August 2010

Evidence-based foot care in patients with diabetes #5454319

The medical literature provides a range of evidence on which to base treatment decisions regarding care of the diabetic foot, but the practitioner must interpret and evaluate that evidence in the context of his or her own clinical expertise.

By Cordell Atkins, PT, DPT, CWS, CDE, CPed

Since the early 1990s evidence based medicine has been an interesting topic of conversation in the medical community. Evidence based medicine has been used to seek guidance on the safest and most effective treatments for a variety of illnesses and diseases, reduce needless disabilities and loss of function, and reduce wasteful expenditures by third party payers and patients.

So what is evidence based medicine? In 1996, David L. Sackett, MD, wrote: “Evidence based medicine is the conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients. The practice of evidence based medicine means integrating individual clinical expertise with the best available external clinical evidence from systematic research.”1 Evidence based practice integrates relevant, reliable, pertinent, and trustworthy research information with clinical expertise and the patient’s specific needs and problems.

Levels of evidence

Evidence based care often requires searching published sources for evidence to help direct and guide care for the specific clinical question. Sources are often obtained from searches in databases such as PubMed, EBSCO, Cochrane Collaboration, association resources or collections, government sites, and other electric resources. The clinician or practitioner must be able to evaluate the evidence obtained for its usefulness, importance, and validity as related to the specific clinical question.

There is a hierarchy of evidence used to rank the strength and validity of the evidence from expert opinion to systematic reviews and meta-analyses (see table 1). Randomized controlled trials (RCT) assess the efficacy of an intervention. Efficacy is the capacity or power to produce an effect. (Levels I and II)  Observational studies, cohort, case control, case series and case reports address effectiveness—the quality or amount of the effect in practice, outside the laboratory or other controlled environment. (Level III).  Evidence from expert committees, opinions or clinical experience may introduce bias in the evidence (Level IV).

The clinician or practitioner can incorporate the published evidence, the individual patient’s needs or problems, and their own clinical expertise to develop a plan of care. Additionally, clinical guidelines or algorithms may be available to assist in care planning. These guidelines are generally developed by a multidisciplinary team with support from professional organizations, institutions or governmental agencies that publish the guidelines. The American Diabetes Association; the American College of Foot and Ankle Surgeons; the Wound, Ostomy, Continence Nurses Society; the American Pharmaceutical Association; the American Orthopedic Foot and Ankle Society; the International Working Group on the Diabetic Foot and the Infectious Diseases Society of America have all developed diabetic foot ulcer guidelines as a resource for clinicians and practitioners.

Guideline development is generally accomplished by a group of stakeholders concerned and interested in a certain clinical question or condition. The group will identify and gather evidence, assess the evidence for relevance, summarize and categorize the evidence and then translate the evidence, or lack of evidence, into clinical practice guidelines. As the evidence is being interpreted, the opinion of the group will be needed to create recommendations in the absence of evidence, or to assess other  issues such as the generalizability of the evidence2–for example, whether the results of a small RCT can be applied to a large population. Additionally, the opinions or conclusions of a speciality group may differ from that of a multidisciplinary group when presented with the same evidence. The multidisciplinary group tends to represent a more deversified viewpoint.

In a study published in 1998, Schuster reported that 30% to 40% of patients were not receiving care directed by evidence based guidelines and 20% to 30% were receiving care that was inappropriate, unnecessary, potentially dangerous or contraindicated.3 These data unfortunately demonstrate that there appears to be a gap between evidence based research and application in actual clinical practice.


According to the Centers for Disease Control and Prevention 2007 statistics,4 23.6 million people in the U.S. have diabetes. Unfortunately 5.7 million are undiagnosed. Complications of diabetes include heart disease, stroke, high blood pressure, blindness, kidney disease, nervous system disease, amputation, and dental disease.

Appropriate diabetic care can reduce the occurrence of diabetic complications. The Diabetes Control and Complications Trial (DCCT) demonstrated that tight glycemic control can reduce the occurrence of complications and even slow the progression of existing complications.5-12 In a follow up study of the original DCCT study, it was shown that the effects of early tight glycemic control demonstrated positive effects on neuropathy more than 10 years later.13 With regard to clinical practice, the newly published evidence strongly indicates that tight glycemic control should be the initial intervention for the care and prevention of diabetic complications and especially neuropathic complications.l3

The diabetic foot

In spite of all the published evidence for care and prevention of diabetic complications, these complications continue. More than 60% of all non-traumatic amputations occur in patients with diabetes. In the U.S. in 2004 there were approximately 71,000 lower extremity amputations in people with diabetes.4 According to the International Diabetes Federation, an amputation in a person with diabetes occurs every 30 seconds worldwide.14

Preventive foot care

Benjamin Franklin’s old saying “an ounce of prevention is worth a pound of cure” is probably very appropriate when discussing diabetic foot complications. Effective preventive care and management of the diabetic foot relies on assessment and risk identification. To prevent foot complications, it is essential to identify, assess, and screen those at risk. Several publications have confirmed this requirement for proper care of the diabetic foot and diabetic foot ulcerations.15-19

Everyone with diabetes should have an annual foot exam. The initial screening allows the clinician to examine and asses the foot for loss of protective sensation (LOPS),20-22 bony deformities, joint mobility, peripheral circulation, skin integrity, and callus formation. Gait and balance should also be evaluated. Many people with diabetes are at a low risk for foot ulceration while others may be classified as high risk.23,24 Those at high risk may have LOPS, foot deformities, peripheral arterial disease (PAD), or a history of previous foot ulcers. Table 217 demonstrates the risk categories with their definitions, treatment recommendations, and suggested follow-up visits for foot examinations that were developed by a multidisciplinary Task Force of the Foot Care Interest Group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists.

Diabetic foot ulcers

Even with good preventive care, diabetic foot ulcers may occur. Published literature demonstrates that diabetic foot ulcers are a result of either PAD and/or diabetic peripheral neuropathy, with additional causative factors such as bony deformities, callus buildup, and trauma.25-28 The lifetime risk of foot ulceration in an individual with diabetes is about 15%.29 The published two-year cost of caring for a diabetic foot ulcer in 1999 was about $28,000.30


A key component of providing evidence based care is a thorough and comprehensive evaluation of the foot and the ulcer including a patient history and physical examination.17 The evaluation has several components that provide data to the clinician. It should include a vascular assessment to rule out arterial disease31,32 and a neurological assessment to assess LOPS.33 Additional laboratory tests that may assist the clinician in the assessment could include a prealbumin test to assess protein deficiency,34 a lipid profile to assess risk for developing cardiovascular disease,35 and, if not already ordered by the primary care physician, a hemoglobin A1c test.36 The data gathered, combined with applicable published evidence and clinician expertise in assessing the patient’s specific needs, should lead to optimal care for the patient.

Infection, debridement and wound care

Infection occurs when bacteria is greater than the host defense mechanism. The classic signs of soft tissue infection are redness, heat, pain, and swelling. Many individuals with neuropathy may have an impaired neuroinflammatory response and may not have the normal physiological response to pain. Other methods may be needed to assess for infection. Additional symptoms may include but are not limited to exudates, delayed healing, friable or discolored granulation tissue, foul odor, and wound breakdown.37 The use of erythrocyte sedimentation rate (ESR) and C-reactive protein as markers for bone infection, or osteomyelitis, has been supported by recent evidence.38,39

Necrotic and devitalized tissue is a source of bacterial growth and reduces the body’s ability to fight infection. Debridement and removal of the nonviable tissue help the diabetic ulcer to heal more rapidly.40,41 Diabetic wounds tend to be chronic in nature, and it is important to have a proper wound bed for healing. The goal of debridement is to convert the stagnant chronic wound bed of the diabetic ulcer into an active, acute wound by removing all necrotic, dysvascular, nonviable tissue to obtain a red granular wound bed.42 The most effective treatment of an infected bone is debridement of the infected bone, followed by an adequate course of antibiotics.43,44 Thorough surgical debridement has been shown to be effective in wound healing, and other methods such as enzymatic, mechanical, biological, or autolytic debridement may be appropriated depending on the status of the wound, the patient condition, or professional licensing restrictions.45-48

After the wound has been debrided and cleaned, it is necessary to maintain an environment that facilitates continued wound healing. Studies published in the 1950s and ‘60s by Odland,49 Winter,50 and Hinman and Maibach51 demonstrated that a clean, moist, occluded wound healed more rapidly than a wound left open to the air. Continued research has supported moist wound healing.52,53 An appropriate dressing should allow for moist wound healing but should also provide protection to the periwound area; reduce physical trauma, friction and shear; protect from external contamination; and, in today’s economic environment, be cost effective.54-57

Offloading the wound

Diabetic foot ulceration may be a result of increased pressure on the foot due to foot deformity, decreased joint mobility, or neuropathy. Pressure reduction in the area of high pressure, or offloading, has been the mainstay in preventing and healing diabetic neuropathic ulcers.58-61 Pressure relief is essential to maximize the healing potential of a diabetic wound. It has been said “it’s not what you put on the wound, it’s what you take off“62 that facilitates healing in diabetic neuropathic wounds.

Crutches, walkers, wheelchairs, custom shoes, custom inserts, Charcot Restraint Orthotic Walker (CROW) boots, relief boots and total contact casting have been used and are acceptable methods of offloading the diabetic foot.63,64 Of all the offloading techniques, none has been studied more than the total contact cast (TCC). Another method, the instant total contact cast (iTCC),65 has demonstrated success in healing wounds using the principle of pressure offloading 24/7, as with the total contact cast.

Not all patients are good candidates for the TCC or the CROW boot, both the TCC and the CROW tend to be somewhat large and heavy. Individuals of smaller stature or even the morbidly obese may find these difficult to use. Other devices, such as a below knee walking boot, or CAM (controlled ankle motion) walker, have been successful for pressure offloading in patients who cannot easily tolerate the TCC. The major success, wound closure, comes when the patient wears the boot 24/7 as with the TCC.

Adjuvant agents and hyperbaric oxygen

Adjuvant agents have been divided into topical agents, devices to accelerate healing, and systemic agents for patient treatment.

Topical agents that have demonstrated positive research outcomes in the care of the diabetic foot ulcer are platelet-derived growth factor (PDGF)66-68 and other cytokine growth factors.69-71 The use of these topical agents can be expensive, and not all third party payers are willing to cover the costs.

Devices that have been evaluated and have demonstrated a positive and sustainable improvement in diabetic foot wounds are negative pressure wound therapy (NPWT), and electrical stimulation.  NPWT has also been called vacuum-assisted wound closure. NPWT aids in wound healing by reducing edema, removing excess fluid and bacterial products and assisting to draw the edges of the wound together by a vacuum effect under the dressing.72-74 Use of NPWT can be expensive and not all payers provide coverage for the device. In addition, there are some contraindications for its use, including untreated osteomyelitis and inadequate debridement.75

The use of electrical stimulation may be beneficial in diabetic wound healing by affecting protein synthesis, cell migration and reduction of bacterial growth.76,77 The electrical stimulation waveform that has the most evaluation and use in wound care is monophasic high-voltage pulse current (HVPC).  HVPC devices provide polarity selection and a variation of the pulse width that appear to be important in wound healing.78 Two methods have been reported in the literature for application of the electrodes in wound healing.79,80 Electrical stimulation is contraindicated in cases of malignancy, evidence of osteomyelitis, cardiac pacemaker, and electrode placement over or near the phrenic nerve, carotid sinus or laryngeal musculature. The Centers for Medicare and Medicaid Services (CMS) coverage policy81 states that electrical stimulation is covered for diabetic ulcers when used as adjunct to standard wound therapy and not as an initial treatment modality, and when the patient has undergone at least 30 consecutive days of treatment with standard wound therapy with no measurable signs of healing.

Hyperbaric oxygen therapy (HBOT) is the medical use of oxygen at a level higher than atmospheric pressure. HBOT increases the partial pressure of oxygen in all the tissues of the body.  The systemic use of oxygen requires a doctors order as oxygen is considered a drug. HBOT used as a systemic agent has been associated with a reduction in amputation rates in patients who were at risk of below knee or above knee amputation due to severe ischemia, underlying osteomyelitis, or both.82 The Wound Healing Society has given HBOT a level I evidence rating in their “Guidelines for the treatment of diabetic ulcers.”49 CMS has established guidelines for reimbursement for the use of HBOT83 in the care and treatment of diabetic foot wounds:

  • Type 1 or Type 2 Diabetes Mellitus, with lower extremity wound due to DM
  • Wagner grade III or higher
  • Failed standard wound care (no measurable signs of healing for 30 days)
  • Wound must be re-evaluated every 30 days during HBOT course
  • Continued HBOT will not be covered if there are no measurable signs of healing during the 30 day period.


Providing evidence based care for the diabetic foot requires the clinician to integrate personal clinical expertise with the best available external clinical evidence from systematic research while assessing what is best for the patient’s specific needs and problems. Because diabetes and diabetic foot care is such a large concern socially, emotionally, and financially, a great deal of research has been done and will continue to be done to resolve the underlying disease and complications. The truly concerned clinician will have to continue to keep abreast of the most current, relevant, reliable, and pertinent research and care guidelines to provide the best evidence based care.

There are many more evidence based articles to support the care of the diabetic foot than those referenced in the preceding text. Table 3 provides a partial list of additional references, with the associated level of evidences, for the care of the diabetic foot.

Cordell “Corky” Atkins PT, DPT, CWS, CDE, CPed, is the manager of the Intermountain Diabetic Foot Clinic in Salt Lake City, UT.


1.  Sackett DL, Rosenberg WM, Gray JA, et al. Evidence based medicine: what it is and what it isnt. BMJ 1996;312(7023):71-72.

2. Shekelle PG, Woolf SH, Eccles M, Grimshaw J. Developing guidelines. BMJ 1999;318(7183):593-596.

3. Schuster MA, McGlynn EA, Brook RH. How good is the quality of care in the United States? Milbank Q 1998;76(4);517-563.

4.  CDC National Diabetes Fact Sheet, 2007.  Available at: .  Accessed May 20, 2010.

5.  The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. The Diabetes Control and Complications Trial Research Group. N Engl J Med 1993;329(14):977-986.

6.  Effect of intensive diabetes treatment on the development and progression of long-term complications in adolescents with insulin-dependent diabetes mellitus: Diabetes Control and Complications Trial. J Pediatr 1994;125(2):177-188.

7. Reichard P, Nilsson BY, Rosenqvist U. The effect of longterm intensified insulin treatment on the development of microvascular complications of diabetes mellitus. N Engl J Med 1993;329(5):304-309

8. Intensive blood glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complication in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study Group. Lancet 1998;352(9131):837-853.

9. Effect of intensive blood glucose control with metformin on complication in overweight patients with type 2 diabetes (UKPDS 34). UK Prospective Diabetes Study Group. Lancet 1998;352(9131):854-865.

10. Ohkubo Y, Kishikawa H, Araki E, et al. Intensive insulin therapy prevents the progression of diabetic microvascular complications in Japanese patients with NIDDM: A randomized prospective 6-year study. Diab Res Clin Pract 1995;28(2):103-117.

11. Nathan DM, Cleary PA, Backlund JY, et al; Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research Group. Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes. N Eng J Med 2005;353(25):2643-2653.

12. Gerstein HC, Miller ME, Byington RP, et al; Action to Control Cardiovascular Risk in Diabetes Study Group. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med 2008;358(24):2545-2559.

13. Albers JW, Herman WH, Pop-Busui R, et al. Effect of prior intensive insulin treatment during the Diabetes Control and Complications Trial (DCCT) on peripheral neuropathy in type 1 diabetes during the Epidemiology of Diabetes Interventions and Complications (EDIC) Study. Diabetes Care 2010;33(5):1090-1096.

14.  International Diabetes Federation Position Statement – The diabetic foot. The diabetic foot: amputations are preventable. May 2005. Accessed May 29, 2010.

15.  Mayfield JA, Reiber GE, Sanders LJ, et al; American Diabetes Association. Preventive foot care in diabetes. Diabetes Care 2004;27 suppl 1:S63-S64.

16.  Singh N, Armstrong DG, Lipsky BA. Preventing foot ulcers in patients with diabetes. JAMA 2005;293(2):217-228.

17.  Boulton AJM, Armstrong DG, Albert SF, Frykberg RG, Comprehensive Foot Examination and Risk Assessment: A report of the Task Force of the Foot Care Interest Group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists. Diabetes Care 2008;31(8):1679-1685.

18.  Snyder RJ, Kirsner RS, Warriner RA 3rd, et al. Consensus recommendations on advancing the standard of care for treating neuropathic ulcers in patients with diabetes. Ostomy Wound Manage 2010;56(4 Suppl):S1-S24.

19. Armstrong DG. Loss of protective sensation: a practical evidence-based definition. J Foot Ankle Surg 1999;38(1):79-80.

20.  Birke JA, Sims DS. Plantar sensory threshold in the ulcerative foot. Lepr Rev 1986;57(3):261-267.

21. Armstrong DG. The 10-g monofilament: the diagnostic divining rod for the diabetic foot? Diabetes Care 2000;23(7):887.

22. Rith-Najarian SJ, Stolusky T, Gohdes DM. Identifying diabetic patients at risk for lower extremity amputation in a primary health care setting. Diabetes Care 1992;15(10):1386-1389.

23. Pham H, Armstrong DG, Harvey C, et al. Screening techniques to identify patients at high risk for diabetic foot ulceration: a prospective multicenter trial. Diabetes Care 2000;23(5):606-611.

24. Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation. Basis for prevention. Diabetes Care 1990;13(5):513-521.

25. Boulton AJ, Vileikyte L, Ragnarson-Tennvall G, Apelqvist J. The global burden of diabetic foot disease. Lancet 2005;366(9498):1719-1724.

26.  Sanders LJ. Diabetes mellitus: prevention of amputation. J Am Podiatric Med Assoc 1994;84(7):322-328.

27.  Reiber GE, Vileikyte L, Boyko EJ, et al. Causal pathways for incident lower-extremity ulcers in patients with diabetes from two settings. Diabetes Care 1999;22(1):157-162.

28.  Reiber GE, Ledoux WR. Epidemiology of diabetic foot ulcers and amputations: evidence for prevention. In: Williams R, Hermanw, Kinounth AL,Wareham NJ, eds. The evidence base for diabetes care. Hoboken, NJ: John Wiley & Sons; 2002:641-665.

29.  Palumbo PJ, Melton LJ. Peripheral vascular disease and diabetes. In: Harris MI, Hamman RF, eds. Diabetes in America. Washington, DC: US Government Printing Office; 1985:XV,1–21.

30.  Ramsey SD, Newton K, Blough D, et al. Incidence, outcomes, and cost of foot ulcers in patients with diabetes. Diabetes Care 1999;22(3):382-387.

31.  Sahili D, Eliasson B, Svensson M, et al. Assessment of toe blood pressure is an effective screening method to identify diabetes patients with lower extremity arterial disease. Angiology 2004;55(6):641-651.

32.  American Diabetes Association. Peripheral arterial disease in people with diabetes. Diabetes Care 2003;26(12):3333-3341.

33. Kamei N, Yamane K, Nakanishi S, et al. Effectiveness of Semmes-Weinstein monofilament examination for diabetic peripheral neuropathy screening. J Diabetes Complications 2005;19(1): 47-53.

34. Pompeo M. Misconceptions about protein requirements for healing; results from a prospective study. Ostomy Wound Manage 2007;53(8):30-32.

35.  Young MJ, McCardle JE, Randall LE, Barclay JI. Improved survival of diabetic foot ulcer patients 1995-2008: possible impact of aggressive cardiovascular risk management. Diabetes Care 2008;31(11):2143-2147.

36.  American Diabetes Association. Standards of medical care in diabetes- 2010. Diabetes Care 2010;33(supp 1):S11-S61.

37. Gradner SE, Frantz RA, Doebbeling BN. The validity of the clinical signs and symptoms used to identify localized chronic wound infection. Wound Repair Regen 2001;9(3):178-186.

38. Rabajohn L Roberts K, Troiano M, et al. Diagnostic and prognostic value of erythrocyte sedimentation rate in contiguous osteomyelitis of the foot and ankle. J foot Ankle Surg 2007;46(4)232-237.

39. Fleischer AF, Didyk AA, Woods JB, et al. Combined clinical and laboratory testing improves diagnostic accuracy for osteomyelitis in the diabetic foot. J Foot Ankle Surg 2009;48(1)39-46.

40.  Brem H, Sheehan P, Boulton AJ. Protocol for treatment of diabetic foot ulcers. Am J Surg 2004;187(5A):1S-10S.

41.  Moss SE, Klein R, Klein BE, Wong TY. Retinal vascular changes and 20-year incidence of lower extremity amputations in a cohort with diabetes. Arch Intern Med 2003;163(20):2505-2510.

42.  Dinh TL, Veves A. Treatment of diabetic ulcers. Dermatol Ther 2006;19(6):348-355.

43. Steed DL, Donohoe D, Webster MW, Lindsley L. Effect of extensive debridement on the healing of diabetic foot ulcers. Diabetic Ulcer Study Group.  J Am Coll Surg 1996;183(1):61-64.

44. 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.

45. Alvarez OM, Mertz PM, Eaglstein WH. The effect of occlusive dressings on collagen synthesis and re-epithelialization in superficial wounds. J Surg Res 1983;35(2):142–148.

46. Falanga V. Wound bed preparation and the role of enzymes: a case for multiple actions of therapeutic agents. Wounds 2002;14(2):47-57.

47. Jensen JL, Seeley J, Gillin B. Diabetic foot ulcerations. A controlled, randomized comparison of two moist wound healing protocols: Carrasyn hydrogel wound dressing and wet-to-moist saline gauze. Adv Wound Care 1998;11(7 Suppl):1-4.

48.  Steed DL, Attinger C, Colaizzi T, et al. Guidelines for the treatment of diabetic ulcers. Wound Repair Regen 2006;14(6):680-692.

49. Odland G. The fine structure of the interrelationship of cells in the human epidermis. J Biophys Biochem Cytol 1958;4(5):529-535.

50. Winter GD. Formation of the scab and the rate of epithelization of superficial wounds in the skin of the young domestic pig. Nature 1962;193:293-294.

51. Hinman CD, Maibach H. Effect of air exposure and occlusion on experimental human skin wounds. Nature 1963;200:377-378.

52.  Nemeth AJ, Eaglstein WH, Taylor JR, et al. Faster healing and less pain in skin biopsies treated with an occlusive dressing. Arch Dermatol 1991;127(11):1679-1983.

53.  Phillips TJ, Kapoor V, Provan A, Ellerin T. A randomized prospective study of a hydroactive dressing vs conventional treatment after shave biopsy excision. Arch Dermatol 1993;129(7):859-860.

54. Sayag J, Meaume S, Bohbot S. Healing properties of calcium alginate dressings. J Wound Care 1996;5(8):357-362.

55. Lalau JD, Bresson R, Charpentier P, et al. Efficacy and tolerance of calcium alginate versus Vaseline gauze dressings in the treatment of diabetic foot lesions. Diabetes Metab 2002;28(3):223–229.

56. Ohlsson P, Larsson K, Lindholm C, Moller M. A cost effectiveness study of leg ulcer treatment in primary care. Comparison of saline-gauze and hydrocolloid treatment in a prospective, randomized study. Scand J Prim Health Care 1994;12(4):295-299.

57. Harding K, Price P, Robinson B, et al. Cost and dressing evaluation of hydrofiber and alginate dressings in the management of community-based patients with chronic leg ulcerations. Wounds 2001;13(6):229-236.

58.  Duckworth T, Betts RP, Franks CI, Burke J. The measurement of pressures under the foot. Foot and Ankle 1982;3(3):130-141.

59.  Boulton AJM. The importance of abnormal foot pressure and gait in causation of foot ulcers. In: Connor H, Boulton AJM, Ward JD, eds. The foot in diabetes. Chilchester: John Wiley and Sons; 1987:11–26.

60.  Cavanagh PR, Ulbrecht JS, Caputo GM. Biomechanical aspects of diabetic foot disease: aetiology, treatment, and prevention. Diabet Med 1996;13(Suppl 1):S17-S22.

61.   Armstrong DG, Peters EJ, Athanasiou KA, Lavery LA. Is there a critical level of plantar foot pressure to identify patients at risk for neuropathic foot ulceration? J Foot Ankle Surg 1998;37(4):303-307.

62.  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-S9.

63. Reiber GE, Smith DG, Wallace C, et al. Effect of therapeutic footwear on foot reulceration in patients with diabetes: a randomized controlled trial. JAMA 2002;287(19):2552-2558.

64. Uccioli L, Faglia E, Monticone G, et al. Manufactured shoes in the prevention of diabetic foot ulcers. Diabetes Care 1995;18(10):1376-1378.

65.  Armstrong DG, Short B, Espensen EH, et al. Technique for fabrication of an “instant total-contact cast” for treatment of neuropathic diabetic foot ulcers. J Am Podiatr Med Assoc 2002;92(7):405-408.

66.  Steed DL. Clinical evaluation of recombinant human platelet derived growth factor for the treatment of lower extremity diabetic ulcers. Diabetic Ulcer Study Group. J Vasc Surg 1995;21(1):71-81.

67. Wieman TJ, Smiell JM, Su Y. Efficacy and safety of a topical gel formulation of recombinant human plateletderived growth factor-BB (becaplermin) in patients with chronic neuropathic diabetic ulcers: a phase III randomized, placebo-controlled double-blind study. Diabetes Care 1998;21(5):822-827.

68.  d’Hemecourt PA, Smiell JM, Karim MR. Sodium carboxymethylcellulose aqueous-based gel versus becaplermin gel in patients with non-healing lower extremity ulcers. Wounds 1998; 10(3):69-75.

69. Steed DL, Goslen BG, Holloway GA, et al. Randomized prospective double-blind trial in healing chronic diabetic foot ulcers. CT-102 activated platelet supernatant, topical versus placebo. Diabetes Care 1992;15(11):1598–1604.

70. Holloway G, Steed D, DeMarco M, et al. A randomized, controlled multicenter, dose response trial of activated platelet supernatant, topical CT-102 in chronic, non-healing, diabetic wounds. Wounds 1993;5:198-206.

71. Atri SC, Misra J, Bisht D, Misra K. Use of homologous platelet factors in achieving total healing of recalcitrant skin ulcers. Surgery 1990;108(3):508-512.

72.  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.

73.  McCallon SK, Knight CA, Valiulus JP, et al. Vacuum-assisted closure versus saline-moistened gauze in the healing of postoperative diabetic foot wounds. Ostomy Wound Manage 2000;46(8):28-34.

74. Armstrong DG, Lavery LA; Diabetic Foot Study Consortium. Negative pressure wound therapy after partial diabetic foot amputation: a multicentre, randomised controlled trial. Lancet 2005;366(9498):1704-1710.

75. Agency for Healthcare Research and Quality. Negative pressure wound therapy devices. Available at: Accessed July 25, 2010.

76.  Houghton PE, Kincaid CB, Lovell M, et al. Effect of electrical stimulation on chronic leg ulcer size and appearance. Phys Ther 2003;83(1):17-28.

77. Lundeberg TC, Eriksson SV, Malm M. Electrical nerve stimulation improves healing of diabetic ulcers. Ann Plast Surg 1992;29(4):328-331.

78.  Gentzkow GD. Electrical stimulation to heal dermal wounds. J Dermatol Surg Oncol 1993;19(8):753-758.

79.  Baker LL, Rubayi S,Villar F, DeMuth SK. Effect of electrical stimulation waveform on healing of ulcers in human beings with spinal cord injury. Wound Repair Regen 1996;4(1):21-28.

80.  Gentzkow GD, Pollack SV, Kloth LC. Improved healing of pressure ulcers using Dermapulse, a new electrical stimulation device. Wounds 1991;3(5):158-170.

81.  Centers for Medicare & Medicaid Services. Medicare coverage issues manual. November 8, 2002. Available at: Accessed May 31, 2010.

82. Faglia E, Favales F, Aldeghi A, et al. Adjunctive systemic hyperbaric oxygen therapy in treatment of severe prevalently ischemic diabetic foot ulcer. A randomized study.  Diabetes Care 1996;19(12):1338-1343.

83. CMS Coverage Memorandum CAG00060N 08.30.02 Transmittal AB-02-183 12.22.02 Effective 04.01.03

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