissue.6 During sharp debridement, one uses a scalpel, curette, tissue nipper or other tool to remove all non-vital tissue. This also removes potential contaminants, bacterial burden or biofilm from the bed and edges of a wound.6

Sharp debridement is quick, highly selective and is applicable to almost all wound types.7-10 In fact, wound healing centers utilizing less frequent debridement note increased time to healing, independent of the treatment group.9 However, if a patient has vascular compromise, a densely adherent eschar or a clotting disorder, sharp debridement is contraindicated. 

What You Should Know About Hydrosurgical And Ultrasonic Debridement 

Hydrosurgery is a form of debridement which aims to provide a clean, granular and healthy wound bed via a powerful stream of saline (approximately 15,000 psi) through a sterile circuit.11 With a parallel orientation to the wound bed, hydrosurgical debridement enables clinicians to remove all debris from the wound bed with surgical precision while preserving healthy tissue that may be compromised during sharp excisional debridement. 

In an animal model comparing hydrosurgical to sharp surgical debridement, Hirokawa and colleagues found that hydrosurgical debridement techniques caused less blood loss, minimized damage to healthy tissue, improved inflammation in the wound bed and less deep dense inflammatory cell infiltration.12 Authors in another study found more vascular endothelial cells after hydrosurgical debridement as well as a thinner, reactive fibrotic layer.13 Hirokawa and coworkers also found that debridement time and time to healing were significantly shorter with hydrosurgical debridement versus surgical debridement.12,13 Hydrosurgical debridement is reportedly most effective in fibrous, necrotic and granular tissue beds.11 However, this debridement technique is not suited for desiccated eschars.11 

Wang and colleagues have demonstrated that ultrasonic debridement is superior to standard wound care (see second photo above).14 One can perform ultrasonic debridement through direct contact or indirect contact, and with high (one MHz to 10 MHz) and low (20 to 60 kHz) frequencies and intensities. A systematic review of ultrasound therapy found that both low-frequency, low-intensity and low-frequency, high-intensity ultrasound therapy have wound healing benefits.15 In their meta-analysis, Voigt and colleagues specifically noted early healing with diabetic ulcerations when researchers employed either low-frequency, low-intensity noncontact ultrasound debridement or low-frequency, high-intensity contact ultrasound debridement.15 On a cellular level, ultrasound debridement may cause conformational changes in proteins and stimulate signal transduction pathways.16 For example, researchers have attributed growth factor production, collagen production, increased angiogenesis, macrophage and leukocyte response, and increased nitric oxide to ultrasonic debridement.16 

While all ultrasound debridement produces thermal and nonthermal effects, clinicians frequently use direct-contact, low-frequency ultrasound with a probe to remove all non-viable soft-tissue and help promote a healthier wound bed.15 This type of ultrasound also produces bubble cavitation, a nonthermal, acoustic phenomenon which tests the tensile strength of each cell with shearing force and selectively removes proteinaceous material from the wound base.17 As the tensile strength of healthy cells is stronger than that of necrotic tissue, ultrasound debridement allows one to perform targeted debridement of necrotic tissue without damage to healthy tissue.17 This is a form of mechanical energy release.18 The mixture of direct-contact, low-frequency ultrasound and the hydrodynamic effects like bubble cavitation causes necrotic tissue fragmentation, emulsion and overall destruction.19 

Ultrasonic debridement also removes bacteria and debris from wound beds. However, this creates a concern for possible aerosol contamination, necessitating the use of proper protective equipment for providers and patients.17 

Key Considerations With Enzymatic Debridement 

Enzymatic debridement ideally removes wound debris (specifically collagen, fibrin and elastin) without harming healthy tissue through proteolytic enzyme activity.20-22 Clinicians have used enzymatic debridement for nearly 50 years and one can employ this debridement method for wounds in patients with multiple comorbidities and complications.23 Enzymatic debridement is effective for a large range of wound types, including pressure, surgical, diabetic, burn, partial-thickness and chronic leg ulcerations.20,21,23-26 

Enzymatic debridement agents come in various forms with different sources and activity. Collagenase-based products are proteinases clinicians may employ for necrotic tissue in burns and dermal ulcers (see third photo above).27 Specifically, collagenase products allow for keratinocyte and fibroblast migration through increased wound bed permeability and release of stimulatory peptide fragments.23 However, the exact mechanism is not understood. In a study examining collagenase clostridium, researchers showed that keratinocyte migration increased twofold in comparison to carboxymethyl cellulose and platelet-derived growth factor-BB (PDGF-BB).28 

The literature suggests enzymatic debridement is effective in necrotic and sloughy tissue, and can be cost-effective in comparison to wet-to-dry dressings or autolytic debridement.20,23,26 However, it is most effective in combination with other debridement methods, such as surgical debridement.29 Overall, enzymatic debridement is a safe, cost-efficient and effective wound debridement tool, either in combination with other therapies or individually, in many populations.22,23,26,29 

Understanding Biological And Mechanical Debridement 

Medical maggot therapy involves the use of medical-grade larvae from a variety of fly species to remove devitalized tissue from the wound bed without causing harm to healthy and periwound skin.30 However, some studies have suggested that clinicians consider the protection of epithelialized skin due to possible debridement by the larvae.31 One may utilize biological debridement in wounds with and without infection, and various researchers have assessed this modality for a variety of wounds including chronic, trophic, malignant, diabetic, leg and traumatic wounds.30-34 In fact, multiple authors have found that biological debridement is as powerful as more traditional debridement techniques for diabetic foot ulcers.35,36 

Unfortunately, medical maggot therapy is not ideal in dry wounds or extremely wet or deep wounds. Maggots need a moist wound environment for survival but may suffocate in heavy exudate or deeper wounds.29 This treatment can also increase pain during the debridement period.37 

Biological debridement has other benefits besides removing devitalized tissue. Microbiotic activity can persist in chronic wounds. However, Margolin and Gialanella have presented empirical evidence that medical maggots lyse bacteria and fungi in the wound bed.38 Medical maggots are also effective in combatting methicillin-resistant Staphylococcus aureus (MRSA), Pseudomonas aeruginosa, vancomycin-resistant Enterococcus (VRE), Escherichia coli, Klebsiella pneumoniae and Candida albicans.33,38 The effect on the bacteria caused by maggot therapy begins as soon as 24 hours from application.37 This property of larvae debridement therapy is attributed to phenylacetic acid and phenylacetaldehyde production in maggot byproducts.31 Outside of antimicrobial properties, maggots also release growth factors to stimulate fibroblasts and increase granular tissue in the wound bed.31 

Clinicians hesitate to use this therapy at times due to anticipated patient resistance. Biological debridement modalities are generally accepted by patients in a wide range of settings, including hospitals and clinical offices.39 However, consensus on the cost-effectiveness of medical maggot therapy remains elusive at this time.30,31 

Mechanical debridement debrides both vital and devitalized tissue (see fourth photo above). Types of mechanical debridement include wet-to-dry dressings, whirlpool and soft fiber scrubs. Wounds with more necrotic than granular tissue would benefit from mechanical debridement. 

Wet-to-dry dressings need frequent changes (three to four times per day) to be effective and can be painful to patients. Research shows there are better and more cost-effective ways to debride than wet-to-dry dressings.40 Additionally, Dale and Wright noted that eliminating a wet-to-dry dressing from their home health protocol decreased emergent wound care examinations, improved healing rates, lowered adverse reactions, increased physician and patient satisfaction, and reduced supply costs.41 

Slough in wounds is problematic in that it prevents accurate depth measurement, disrupts visualization of the wound bed and impedes wound healing by providing a reservoir for pathogens.42 Monofilament wound debridement pads, another type of mechanical debridement, show promise in recent studies. These single-use pads can be valuable to practitioners who lack sufficient training in sharp debridement.43 Some debridement pads are also being enhanced with various topical products. For example, a surfactant, a molecule naturally occurring in the lungs, is added to some pads to lower liquid surface tension and assist in mechanical debridement. In a comparison to saline-dampened gauze, this enhanced pad showed improvement in moisture of the skin, lower bacterial levels and reduced hyperkeratosis.44 

While mechanical debridement is one of the most traditionally-utilized forms of debridement, it is beginning to fall out of favor for sharp debridement and adjunct debridement techniques. However, mechanical debridement pads are beginning to emerge as a way for patients to debride their wounds safely between physician appointments or in rural areas where medical care is limited. 

Analyzing Autolytic And Laser Debridement In Wound Care 

Autolytic debridement uses a patient’s neutrophils and macrophages to debride the wound with the body’s own proteolytic enzymes instead of pharmacologically-generated enzymes.1,45,46 This allows for the enzymes to specifically debride only the necrotic tissue. This debridement technique is uncomplicated and open to a wide range of practitioners and skill sets. When it comes to autolytic debridement, clinicians commonly use it as a pre-debridement technique prior to a skilled specialist implementing sharp or biological debridement. One may also employ this type of debridement when injury risk is otherwise too high for other debridement methods. One example may be unknown wound depth, which can make sharp debridement too invasive. 

One can perform autolytic debridement with occlusive dressings, such as hydrocolloids, hydrogels or films, over the wound (see right photo on page 40).46-48 Some studies have found that a moist wound bed environment can accelerate autolytic debridement by 50 percent.49 These dressings create a moist and hypoxic wound environment that facilitates autolysis.45 Clinicians typically leave these dressings in place for two to three days and use saline to remove liquified tissue.46 While this process can be long, it allows for pain-free and highly specific wound debridement.45,46 Autolytic debridement is also cost-effective.49 Unfortunately, this method of debridement is contraindicated in infected, deep or avascular wounds due to the need for a moist wound environment with good vascular supply to be effective.46 

Low level laser therapy is the delivery of light energy in a safe, controlled manner that is absorbed by chromophores and transformed into chemical energy.50 Devices developed for this type of debridement include helium-neon and carbon dioxide lasers. Researchers have demonstrated that benefits of low level laser therapy on wounds include tissue repair acceleration, wound contraction and inflammation modulation.51 Biochemically, studies show laser photostimulation increases cell proliferation, adenosine triphosphate (ATP) synthesis, nucleic acid production and cell division.50 

Numerous studies suggest low level laser therapy is useful in wound healing. Greater wound contraction occurred in a low level laser therapy group versus a sham group.52 In a rat model study, therapy with a 633-nm laser improved wound healing by 40.3 percent.53 Low level laser therapy is also useful in treating venous stasis wounds.54 Biomedical and cellular research has revealed that cells stimulated with lasers had a marked increase in leukocyte phagocytosis of Staphyloccus aureus.55 Other microscopic in-vivo studies showed that DNA/RNA synthesis improved with laser treatments on wounds.56 In another article, Mester and colleagues histologically examined wound beds after laser therapy and found that type I and type III procollagen levels markedly increased after laser treatments in comparison to the control group.57 

On the other hand, many studies show no benefit of using low level laser therapy or showed that the wound type and size were significant factors.58,59 Further studies with an increased number of patients are necessary to explore the efficacy of low level laser therapy in wound healing. 

In Conclusion 

While there are a large number of debridement techniques for diabetic foot ulcerations, many are adjunct therapies clinicians may use with proper wound care. Management of infection, offloading, vascular intervention as necessary and good sharp debridement still constitute the standard of care for diabetic foot ulcers. Further research is needed for every debridement technique as many prior studies compared these techniques to a wet-to-dry dressing standard of care. However, each of these debridement techniques show promise to improve the healing rates of diabetic foot ulcerations.

Dr. Ansert is a first-year podiatric surgical resident at Saint Vincent Hospital in Worcester, Mass. 

Dr. Murry is a first-year podiatric surgical resident at Saint Vincent Hospital in Worcester, Mass. 

Dr. Cohen is a second-year podiatric surgical resident at Saint Vincent Hospital in Worcester, Mass. 

Dr. Tickner is the Medical Director of the Saint Vincent Hospital/RestorixHealth Wound Healing Center in Worcester, Mass. He is a global wound care consultant and is involved in podiatric wound care education at Saint Vincent Hospital. 

Features
38
46
By Elizabeth Ansert, MA, DPM, MBA, Weldon Murry, DPM, Donald Cohen, DPM
and Anthony Tickner, DPM, FACCWS, FAPWCA, FAPWH
References

1. Edwards J, Stapley S. Debridement of diabetic foot ulcers. Cochrane Database Syst Rev. 2010;1:CD003556. 

2. Elraiyah T, Domecq JP, Prutsky G, et al. A systematic review and meta-analysis of débridement methods for chronic diabetic foot ulcers. J Vasc Surg. 2016;63(2 Suppl):37S-45S. 

3. Braun LR, Fisk FA, Lev-Tov H, Kirsner RS, Isseroff RR. Diabetic foot ulcer: an evidence-based treatment update. Am J Clin Dermatol. 2014;15(3):267-281. 

4. Wilcox JR, Carter MJ, Covington S. Frequency of debridements and time to heal: a retrospective cohort study of 312,744 wounds. JAMA Dermatol. 2013;149(9):1050-1058. 

5. Piaggesi A, Schipani E, Campi F, et al. Conservative surgical approach versus non-surgical management for diabetic neuropathic foot ulcers: a randomized trial. Diabet Med. 1998;15(5):412-417. 

6. Fonder MA, Lazarus GS, Cowan DA, Aronson-Cook B, Kohli AR, Mamelak AJ. Treating the chronic wound: a practical approach to the care of nonhealing wounds and wound care dressings. J Am Acad Dermatol. (2008);58(2):185-206. 

7. 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. 

8. 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. 

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(1):61-64. 

10. Armstrong DG, Lavery LA, Vazquez JR, Nixon BP, Boulton AJM. How and why to surgically debride neuropathic diabetic foot wounds. J Am Podiatr Med Assoc. 2002;92(7):402-404. 

11. Granick M, Jacoby M, Noruthrun S, Datiashvili RO, Ganchi PA. Clinical and economic impact of hydrosurgical debridement on chronic wounds. Wounds. 2006;18(2):35-39. 

12. Hirokawa E, Sato T, Fujino T, Gotoh Y, Yokogawa H, Ichioka S. Hydrosurgical debridement as an approach to wound healing: an animal thermal burn model. J Wound Care. 2019;28(5):304-311. 

13. McAleer JP, Kaplan EM, Persich G, Axman W. A prospective randomized study evaluation the time efficiency of the VERSAJET hydrosurgery system and traditional wound debridement. Presented at: ACFAS 63rd Annual Scientific Conference; March 9-13, 2005; New Orleans, La. 

14. Wang R, Feng Y, Di B. Comparisons of negative pressure wound therapy and ultrasonic debridement for diabetic foot ulcers: a network meta-analysis. Int J Clin Exp Med. 2015;8(8):12548-12556. 

15. Voigt J, Wendelken M, Driver V, Alvarez OM. Low-frequency ultrasound (20-40 kHz) as an adjunctive 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. 

16. 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(8):24-39. 

17. Gray D, Acton C, Chadwick P, et al. Consensus guidance for the use of debridement techniques in the UK. Wounds UK. 2011;7(1):77- 84. 

18. Cimino WW, Bond LJ. Physics of ultrasonic surgery using tissue fragmentation: part I. Ultrasound Med Biol. 1996;22(1):89-100. 

19. Alvarez OM, Wendelken ME, Granick MS. Debridement of venous leg ulcers with direct-contact, low-frequency ultrasound: results of a randomized, prospective, controlled, clinical trial. Eplasty. 2019;19:pb2. 

20. Kavitha KV, Tiwari S, Purandare VB, Khedkar S, Bhosale SS, Unnikrishnan AG. Choice of wound care in diabetic foot ulcer: a practical approach. World J Diabetes. 2014;5(4):546- 556. 

21. Ramundo J, Gray M. Enzymatic wound debridement. J Wound Ostomy Contin Nurs. 2008;35(3):273-280. 

22. McCallon SK, Weir D, Lantis II JC. Optimizing wound bed preparation with collagenase enzymatic debridement. J Am Coll Clin Wound Spec. 2014;6(1-2):14-23. 

23. Tallis A, Motley TA, Wunderlich RP, et al. Clinical and economic assessment of diabetic foot ulcer debridement with collagenase: results of a randomized controlled study. Clin Ther. 2013;35(11):1805-1820. 

24. König M, Vanscheidt W, Augustin M, Kapp H. Enzymatic versus autolytic debridement of chronic leg ulcers: a prospective randomised trial. J Wound Care. 2005;14(7):320-323. 

25. Marazzi M, Stefani A, Chiaratti A, Ordanini MN, Falcone L, Rapisarda V. Effect of enzymatic debridement with collagenase on acute and chronic hard-to-heal wounds. J Wound Care. 2006;15(5):222-227. 

26. Waycaster C, Milne CT. Clinical and economic benefit of enzymatic debridement of pressure ulcers compared to autolytic debridement with a hydrogel dressing. J Med Econ. 2013;16(7):976-986. 

27. Smith RG. Enzymatic debriding agents: an evaluation of the medical literature. Ostomy Wound Manage. 2008;54(8):16-34. 

28. Riley KN, Herman IM. Collagenase promotes the cellular responses to injury and wound healing in vivo. J Burns Wounds. 2005;4:e8. 

29. Motley TA, Gilligan AM, Lange DL, Waycaster CR, Dickerson Jr JE. Cost-effectiveness of clostridial collagenase ointment on wound closure in patients with diabetic foot ulcers: economic analysis of results from a multicenter, randomized, open-label trial. J Foot Ankle Res. 2015;8(1):7. 

30. Sun X, Jiang K, Chen J, et al. A systematic review of maggot debridement therapy for chronically infected wounds and ulcers. Int J Infect Dis. 2014;25:32-37. 

31. Gupta, A. A review of the use of maggots in wound therapy. Ann Plast Surg. 2008;60(2):224-227. 

32. Steenvoorde P, Jacobi CE, Van Doorn L, Oksam J. Maggot debridement therapy of infected ulcers: patient and wound factors influencing outcome–a study on 101 patients with 117 wounds. Ann R Coll Surg Engl. 2007;89(6):596-602. 

33. Pinheiro MARQ, Ferraz JB, Junior MAA, et al. Use of maggot therapy for treating a diabetic foot ulcer colonized by multidrug resistant bacteria in Brazil. Ind J Med Res. 2015;141(3):340. 

34. Wang S, Wang J, Lv D, Diao Y, Zhang Z. Clinical research on the bio-debridement effect of maggot therapy for treatment of chronically infected lesions. Orthop Surg. 2010;2(3):201- 206. 

35. Azad AK, Wan Azizi WS, Adham SA, Yee BL. Maggot debridement therapy for diabetic foot ulcer: experience from maggot treatment centers. Asian J Pharm Pharmacol. 2016;2(1):23-25. 

36. Opletalová K, Blaizot X, Mourgeon B, et al. Maggot therapy for wound debridement: a randomized multicenter trial. Arch Derm. 2012;148(4):432-438. 

37. Mumcuoglu KY, Davidson E, Avidan A, Gilead L. Pain related to maggot debridement therapy. J Wound Care. 2012;21(8):400-405. 

38. Margolin L, Gialanella P. Assessment of the antimicrobial properties of maggots. Int Wound J. 2010;7(3):202-204. 

39. Petherick ES, O’Meara S, Spilsbury K, Iglesias CP, Nelson EA, Torgerson DJ. Patient acceptability of larval therapy for leg ulcer treatment: a randomised survey to inform the sample size calculation of a randomised trial. BMC Med Res Methodol. 2006;6(1):43. 

40. Capasso VA, Munro BH. The cost and efficacy of two wound treatments. AORN J . 2003;77(5):984–992, 995–997, 1000–1004. 

41. Dale BA, Wright DH. Say goodbye to wet-to-dry wound care dressings: changing the culture of wound care management within your agency. Home Healthc Nurse. 2011;29(7):429- 440. 

42. Young S. Management of slough in diabetic foot wounds. Diab Foot J. 2014;17(1):29–33. 

43. Stang D. Is the scapel the only way to debride? Diab Foot J. 2013;16:74-78. 

44. Young, T. The role of surfactants in mechanical debridement. Wounds UK. 2019;15(1):72- 74. 

45. Alexiadou K, Doupis J. Management of diabetic foot ulcers. Diab Ther. 2012;3(1):4. 

46. Ayello EA, Cuddigan JE. Debridement: controlling the necrotic/cellular burden. Adv Skin Wound Care. 2004;17(2):66-75. 

47. Hilton JR, Williams DT, Beuker B, Miller DR, Harding KG. Wound dressings in diabetic foot disease. Clin Inf Dis. 2004;39(Suppl 2):S100-S103. 

48. Cuschieri L, Debosz J, Miller P, Celis M. Autolytic debridement of a large, necrotic, fully occluded foot ulcer using a hydrocolloid dressing in a diabetic patient. Adv Skin Wound Care. 2013;26(7):300-304. 

49. Edwards J, Stapley S. Debridement of diabetic foot ulcers. Cochrane Database Syst Rev. 2010;1:CD003556. 

50. Yazdanpanah L, Nasiri M, Adarvishi S. Literature review on the management of diabetic foot ulcer. World J Diabetes. 2015;6(1):37. 

51. Andrade FSSD, Clark RMO, Ferreira ML. Effects of low-level laser therapy on wound healing. Rev Col Bras Cir. 2014;41(2):129–33. 

52. Franken PA, Hill AE. Laser debridement of wounds. U.S. Patent No. 5,207,671. 4 May 1993. 

53. Tchanque-Fossuo CN, Ho D, Dahle SE, et al. A systematic review of low-level light therapy for treatment of diabetic foot ulcer. Wound Repair Regen. 2016;24(2):418–26. 

54. Al-Watban FAH. Laser therapy converts diabetic wound healing to normal healing. Photomed Laser Surg. 2009;27(1):127-135. 

55. Hopkins JT, McLoda TA, Seegmiller JG, Baxter GD. Low-level laser therapy facilites superficial wound healing in humans: a triple-blind, sham-controlled study. J Athl Train. 2004;39(3):223-9. 

56. Sugrue ME, Carolan J, Leen EJ, Feeley TM, Moore DJ, Shanik GD. The use of infrared laser therapy in the treatment of venous ulceration. Ann Vasc Surg. 1990;4(2):179-181. 

57. Mester E, Mester AF, Mester A. The biomedical effects of laser application. Lasers Surg Med. 1985;5(1):31-39. 

58. Saperia D, Glassberg E, Lyons RF, et al. Demonstration of elevated type I and type III procollagen mRNA levels in cutaneous wounds treated with helium-neon laser. Proposed mechanism for enhanced wound healing. Biochem Biophys Res Commun. 1986;138(3):1123- 1128. 

59. Allendorf JD, Bessler M, Huang J, Kayton ML, Laird D, Nowygrod R. Helium-neon laser irradiation at fluences of 1, 2, and 4 J/ cm2 failed to accelerate wound healing as assessed by both wound contracture rate and tensile strength. Treat MR Lasers Surg Med. 1997;20(3):340-345. 

Additional References 

60. Falabella AF. Debridement and wound bed preparation. Derm Ther. 2006;19(6):317-325. 

61. Schindl M, Kerschan K, Schindl A, Schön H, Heinzl H, Schindl L. Induction of complete wound healing in recalcitrant ulcers by low-intensity laser irradiation depends on ulcer cause and size. Photodermatol Photoimmunol Photomed. 1999;15(1):18-21. 

62. Kajagar BM, Godhi AS, Pandit A, Khatri S. Efficacy of low level laser therapy on wound healing in patients with chronic diabetic foot ulcers—a randomised control trial. Ind J Surg. 2012;74:359-363. 

Resource Center
Back to Top