Secondary Logo

Journal Logo


Best Practices for the Management of Foot Ulcers in People with Diabetes

Woo, Kevin Y. PhD, RN; Botros, Mariam DCh; Kuhnke, Janet RN, MSc, ET; Evans, Robyn MD, MSc; Alavi, Afsaneh MD

Author Information
doi: 10.1097/01.ASW.0000436385.24508.d5

Diabetes is one of the leading chronic diseases that has become an epidemic worldwide.1 According to the International Diabetes Federation, the global number of people with diabetes will increase from 246 million or 5.9% in 2007 to 380 million or 7.1% by 2025.1 Of persons with diabetes (PWDs), 2% to 3% will develop a foot ulcer annually, whereas the lifetime risk of developing a foot ulcer is as high as 25%, primarily because of neuropathy and potential coexisting vascular disease.2 Following patients with diabetes and neuropathy for 1 year, it was estimated that 7.2% of this population would develop their first foot ulcer.3 More than 80% of all nontraumatic amputations in diabetes are preceded by foot ulcers that should be considered as one of the prognostic indicators for advanced diabetes.4 In most countries, the healthcare system costs of diabetic foot ulcers are exorbitant and include a high likelihood of hospitalizations. In the United States, the care of diabetes-related foot ulcers constitutes 25% to 50% of the total costs associated with diabetic care.1 Despite these staggering statistics, foot ulcers and related adverse sequelae in PWDs are deemed highly preventable.5

For optimal patient outcomes, the care of people with diabetic foot ulcers requires a systematic approach following the wound bed preparation paradigm and the existing best practice recommendations.6–9 Integral to the recommended best practices is the primary emphasis on addressing patient concerns and the causative factors prior to instituting local wound care. Foot ulcers are often precipitated by neuropathy and complicated by vascular insufficiency that necessitates thorough evaluation and specific intervention to promote healing. Local wound care of wounds with healing potential usually involves 3 core components: Debridement of nonviable tissue, Infection management, and Moisture balance (DIM).10 By applying the principles to optimal wound healing, it has been demonstrated that 50% surface area reduction at week 4 is predictive of complete wound closure at week 12.11 If the wound is not healing at the expected rate, advanced therapies may be considered. If the wound cause cannot be corrected, compromising healing potential, local wound care should focus on maintenance to prevent secondary infection and further deterioration.10 This article summarizes key evidence and recommendations regarding prevention and management of diabetic foot ulcers that clinicians can translate into practice.


  • 1. Evaluate diabetes management and conduct a systematic assessment of the PWD including A1c, blood pressure, cholesterol, diet, exercise, and smoking history.

Inadequate management of diabetes can put individuals at risk for a number of serious complications including foot ulceration. Hyperglycemia triggers a constellation of metabolic events leading to excessive production of advanced glycation end-products and overproduction of oxygen free radicals that can delay healing of foot ulcers12 (Figure 1).

Figure 1
Figure 1:

Recognizing the multifaceted nature of diabetes management and risk factors for foot ulcers,12 several salient factors should always be part of a careful patient history, and their associated risks for foot ulceration are summarized in Table 1. Practitioners may consider close monitoring, early referral to specialists, and intensive treatment based on the risk profile.

Table 1
Table 1:
  • 2. Conduct a lower-leg and foot assessment to differentiate neuropathic, neuroischemic, and ischemic diseases (ulcers).

A thorough foot examination should be conducted at least on an annual basis to identify risk factors that can lead to foot ulcers in order to institute early intervention. Only half of the individuals with diabetes, however, receive routine foot examinations by their healthcare providers.13 To help identify the key and relevant risk factors, Inlow et al14 developed a 60-second diabetic foot screening tool that allows clinicians to quickly assess for the skin, nail, foot deformity, footwear, temperature (hot and cold), range of motion, loss of sensation, pedal pulses, dependent rubor, and erythema. The key elements and supporting evidence are summarized in Table 2. The interrater reliability of Inlow’s 60-second foot screening tool has been supported by high intraclass correlation coefficients ranged from 0.83 to 0.93.15 There is a need to explore if the PWD understands the implications of various risk factors and the importance of self-care practices in diabetic foot ulcer prevention.

Table 2
Table 2:

Neuropathic Foot

Diabetic neuropathy is present in almost 60% of diabetic patients with foot ulcers5; associated nerve dysfunction may be described as sensory, autonomic, or motor. Sensory neuropathy removes the protective sensation rendering the individual to be less aware of potential or actual trauma to his or her skin. To screen for individuals with sensory neuropathy, the 5.07 (10 g) Semmes-Weinstein monofilament test is recommended. Individuals with significant sensory impairment (4 of the 10 points in Figure 2) are likely to develop foot ulcers (odds ratio [OR], 5.4; 2.6–11.6).16

Figure 2
Figure 2:
10 SITES FOR MONOFILAMENT TESTING©Canadian Assocation of Wound Care. Reprint with permission.

Autonomic neuropathy is associated with decreased production of sweat and components of the natural moisturizing factor leaving the skin dry that leads to disruption of the epidermal barrier.17 The skin should be inspected for dryness, especially the presence of fissures or cracks that may become a portal of entry for bacteria. Areas with blisters, cuts, scratches, redness, or hemorrhage are indicative of local damage from local trauma, friction, or shear commonly caused by walking barefoot and poorly fitting footwear. Callus formation is a reaction to increased local pressure and heralds impending skin breakdown and ulceration (relative risk [RR], 11.0).18 By recognizing early signs of injury from pressure and friction, prompt interventions can be instituted to prevent actual ulceration. Fungal infection is not uncommon in PWDs. The most occlusive areas are the fourth and fifth toe web spaces allowing excessive moisture accumulation that promotes fungal proliferation as evident by skin maceration in the area. A plethora of antifungal agents are available for local or systemic management.

Motor neuropathy interferes with the normal signaling to the lumbrical and interosseus muscles, leading to atrophy and wasting of the muscles, foot deformity, upper displacement of fat pads, and altered foot biomechanics.19 Common foot deformities including foot drop, equinous deformity, hammertoes, and prominent plantar metatarsal heads12 create areas that sustain high impact and pressure and are prone to ulcer formation (especially with ill-fitting and poorly designed footwear).

Ischemic foot

Diabetes is associated with a 2- to 3-fold increased risk of accelerated atherosclerosis.20 Poor arterial blood supply compromises not only the delivery of oxygen and nutrients to the skin but also the availability of white blood cells to defend the host against bacterial invasion if the skin is broken down. The severity of macrovascular and microvascular disease may hinge upon the duration and degree of diabetes, severity of dyslipidemia, obesity, hypertension, smoking, and family history of atherosclerosis and anatomical location (proximal versus distal). Over time, chronic hemodynamic and metabolic damages to the endothelium result in functional and structural changes. The typical changes may involve thickening of the basement membrane and sclerosis of capillary walls.20 Common tests for vascular assessment are summarized in Table 3. Although measuring ankle-brachial pressure index (divide ankle systolic blood pressure by brachial systolic blood pressure obtained by a handheld Doppler) and palpation for pedal pulses are considered the most convenient noninvasive diagnostic method for detecting peripheral vascular disease (PVD), false elevation is not uncommon in people with diabetes due to noncompressible arteries associated with advanced atherosclerosis and vascular calcification. To improve the accuracy, the Wound, Ostomy and Continence Nurses Society’s Wound Committee has published a quick clinical guide for the performance of ankle-brachial pressure index.

Table 3
Table 3:

In general, an ankle-brachial pressure index of less than 0.5 indicates significant PVD (Table 3).

The loss of triphasic waveform, as indicated by pulsed wave Doppler, indicates stiff atherosclerotic vessels, providing further validation for the presence of arterial disease. A full segmental arterial Doppler examination should be obtained to provide accurate assessment of lower-extremity arterial disease (82% sensitivity and 92% specificity).21

Vascular tests should be considered in consultation with the clinical team and patient and in conjunction with the clinical signs of arterial disease. According to a systematic review,22 the complaint of claudication increases the likelihood of PVD (likelihood ratio [LR], 3.30; 95% confidence interval [CI], 2.30–4.80). Physical findings of atrophic skin, cool skin, blue/purple skin, or absence of lower limb hair (LR, 1.50; 95% CI, 1.20–1.70) and clinical assessment of capillary refill time (LR, 1.90; 95% CI, 1.20–3.20) are considered to be valuable for identifying advanced PVD. Individuals with ischemic foot would warrant a thorough assessment by a vascular specialist to determine the most appropriate interventions based on the location, the involved angiosomes, and the extent of arterial compromise.23

Neuroischemic foot

Clinicians should recognize that neuropathy and PVDs often coexist, which was previously discussed.

  • 3. Optimize plantar pressure redistribution to prevent and treat diabetic foot ulcers.

In general, plantar pressure redistribution should be considered for all individuals with neurotrophic foot ulcers (Table 4). Most experts advocate the pneumatic walker (made nonremovable with flexible cohesive bandage or casting material to increase adherence) or the total contact cast (TCC) for forefoot ulcers.24 The the TCC is an effective pressure redistribution measure but contraindicated in the presence of ischemia or deep infection or if trained professionals are not available to apply and manage the TCC. Deep-toed shoes and orthotics are more appropriate for maintenance after healing to prevent recurrence. Individuals with ulcers that are located in the heel area could benefit from modified shoes (pneumatic walkers and contact casts will actually increase local pressure). All persons with neurotrophic foot ulcers should see a foot specialist with appropriate training (eg, podiatrist, chiropodist, pedorthist, occupational therapist, physiotherapist, foot care nurse, or physician). Reevaluation, including further education and rationale for the devices, should occur at regular intervals (2–6 weeks with an active ulcer, 6–12 weeks with deformity or previous ulcer, 6–12 months with neuropathy alone). Despite best practice recommendations, clinicians need to consider the patient’s financial and vocational demands, as well as his/her mobility to individualize a realistic and achievable plan of care.25

Table 4
Table 4:
  • 4. Address the individual’s concerns and modify a plan of care to promote self-care and treatment adherence.

The paradigm that shifts the focus to self-management and patient engagement is the cornerstone of chronic disease management. Self-management support is “the systematic provision of education and supportive interventions, by healthcare staff (and others), to increase patients’ skills and confidence in managing their health problems, including regular assessment of progress and problems, goal setting, and problem-solving support.”26

Without appropriate interventions to support self-management, studies27,28 document that less than one-third of patients with diabetes and active ulcers were actually wearing downloading devices during activities on a regular basis. Chin et al29 identified a number of action cues from family, friends, and healthcare professionals that may enhance daily foot examination by people with diabetes. Valk et al28 identified 9 randomized controlled trials (RCTs) that evaluated patient education to prevent diabetic foot ulceration. The evidence is weak, with only 1 study of high-risk individuals with diabetes that reported a reduction in ulcer incidence (Peto OR, 0.28; 95% CI, 0.13–0.59) and reduced amputation rate (Peto OR, 0.32; 95% CI, 0.14–0.71) 1 year after intensive educational interventions. Ismail et al30 identified 25 trials that utilized various psychological interventions (eg, problem solving, contract setting, goal setting, self-monitoring of behaviors) to improve diabetic self-management. Patients allocated to psychological therapies demonstrated improvement in A1c (12 trials, standardized effect size = -0.32; -0.57 to -0.07) and reduction of psychological distress including depression and anxiety (5 trials, -0.5; -0.95 to -0.20).

Individuals living with foot ulcers experience poor quality of life because of limited mobility, social isolation, disruption to work and leisure activities, sleep disturbance, depression, and pain.31,32 According to a systematic review,33 the prevalence of depression is 3 times higher in type 1 diabetes (12% [range, 5.8%–43.3%] vs 3.2% [range, 2.7%–11.4%]) and 2 times higher prevalence of depression in people with type 2 diabetes (19.1% [range, 6.5%–33%] vs 10.7% [range, 3.8%–19.4%]) than in those without diabetes. The impact of depression and related distress on individuals with diabetes cannot be underestimated.

In a 5-year follow-up study of a cohort of PWDs, Winkley et al34 explored the association between depressive disorders and mortality. Matched with age and gender, participants with a documented history of depression were associated with 2-fold increased risk in mortality (hazard ratio, 2.09; 95% CI, 1.34–3.25) compared with those without depression. Healing of diabetic foot ulcers can be predicted by depression.35

Similarly, PWDs who report pain most or all of the time had statistically and clinically significantly poorer health-related quality of life than those who did not report pain.36 However, pain in diabetes is often underestimated and undertreated.37

  • 5. Optimize local wound environment for healing through debridement, infection control (bacterial burden control), and moisture balance (DIM).


Nonviable tissue including eschar or soft slough promotes bacteria growth and creates a proinflammatory environment that inhibits healing.38 However, not all wounds need and benefit from debridement. The decision to perform debridement should take into consideration whether complete wound closure is realistic and achievable. For wounds with the ability to heal, surgical debridement of callus and abnormal surface granulation with a curette, scissors, or scalpel blade has been considered to be the most effective way to destroy the biofilm structure and reduce the number of senescent cells that impede healing.39 In a 143-patient study by Saap and Falanga,40 wound closure of diabetic foot ulcers was predicted by whether the ulcers were adequately debrided (OR, 2.4; 95% CI, 1.0–5.6). Removal of hyperkeratosis and callus has been shown to reduce the risk of diabetic foot ulcers by lowering overall peak plantar pressure by 29%.41 Edwards and Stapley42 reviewed RCTs pertaining to debridement of diabetic foot ulcers. Combining results from 3 RCTs suggests hydrogels are superior to gauze or standard ulcer care to assist tissue autolytic debridement and healing in diabetic foot ulcers (RR, 1.84; 95% CI, 1.3–2.61). For wounds that do not have the potential for healing, debridement is contraindicated. Without adequate blood supply and immune defense, debridement can increase the risk of infection (especially when moisture is donated into the wound) and create a larger and deeper wound that does not heal. It is recommended that nonhealable wounds be kept dry and only loose-hanging slough be removed under judicious consideration (Figure 3).

Figure 3
Figure 3:


Individuals with diabetes are susceptible to wound infection as a result of immunodeficiency, neuropathy, and arteriopathy. Mowat et al43 documented an in vitro leukocyte chemotaxis defect in PWDs. Phagocytosis and bactericidal capacity were significantly reduced in the presence of hyperglycemia. Galkowska et al44 compared ulcer margin of foot biopsies in PWDs (n = 12) to normal controls (n = 5) and found no increased ratio of the CD4 and CD8 T lymphocytes indicating a relative lymphocyte response defect. Loots et al45 examined the cellular infiltrate patterns of punch biopsies from acute and chronic wounds including PWDs and foot ulcers. The CD4/CD8 ratio in all chronic wounds was significantly lower (P < .0027) compared with acute wounds. In light of the ubiquitous presence of microbes, proposed clinical presentations (Table 5) may help to distinguish whether significant bacterial damage occurs in the upper superficial or extends to the lower deep compartments.46 Early assessment and prompt treatment may help to prevent untoward outcomes.

Table 5
Table 5:

Increased surface bacterial burden may be treated with topical antimicrobials, whereas systemic treatment is required for lower compartment involvement (Figure 4). There is no one individual sign or symptom that will accurately confirm the diagnosis of wound infection, but a combination of 2 or more indicators should be sought for the diagnosis in each level (Table 5).46,47 Wounds that probe to bone (OR, 6.7; 95% CI, 2.3–19.9) exist for more than 30 days (OR, 4.7; 95% CI, 1.6–13.4), recur (OR, 2.4; 95% CI, 1.3–4.5), and relate to trauma (OR, 2.4; 95% CI, 1.1–5.0) and PVD (OR, 1.9; 95% CI, 1.0–3.6) are independent risk factors for foot infection.48 Furthermore, osteomyelitis should be suspected if ulcers probe to bone (sensitivity = 38%–87%, specificity = 85%–91%; positive predictive value = 53%–89%; negative predictive value = 56%–98%).49–51 Although magnetic resonance imaging is more sensitive and specific for the diagnosis of osteomyelitis, changes in radiographic appearance over a 2-week interval are considered as a viable alternative.47 Elevations in erythrocyte sedimentation rate and C-reactive protein, in the absence of other inflammatory conditions, are both valuable diagnostic indicators to validate the diagnosis of osteomyelitis.47,52 To manage damage associated with increased bacterial burden in the upper or superficial compartment, an array of antibacterial dressings (cadexomer iodine,53 silver dressings54) or topical antimicrobial agents (silver sulfadiazine, mupirocin, fusidic acid, or polysporin-gramicidin cream) have been used. There was no evidence that any particular topical agent was associated with better clinical outcomes compared with another.55,56 When individuals exhibit signs associated with deep and surrounding wound infection, systemic antimicrobial therapies should be considered (Figure 4). Although most infections are caused by gram-positive cocci, broad-spectrum antibiotic therapy may be needed for long-standing and refractory ulcers.47 Systematic reviews of trials to evaluate the effectiveness of antimicrobial treatment for diabetic foot ulcers fail to support the superiority of any intravenous or oral antibiotic regimen over any other.57 When wound healing is not a realistic goal, use of topical antiseptic agents that are often considered to be cytotoxic may be appropriate (Figure 4).

Figure 4
Figure 4:


Moisture balance is a critical element during the entire healing process. Although a desiccated wound environment can slow keratinocyte migration, too much moisture can cause damage to the surrounding skin and promote bacteria growth.47 A variety of dressings have been developed to maintain moisture balance. For instance, foam dressings wick up and lock in a large volume of exudate. Alginate and hydrofibers are also capable of handling copious exudate, while the gelling effect of these materials will keep the wound base moist without maceration. Hydrogels and occlusive dressings are usually indicated for dry wounds.

Despite the availability of different types of dressings, previous systematic reviews58–61 of RCTs have failed to reveal the benefit of one dressing class over another in various chronic wound types. Furthermore, there was no significant difference between modern advanced moisture-controlling dressings and daily application of normal saline gauze in healing outcomes. However, saline gauze usually requires frequent dressing changes to maintain moisture balance, increasing the likelihood of pain (compared with foam dressings [RR, 0.27; 95% CI, 0.10-0.69]) and discomfort (weighted mean difference [WMD] = 1.5; 95% CI, 0.63-2.37) as well as higher nursing costs (WMD= -30.5; 95% CI, -37.71 to -23.29, favoring foam dressings).58

  • 6. Consider the use of biological agents and adjunctive therapies for stalled wounds despite optimal treatment and potential for healing.

Neuropathy reduces growth factor production and leukocyte activities that are crucial to wound healing.5 Advance therapies (such as biological agents, skin substitutes, hyperbaric oxygen therapy, negative-pressure wound therapy) may have a role in chronic wounds but only after debridement, infection, and moisture balance are addressed.62 Clinicians ask if there is sufficient evidence to support advanced therapies. Analysis of pooled data from 3 RCTs of 140 people with a diabetic foot ulcer demonstrated an increase in the rate of ulcer healing (RR, 5.20; 95% CI, 1.25–21.66; P = .02) in favor of hyperbaric oxygen therapy at 6 weeks, but long-term benefits remained unequivocal. There was no difference in major amputation rate according to results from 5 trials with 312 participants (RR, 0.36; 95% CI, 0.11–1.18).63 Negative-pressure wound therapy has been widely used. In a recent review of 7 RCTs involving 580 patients with diabetic foot ulcers, 5 studies documented accelerated wound healing with the treatment of negative-pressure wound therapy.64

  • 7. Establish and empower an interprofessional team to improve care of PWDs and foot ulcers

The optimal care of individuals with chronic leg and foot ulcers is complex and time-consuming and requires the support of an interprofessional team. Management of these ulcers involves a detailed examination and discussion with patients to adequately address their concerns. The management of a chronic wound may be further complicated by the fragmentation of communication and services between acute, chronic, and home care.65

An interprofessional team approach that draws on the required expertise from a number of healthcare professionals, including diabetic education, medicine, nursing, infection control, chiropody, rehabilitation, and nutrition, is required to address the complexity of diabetic foot ulcer care.66 A patient education sample handout is illustrated in Table 6.

Table 6
Table 6:
PATIENT HANDOUTYou need to ensure that your feet last a lifetime. The care of your feet can be summarized with the 12 words beginning with the letter “S” in the chart below. You can prevent foot complications: Act to protect your own feet.


People with diabetes are at risk for foot problems, including skin ulcerations. This article highlighted the need to complete a comprehensive and holistic assessment to include laboratory evaluation, physical examination, lifestyle modifications, and patients’ perception and readiness to participate in self-management of the disease. Lower leg and foot assessment should be part of routine practice at each patient encounter to identify risks and needs for early intervention. Although debridement, infection management, and moisture balance are the key elements to optimize local wound environment for healing, clinicians must consider all available options to redistribute plantar pressure. The care of an active foot ulcer would necessitate involvement of an interprofessional team and ongoing psychosocial support.


This article focuses on the current state of care recommendations for persons living with diabetic foot ulcers. These include the following:

  • Perform a comprehensive clinical assessment that includes A1c, blood pressure, cholesterol, diet, exercise, and smoking history.
  • Conduct a lower-leg and foot assessment to differentiate neuropathic from neuroischemic diseases (ulcers).
  • Optimize plantar pressure redistribution to prevent and treat diabetic foot ulcers.
  • Address the individual’s concerns and modify plan of care to promote self-care and treatment adherence.
  • Optimize local wound environment for healing through debridement, infection control (bacterial burden control), and moisture balance (DIM).
  • Consider the use of biological agents and adjunctive therapies for stalled wounds despite optimal treatment and potential for healing.
  • Establish and empower an interprofessional team to improve the care of persons with diabetes and foot ulcers.


1. Boulton AJ, Vileikyte L, Ragnarson-Tennvall G, Apelqvist J. The global burden of diabetic foot disease. Lancet 2005; 366 (9498): 719–24.
2. Brem H, Sheehan P, Rosenberg H, Schneider JS, Boulton AJ. Evidence-based protocol for diabetic foot ulcers. Plast Reconstr Surg 2006; 117 (Suppl 7): 193S–209S.
3. Abbott CA, Carrington AL, Ashe H, et al. The North-West Diabetes Foot Care Study: incidence of, and risk factors for, new diabetic foot ulceration in a community-based patient-cohort. Diabet Med 2002; 19: 377–84.
4. Adler AI, Boyko EJ, Ahroni JH, Smith DG. Lower extremity amputation in diabetes. The independent effects of peripheral vascular disease, sensory neuropathy, and foot ulcers. Diabetes Care 1999; 22: 1029–35.
5. Bakker K, Apelqvist J, Schaper NC. Practical guidelines on the management and prevention of the diabetic foot 2011. Diabet Metab Res Rev 2012; 28 (Suppl 1): 225–31.
6. Sibbald GR, Woo KY. The biology of chronic foot ulcers in persons with diabetes. Diabetes Metab Res Rev 2008; 24 (Suppl 1): S25–30.
7. Orsted HL, Searles G, Trowell H, Shapera L, Miller M, Rahman J. Best practice recommendations for the prevention, diagnosis, and treatment of diabetic foot ulcers: update 2006. Adv Skin Wound Care 2007; 20: 655–69.
8. Centre for Clinical Practice at NICE (UK). Diabetic Foot Problems: Inpatient Management of Diabetic Foot Problems. London, UK: National Institute for Health and Clinical Excellence; 2011.
9. Bakker K, Apelqvist J, Schaper NCInternational Working Group on Diabetic Foot Editorial Board. Practical guidelines on the management and prevention of the diabetic foot 2011. Diabetes Metab Res Rev 2012;28 Suppl 1: 225–31.
10. Sibbald RG, Goodman L, Woo KY, et al. Special considerations in wound bed preparation 2011: an update. Adv Skin Wound Care 2011; 24: 415–36.
11. Warriner RA, Snyder RJ, Cardinal MH. Differentiating diabetic foot ulcers that are unlikely to heal by 12 weeks following achieving 50% percent area reduction at 4 weeks. Int Wound J 2011; 8: 632–7.
12. Monteiro-Soares M, Boyko E, Ribeiro J, Ribeiro I, Dinis-Ribeiro M. Predictive factors for diabetic foot ulceration: a systematic review. Diabetes Metab Res Rev 2012; 28: 574–600.
13. Boyko EJ, Ahroni JH, Cohen V, Nelson KM, Heagerty PJ. Prediction of diabetic foot ulcer occurrence using the commonly available clinical information: the Seattle Diabetic Foot Study. Diabetes Care 2006; 29: 1202–07.
14. Inlow S, Orsted H, Sibbald RG. Best practices for the prevention, diagnosis and treatment of diabetic foot ulcers. Ostomy Wound Manage 2000; 46 (11): 55–68.
15. Murphy CA, Laforet K, DaRosa P, Tabamo F, Woodbury MG. Reliability and predictive validity of Inlow’s 60-Second Diabetic Foot Screen Tool. Adv Skin Wound Care 2012; 25: 261–6.
16. Pham H, Armstrong DG, Harvey C, Harkless LB, Giurini JM, Veves A. Screening techniques to identify people at high risk for diabetic foot ulceration; a prospective multicenter trial. Diabetes Care 2000; 23: 606–11.
17. Crawford F, Inkster M, Kleijnen J, Fahey T. Predicting foot ulcers in patients with diabetes: a systematic review and meta-analysis. Q J Med 2007; 100: 65–86.
18. Murray HJ, Young MJ, Hollis S, Boulton AJM. The association between callus formation, high pressures and neuropathy in diabetic foot ulceration. Diabetic Med 1996; 13: 979–82.
19. Cowley MS, Boyko EJ, Shofer JB, Ahroni JH, Ledoux WR. Foot ulcer risk and location in relation to prospective clinical assessment of foot shape and mobility among persons with diabetes. Diabetes Res Clin Pract 2008; 82: 226–32.
20. Khan NA, Rahim SA, Anand SA, Simel DL, Panju A. Does the clinical examination predict lower extremity peripheral arterial disease? JAMA 2006; 295: 536–46.
21. Williams DT, Harding KG, Price P. An evaluation of the efficacy of methods used in screening for lower-limb arterial disease in diabetes. Diabetes Care 2005; 28: 2206–10.
22. Crique MH, Fronek A, Klauber MR, Barrett-Connor E, Gabriel S. The sensitivity, specificity and predictive value of traditional clinical evaluation of peripheral arterial disease: results from non-invasive testing in a defined population. Circulation 1985; 71: 516–522.
23. Alexandrescu V, Söderström M, Vermano M. Angiosome theory: fact or fiction? Scand J Surg 2012; 101: 125–31.
24. Katz IA, Harlan A, Miranda-Palma B, et al. A randomized trial of two irremovable off-loading devices in the management of plantar neuropathic diabetic foot ulcers. Diabetes Care 2005; 28: 555–9.
25. Gale L, Vedhara K, Searle A, Kemple T, Campbell R. Patients’ perspective on foot complications in type 2 diabetes: a qualitative study. Br J Gen Pract 2008; 58: 555–63.
26. Health Council of Canada. Self-management support for Canadians with chronic health conditions. Toronto, ON, Canada: Health Council of Canada; 2012.
27. Knowles EA, Boulton AJ. Do people with diabetes wear their prescribed footwear? Diabet Med 1996; 13: 1064–8.
28. Valk GD, Kriegsman DM, Assendelft WJ. Patient education for preventing diabetic foot ulceration. Cochrane Database Syst Rev 2001; (4): CD001488.
29. Chin YF, Huang TT, Hsu BR. Impact of action cues, self-efficacy and perceived barriers on daily foot exam practice in type 2 diabetes mellitus patients with peripheral neuropathy. J Clin Nurs 2013; 22 (1-2): 61–8.
30. Ismail K, Winkley K, Rabe-Hesketh S. Systematic review and meta-analysis of randomized controlled trials of psychological interventions to improve glycemic control in patients with type II diabetes. Lancet 2004; 363 (9421): 1589–97.
31. Egede LE, Ellis C. Diabetes and depression: global perspectives. Diabetes Res Clin Pract 2010; 87 (3): 302–12.
32. Gask L, Macdonald W, Bower P. What is the relationship between diabetes and depression? A qualitative metasynthesis of patient experience of co-morbidity. Chronic Illn 2011; 7 (3): 239–52.
33. Roy T, Lloyd CE. Epidemiology of depression and diabetes: a systematic review. J Affect Disord 2012; 142 Suppl: S8–21.
34. Winkley K, Sallis H, Kariyawasam D, et al. Five-year follow-up of a cohort of people with their first diabetic foot ulcer: the persistent effect of depression on mortality. Diabetologia 2012; 55: 303–10.
35. Vedhara K, Miles JN, Wetherell MA, et al. Coping style and depression influence the healing of diabetic foot ulcers: observational and mechanistic evidence. Diabetologia 2010; 53: 1590–8.
36. Ribu L, Rustøen T, Birkeland K, Hanestad BR, Paul SM, Miaskowski C. The prevalence and occurrence of diabetic foot ulcer pain and its impact on health-related quality of life. J Pain 2006; 7: 290–9.
37. Bengtsson L, Jonsson M, Apelqvist J. Wound-related pain is underestimated in patients with diabetic foot ulcers. J Wound Care 2008; 17: 433–5.
38. Kirshen C, Woo K, Ayello EA, Sibbald RG. Debridement: a vital component of wound bed preparation. Adv Skin Wound Care 2006; 19: 506–17.
39. Wolcott RD, Rumbaugh KP, James G, et al. Biofilm maturity studies indicate sharp debridement opens a time- dependent therapeutic window. J Wound Care 2010; 19: 320–8.
40. Saap LJ, Falanga V. Debridement performance index and its correlation with complete closure of diabetic foot ulcers. Wound Repair Regen 2002; 10: 354–9.
41. Slater RA, Hershkowitz I, Ramot Y, Buchs A, Rapoport MJ. Reduction of digital plantar pressure by debridement and silicone orthosis. Diab Res Clin Pract 2006; 74: 263–6.
42. Edwards J, Stapley S. Debridement of diabetic foot ulcers. Cochrane Database Syst Rev 2010; (1): CD003556.
43. Mowat A, Baum J. Chemotaxis of polymorphonuclear leukocytes from patients with diabetes mellitus. N Engl J Med 1971; 284: 621–7.
44. Galkowska H, Wojewodzka U, Olszewski WL. Chemokines, cytokines, and growth factors in keratinocytes and dermal end othelial cells in the margin of chronic diabetic foot ulcers. Wound Repair Regen 2006; 14: 558–65.
45. Loots MA, Lamme EN, Mekkes JR, Bos JD, Middelkoop E. Cultured fibroblasts from chronic diabetic wounds on the lower extremity (non–insulin-dependent diabetes mellitus) show disturbed proliferation. Arch Dermatol Res 1999; 291 (2-3): 93–9.
46. Woo K, Sibbald RG. A cross-sectional validation study of using NERDS and STONEES to assess bacterial burden. Ostomy Wound Manage 2009; 55 (8): 40–48.
47. Lipsky BA, Berendt AR, Cornia PB, et al. 2012 Infectious Diseases Society of America clinical practice guideline for the diagnosis and treatment of diabetic foot infections. Clin Infect Dis 2012; 54 (12): e132–73.
48. Lavery LA, Armstrong DG, Wunderlich RP, et al. Risk factors for foot infections in individuals with diabetes. Diabetes Care 2006; 29: 1288–93.
49. Grayson ML, Gibbons GW, Balogh K, Levin E, Karchmer AW. Probing to the bone in infected pedal ulcers. a clinical sign of underlying osteomyelitis in diabetic patients. JAMA 1995; 273: 721–3.
50. Lavery LA, Armstrong DG, Peters EJ, Lipsky BA. Probe to the bone test for diagnosing diabetic foot osteomyelitis: reliable or relic? Diabetes Care 2007; 30: 270–4.
51. Shone A, Burnside J, Chipchase S, Game F, Jeffcoate W. Probing the validity of the Probe-to-the-Bone Test in the diagnosis of osteomyelitis of the foot in diabetes. Diabetes Care 2006; 29: 945.
52. Kaleta JL, Fleischli JW, Reilly CH. The diagnosis of osteomyelitis in diabetes using erythrocyte sedimentation rate: a pilot study. J Am Podiatr Med Assoc 2001; 91: 445–50.
53. Apelqvist J, Ragnarson Tennvall G. Cavity foot ulcers in diabetic patients: a comparative study of cadexomar iodine ointment and standard treatment. An economic analysis alongside a clinical trial. Acta Derm Venereol 1996; 76: 231–5.
54. Woo K, Ayello E, Sibbald RG. Bacteriology, inflammation and healing: a study of nanocrystalline silver dressings in chronic venous leg ulcers. Surg Tech Int. In press
55. Peters EJ, Lipsky BA, Berendt AR, et al. A systematic review of the effectiveness of interventions in the management of infection in the diabetic foot. Diabetes Metab Res Rev 2012; 28 Suppl 1: 142–62.
56. Hinchliffe RJ, Valk GD, Apelqvist J, et al. A systematic 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: S119–137.
57. Peters EJ, Lipsky BA, Berendt AR, et al. A systematic review of the effectiveness of interventions in the management of infection in the diabetic foot. Diabetes Metab Res Rev 2012; 28 Suppl 1: 142–62.
58. Vermeulen H, Ubbink D, Goossens A, de Vos R, Legemate D. Dressings and topical agents for surgical wounds healing by secondary intention. Cochrane Database Syst Rev 2004; (2): CD003554.
59. Dumville JC, O’Meara S, Deshpande S, Speak K. Alginate dressings for healing diabetic foot ulcers. Cochrane Database Syst Rev 2012; (2): CD009110.
60. Dumville JC, Deshpande S, O’Meara S, Speak K. Hydrocolloid dressings for healing diabetic foot ulcers. Cochrane Database Syst Rev 2012; (2): CD009099.
61. Game FL, Hinchliffe RJ, Apelqvist J, et al. A systematic review of interventions to enhance the healing of chronic ulcers of the foot in diabetes. Diabetes Metab Res Rev 2012; 28 Suppl 1: 119–41.
62. Woo K, Ayello EA, Sibbald RG. The edge effect: current therapeutic options to advance the wound edge. Adv Skin Wound Care 2007; 20: 99–117.
63. Kranke P, Bennett MH, Martyn-St James M, Schnabel A, Debus SE. Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev 2012; (4): CD004123.
64. Xie X, McGregor M, Dendukuri N. The clinical effectiveness of negative pressure wound therapy: a systematic review. J Wound Care. 2010; 19: 490–5.
65. Robert Wood Johnson Foundation. Chronic care: making the case for ongoing care. Princeton, NJ: Robert Wood Johnson Foundation; 2010.
66. Woo K, Alavi A, Botros M, et al. A transprofessional comprehensive assessment model for persons with lower extremity leg and foot ulcers. Wound Care Canada 2007; 5 Suppl 1: s34–s47.

diabetic foot ulcer; evidence-based practice

© 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins. All world rights reserved.