Local care of diabetic foot ulcers

INTRODUCTION — 

The local care of diabetic foot ulcers is reviewed. The approach to the patient with a diabetic foot ulcer and surgical management are reviewed separately. (See "Management of diabetic foot ulcers".)

GENERAL CONSIDERATIONS — 

The diabetic foot ulcer is a unique category of chronic wound that requires multiple considerations (algorithm 1). The general evaluation and management of diabetic foot ulcers are discussed separately [1,2]. (See "Evaluation of the diabetic foot" and "Management of diabetic foot ulcers".)

Wound healing in diabetic ulcers is impaired through a lack of response to growth factors and reduced collagen accumulation [3,4]. Chronic diabetic foot ulcers are often colonized with a variety of pathogens. For patients who require operative debridement or incision and drainage for infection, initial empiric antibiotic therapy is transitioned to more specific treatment based on the results and sensitivities of intraoperative cultures. Longer antibiotic therapy may be needed, particularly for the treatment of osteomyelitis [5]. (See "Diabetic foot infections, including osteomyelitis: Treatment", section on 'Empiric antibiotic selection'.)

Anatomic location of the ulcer — The location of a diabetic foot ulcer can provide important clues about the underlying cause and help tailor treatment decisions. Common locations and their implications include:

●Base of the metatarsal (plantar foot ulcer) – These are often caused by pressure and friction from footwear or underlying bony deformities (eg, hammertoes, bunions) [1]. Neuropathy (loss of sensation) and peripheral artery disease (PAD) are risk factors [6]. Management considerations include offloading, footwear modifications, and management of bony deformities [7]. Management of bony deformities may require surgical correction in some cases [8]. Mechanical offloading is crucial to relieve pressure on the ulcer and promote healing. The total contact cast is often the gold standard for these ulcers. Proper footwear with cushioned insoles and adequate toe box space is essential to prevent recurrence [9].

●Heel ulcer – Common causes include pressure from lying or sitting for prolonged periods [10], friction from footwear, and underlying bony prominences. Risk factors involve limited mobility, neuropathy, PAD, chronic venous disease, heart failure, and pedal edema [10]. Management considerations include offloading the heel in a specialized device depending on the patient's mobility; heel boots and mattress overlays may be necessary. Pressure redistribution by repositioning and frequent turning is crucial for patients who cannot get up from bed [11]. Wound care requires a moist wound healing environment and debridement as needed.

●Digital ulcer (toe ulcer) – Trauma such as stubbing the toe, friction rub from ill-fitting footwear, ingrown toenails, and bony deformities are common etiologies. Neuropathy and PAD with resultant ischemia are risk factors [12]. When managing these ulcers, offloading may require toe spacers, custom orthotics, or specialized footwear. Treatment of the underlying cause may include ingrown toenail removal, management of bony deformities, wound care from subsequent ulcers, or treatment of PAD. Digital ulcers are at high risk of these complications due to their location and limited blood supply.

Approach by wound classification — Classifying diabetic foot ulcers based on infection and ischemia status helps guide treatment decisions (algorithm 1) as well as the selection of the appropriate setting for care. We use the wound, ischemia, and foot infection (WIfI [2]) classification, which classifies the wound based on the presence and severity of the wound, infection, and ischemia (figure 1), and which can help set realistic expectations for healing and amputation risk (table 1). (See "Management of diabetic foot ulcers", section on 'Threatened limb classification: WIfI' and "Classification of acute and chronic lower extremity ischemia", section on 'WIfI grades and stages'.)

The initial evaluation includes using validated diagnostics such as an ankle-brachial index or toe-brachial index with toe waveforms and pressures at baseline. Transcutaneous oxygen pressure measurements can also be utilized [13]. (See "Noninvasive diagnosis of upper and lower extremity arterial disease".)

Noninfected, nonischemic wounds — Many of these wounds are low-grade small, superficial ulcers (ie, WIfI wound grade 1) that typically have a clean base, minimal exudate, and no gross signs of infection (no erythema, warmth, or purulent discharge). Foot pulses are often palpable, and toe waveforms are pulsatile with toe pressures (TcPO₂) >60 mmHg. Many such wounds are primarily neuropathic.

Regular sharp debridement of any devitalized tissue is essential. These wounds can typically be debrided in the clinic or at the bedside. When a clinician with expertise in sharp debridement is not available, autolytic hydrogels can be used. For noninfected, well-perfused ulcers that extend to deeper tissues, we suggest initial surgical debridement in an operating room setting.

The wound bed should be kept moist with appropriate dressings (eg, hydrocolloids, hydrogels) to promote healing while maintaining a drier periwound environment to prevent maceration of the wound edges [14]. Close monitoring should look for signs of infection or ischemia. Follow-up appointments are usually frequent, initially weekly or biweekly. With proper care, these ulcers often heal within four to eight weeks.

For ulcers related to areas of increased pressure, mechanical offloading should be implemented to relieve pressure on the ulcer and promote healing. (See 'Anatomic location of the ulcer' above and "Management of diabetic foot ulcers".)

Ischemic, noninfected wounds — Many of these wounds are moderately deep (WIfI wound grade 2 to 3) and may appear pale or dry with minimal exudate. Patients often have diminished or absent peripheral pulses and cool skin. They sometimes have rest pain, although this is less common in those with diabetes and neuropathy. Urgent referral for vascular assessment (eg, angiogram) and possible revascularization (endovascular or open surgery) is critical.

Proper wound care includes keeping the wound dry without debridement to help avoid introducing infection until revascularization can be performed [15]. There should be no expectation of wound healing until adequate blood flow is restored. Following revascularization, the time to wound healing varies depending on the nature and success of revascularization.

For ulcers related to areas of increased pressure, mechanical offloading remains important to prevent further tissue damage while awaiting revascularization. (See 'Anatomic location of the ulcer' above and "Management of diabetic foot ulcers".)

Infected, nonischemic wounds — These wounds may be relatively superficial (WIfI wound grade 1) but are more often extensive (WIfI wound grade 2 or 3) and may involve bone/tendon. Signs of infection may include erythema, warmth, purulent discharge, and malodor. The patient may have systemic symptoms and signs such as fever or an elevated white blood cell count or present overtly septic. Peripheral pulses are usually present.

The treatment of infected wounds includes initial broad-spectrum antimicrobial therapy (algorithm 2) and surgical debridement of all infected or necrotic tissue [16]. Antibiotics are adjusted based on tissue culture and sensitivity. The duration of antimicrobial therapy depends on the infecting organism(s), depth, and severity of infection [17]. (See "Management of diabetic foot ulcers", section on 'Managing infection' and "Diabetic foot infections, including osteomyelitis: Treatment".)

Frequent dressing changes with appropriate wound dressings are warranted. (See 'Wound care' below.)

For ulcers related to areas of increased pressure, mechanical offloading should be implemented to relieve pressure on the ulcer and promote healing. (See 'Anatomic location of the ulcer' above and "Management of diabetic foot ulcers".)

With prompt treatment, healing can occur within a few weeks to months, depending on the size of the wound. Deep infections or osteomyelitis may require a longer duration of treatment.

Infected, ischemic wounds — Infected and ischemic wounds (TcPO₂ <60 mmHg) often present with higher grades of foot infection (WIfI limb stage 3 or 4). These ulcers constitute the highest risk for nonhealing and potential amputation [18-20]. Clinical signs of ischemia are not always obvious, and as such, baseline vascular assessment to quantify distal perfusion is essential.

Progress with healing will be significantly delayed until both infection and ischemia are addressed. Broad-spectrum antibiotics should be initiated (algorithm 2) while awaiting tissue culture results and adjusted based on culture and sensitivity. The selected antibiotics and duration of therapy depend upon the depth and severity of infection [17]. (See "Management of diabetic foot ulcers", section on 'Managing infection' and "Diabetic foot infections, including osteomyelitis: Treatment".)

Despite the presence of ischemia (contrasting to infected, nonischemic wounds above) (see 'Infected, nonischemic wounds' above), aggressive debridement is needed to remove all infected and necrotic tissue [16]. Patients should be referred to a vascular specialist; revascularization may be necessary to achieve wound healing [21]. Hospitalization may be necessary to avoid delays in care.

Frequent dressing changes and offloading any areas of pressure are crucial, even in the presence of ischemia. (See 'Wound care' below and "Management of diabetic foot ulcers".)

Healing time is variable and depends on the success of infection control and revascularization. (See "Management of chronic limb-threatening ischemia".)

WOUND CARE

Care setting — The appropriate care setting depends on many factors, including the wound severity, medical comorbidities, and social factors that may limit access to wound care. Regardless of the care setting, interprofessional collaboration is key to optimal diabetic foot ulcer management. An interdisciplinary team of primary care physicians, podiatrists, wound care specialists, vascular surgeons, infectious disease physicians, physical therapists, nurses, and other health care professionals working together to provide comprehensive care ensures the best possible outcomes for patients.

Primary care/office setting — The primary care role is essential in the initial assessment and diagnosis of diabetic foot ulcers and is suitable for the management of patients with diabetes and a limb at low risk for amputation (ie, WIfI limb stage 1) [22]. This includes small, superficial, noninfected, nonischemic ulcers, and some patients with minor infection and no ischemia or a low grade of ischemia and no infection. The patient must have good glycemic control, be without significant comorbidities, and be able to adhere to self-care instructions and follow-up appointments.

In the clinical setting, basic wound care, such as cleaning and dressing changes, can be performed. For patients with pressure-related ulcers, offloading education and implementation (eg, fitting for appropriate footwear) can also be conducted [22]. Monitoring for complications and referral to specialists, when necessary, can be performed in this care setting. Referral to a wound care specialist or vascular surgeon should be considered for any diabetic foot ulcer that does not show signs of improvement within two to four weeks, shows signs of infection or ischemia, involves bone or deep tissues, requires specialized debridement, or requires revascularization.

Outpatient wound care center — The outpatient wound care center is suitable for any ulcer that does not heal within four weeks of appropriate wound care management or for larger or deeper ulcers with mild-to-moderate infection (infection grade 1 or 2) or ischemia (ischemia grade 1 or 2), but not both. This corresponds to WIfI clinical limb stage 2.

Patients requiring specialized wound dressings or debridement or those who need assistance with offloading devices or wound care should be referred early. The wound care clinic provides a comprehensive wound assessment and treatment planning. This management is usually rendered by coordinating care with other specialists (vascular and infectious disease physicians, podiatrists, and nutritionists).

Advanced wound care therapy, such as negative pressure wound therapy (NPWT), oxygen therapy, and additional diagnostic imaging, can be rendered. Close monitoring of the healing progress and adjustment of treatment as needed is part of the care rendered at a wound care center.

Inpatient hospitalization — Inpatient hospitalization is required for infection requiring intravenous antibiotics, ischemia requiring urgent revascularization, or wounds with extensive tissue loss or complications (eg, gangrene). Higher clinical grades of infection, ischemia, or wound severity correspond with WIfI limb stages 3 or 4, which increases the risk for amputation, even more so when severe infection and ischemia occur together.

Inpatient hospitalization is also appropriate for patients with diabetic foot ulcers with unstable medical conditions or significant social barriers to outpatient care.

Hospitalization allows intensive wound care and infection control. Surgical debridement or amputation may be necessary. Patient care also involves the management of underlying uncontrolled medical conditions such as diabetes or hypertension and, later, coordination of discharge planning and posthospital care.

Debridement — Debridement of necrotic tissue is important for ulcer healing [23]. The frequency of assessment and proper care may contribute more to wound healing than the specific type of debridement. In a review that examined chronic wound care among veterans, the chance of diabetic ulcer healing increased 2.5-fold when debridement was performed at 80 percent of visits and doubled when ischemia was assessed at the first visit [24].

There are few data to guide the choice of debridement (surgical, enzymatic, autolytic, mechanical, and biologic) for diabetic foot ulcers [25]. These types of debridement are reviewed separately. (See "Principles of acute wound management", section on 'Debridement'.)

●Sharp surgical debridement involves the use of a scalpel or scissors to remove necrotic tissue [26]. When clinicians with expertise in sharp debridement are available, we prefer this method for debridement for diabetic foot wounds as with other wounds requiring debridement.

●If a clinician with expertise is not available, as an alternative, we suggest the application of hydrogel, but data are limited to support its efficacy in promoting ulcer healing.

●Enzymatic debridement (topical application of proteolytic enzymes such as collagenase) may be appropriate in certain settings (eg, extensive vascular disease not under team management) [27,28].

●Autolytic debridement may be a good option in patients with painful ulcers, such as using a semiocclusive or occlusive dressing to cover the ulcer so that necrotic tissue is digested by enzymes normally present in wound tissue.

●Larval therapy has been used in some specialty clinics for high-risk patients as an adjunct to serial surgical debridement. There appears to be a benefit from several days of targeted therapy [29]. As an example, in very frail patients for whom the goals are comfort care and lowering the risk of infection, "wound hospice" or "podiatric hospice" using larval therapy may increase the duration of antibiotic-free days [30].

Dressings and other treatments

Dressing selection — After debridement, diabetic foot wounds should be kept clean and moist but free of excess fluid. Dressings should be selected based on ulcer characteristics, such as the extent of exudate, desiccation, or necrotic tissue (table 2). Some dressings simply primarily provide protection, whereas others promote wound hydration or prevent excessive moisture. Wet-to-dry saline dressings are frequently used but can remove both nonviable and viable tissue and may result in a dry wound. Other dressings are impregnated with antimicrobial agents to prevent infection with the aim of enhancing ulcer healing.

For the management of foot ulcers in patients with diabetes, there is no high-quality evidence to suggest any significant differences in wound healing outcomes when comparing the various types of dressings (table 3) [31,32]. (See "Overview of treatment of chronic wounds", section on 'Wound dressings'.)

NPWT should be considered before surgery and in between surgical debridement [33-35].

Role of negative pressure wound therapy — NPWT may improve the healing of diabetic foot ulcers, as well as wounds following diabetic foot surgery [36-45]. Based on randomized trials showing improved wound healing [36-44,46], we suggest NPWT for extensive open wounds following debridement for infection and necrosis or following partial foot amputation, provided there is no residual necrotic tissue or infected bone (osteomyelitis) [47]. NPWT can be considered for diabetic foot ulcers that are slow to heal with standard treatment or have not responded within 30 days, provided the infection is controlled, and ischemia has been excluded.

NPWT, also called vacuum-assisted closure, involves the application of controlled subatmospheric pressure to the surface of the ulcer. NPWT enhances healing by increasing wound perfusion, reducing edema, reducing the local bacterial burden, and increasing the formation of granulation tissue. The indications, contraindications, and uses of NPWT systems are discussed in detail separately. (See "Negative pressure wound therapy".)

For managing postoperative wounds, a multicenter trial followed 162 patients with diabetes for 16 weeks following partial foot amputation [38]. Compared with the control group, the NPWT group had a significantly higher percentage of patients with healed wounds (56 versus 39 percent) and a shorter time to complete closure (42 versus 84 days).

NPWT also decreases the length of hospitalization, complication rates, and costs [48-50]. Among five trials in a systematic review, NPWT significantly increased the chance of foot ulcer healing compared with dressings (risk ratio [RR] 1.40, 95% CI 1.14-1.72) [44]. Among three trials, NPWT reduced the risk of amputation (RR 0.33, 95% CI 0.15-0.70). There was no effect on ulcer recurrence.

Adjuncts to wound healing — Other adjunctive therapies may also help improve the healing of diabetic foot ulcers [51-54]. These include the use of growth factors, NPWT, and others with uncertain benefits, such as hyperbaric oxygen therapy (HBOT), topical oxygen therapy, shockwave therapy, and low-level light therapy.

Growth factors — Growth factors can be considered if the wound is slow to respond to standard treatment or has not responded within 30 days, provided the infection is controlled.

Tissue growth factors promote cellular proliferation and angiogenesis and thereby improve ulcer healing. A systematic review assessed outcomes of 28 trials using 11 different growth factors predominantly used as topical agents, including platelet-derived wound healing formula, autologous growth factor, allogeneic platelet-derived growth factor, transforming growth factor beta 2, arginine-glycine-aspartic acid peptide matrix, recombinant human platelet-derived growth factor (becaplermin), recombinant human epidermal growth factor, recombinant human basic fibroblast growth factor, recombinant human vascular endothelial growth factor, recombinant human lactoferrin, and recombinant human acidic fibroblast growth factor [55]. Overall, the quality of the trial was low, with a high risk of bias. In a meta-analysis of 12 trials, the use of any growth factor compared with placebo or no growth factor significantly increased the number of participants with complete wound healing (53 versus 35 percent). The results were mainly based on platelet-derived wound healing formula (64 versus 26 percent, two trials) and recombinant human platelet-derived growth factor (becaplermin; 48 versus 33 percent, five trials). No clear differences were apparent with respect to amputation rates, but only two trials were included in this analysis.

Platelet-derived growth factor as a gel preparation (becaplermin) is approved by the US Food and Drug Administration as an adjuvant therapy for diabetic foot ulcers [56]. Although effective, its use has been limited by high cost and by postmarketing reports of an increased rate of mortality secondary to malignancy in patients treated with three or more tubes of becaplermin, compared with controls (3.9 versus 0.9 per 1000 person-years; adjusted rate ratio 5.2, 95% CI 1.6-17.6) [57,58].

Others

●HBOT – HBOT may be associated with improved healing as a component of diabetic ulcer management, but the indications for HBOT in the treatment of nonhealing diabetic foot ulcers remain uncertain. Most, but not all [59], meta-analyses of randomized trials suggest that HBOT may offer a benefit in the treatment of diabetic foot ulcers; however, each meta-analysis noted variability in methodologic quality of the included studies [59-64]. The available trials are limited by small sample size and heterogeneity of the wounds being treated (eg, ulcer size, ulcer depth, microbial environment, presence of ischemia) [65-76]. No conclusions could be drawn regarding specific indications for or timing of therapy. A pooled analysis found significantly improved wound healing (odds ratio [OR] 9.99, 95% CI 3.97-25.1) and decreased risk of amputation (OR 0.24, 95% CI 0.14-0.43) for HBOT [61]. A later meta-analysis found similar results [64]. As an example of these effects, in one of the larger trials that included 70 patients with severely ischemic foot ulcers, the amputation rate was 9 percent in the treatment group and 33 percent in the control [67]. In another trial that included 94 patients, significantly more wounds healed completely in the HBOT group compared with a placebo group (52 versus 29 percent) [74]. However, in a later longitudinal cohort of 6259 patients with diabetic foot ulcers, the use of HBOT did not result in better wound healing, and amputation rates were similar to those not receiving the therapy [65].

●Topical oxygen therapy – Topical oxygen therapy/continuous diffusion of oxygen appears to be associated with improved healing of diabetic foot ulcers [77,78]. This therapy involves local administration of oxygen and appears to improve epithelialization by upregulating vascular endothelial growth factor expression and collagen synthesis, improving overall matrix deposition, and altering microbiome ecology [79,80]. Several sham-controlled, double-blind, randomized trials support the use of this therapy, including a multinational study that included 220 subjects, which reported a 4.5-fold greater rate of healing in those receiving active topical oxygen therapy at home compared with placebo [81]. Other similarly designed studies have reported similar findings [82-85].

●Shockwave therapy – Shockwave therapy, which consists of treatment using a handheld probe to deliver high-energy pulses locally to the wound, purportedly increases local perfusion and angiogenesis, disrupts biofilm, and may upregulate growth factors. Observational and small randomized trials suggest that shockwave therapy may improve the healing of chronic diabetic foot ulcers [86-90]. In two proprietary trials, 336 patients were randomly assigned to shockwave therapy (DermaPACE) or usual care consisting of wet-to-dry dressings or debridement. At 24-week follow-up, significantly more patients in the shockwave group achieved complete wound closure compared with usual care (44 versus 30 percent) [91].

●Low-level light therapy – Low-level light therapy uses low-power lasers or light-emitting diodes to alter cellular function and molecular pathways. A systematic review identified four randomized trials that included 131 patients comparing low-level light therapy with either nontherapeutic light therapy or sham treatment for the treatment of diabetic foot ulcers [92-97]. Each of the trials demonstrated beneficial outcomes for the light treatment with no adverse events; however, many limitations were noted with these generally small trials.

In a review of other forms of energy, such as electrical stimulation, ultrasound, normothermic therapy, magnet therapy, and laser therapy, there was no convincing evidence of clear benefit [46]. Other therapies aimed at managing chronic wounds predominantly in patients with peripheral artery disease have been tried, and some initial data appear promising, but further studies are required regarding dose/duration/delivery to provide recommendations on use [98-100]. (See "Investigational therapies for treating symptoms of lower extremity peripheral artery disease", section on 'Stem cell therapy' and "Investigational therapies for treating symptoms of lower extremity peripheral artery disease", section on 'Therapeutic angiogenesis'.)

Wound coverage — The adjunctive use of skin grafts or skin substitutes can improve ulcer healing. Techniques for skin grafting and using skin substitutes are reviewed separately. (See "Skin autografting" and "Skin substitutes".)

A systematic review identified 17 trials using skin grafts or substitutes for the treatment of diabetic foot ulcers [101]. The incidence of completed closure of diabetic foot ulcers was significantly improved for the skin grafts or substitutes compared with standard care (RR 1.55, 95% CI 1.30-1.85). In two trials, there were no significant differences in ulcer recurrence. Based on four trials that directly compared two products, no specific type of skin graft or skin substitute was found to be superior to another. Among two trials that reported the incidence of lower limb amputations, skin grafts and substitutes were also associated with significantly lower risk for amputation, although the absolute risk reduction for amputation was small (RR 0.43, 95% CI 0.23-0.81; risk difference -0.06, 95% CI -0.10 to -0.01).

Among chronic wounds, skin substitutes have been highly studied for promoting the healing of diabetic foot ulcers [101-105]. Many types of skin substitutes have been used in the treatment of diabetic foot ulcers, including epidermal, dermal, and bilayer substitutes [101,106-116]. Human skin grafts and bioengineered skin substitutes (eg, Dermagraft, Apligraf, TheraSkin, Graftskin, EpiFix, Zelen, Graftjacket, Hyalograft 3D, Kaloderm, OrCel) have been studied in individuals with noninfected, nonischemic chronic plantar diabetic foot ulcers [53,110,117-125].

A systematic review identified 17 trials using various skin substitutes (eg, Graftjacket, Hyalograft, Dermagraft, Apligraf, OrCel, Kaloderm) for the treatment of diabetic foot ulcers [101]. Completed closure of diabetic foot ulcers was significantly improved for skin substitutes compared with standard care (RR 1.55, 95% CI 1.30-1.85). In two trials, there were no significant differences in ulcer recurrence. Among two trials that reported the incidence of lower limb amputations, skin grafts, and substitutes were also associated with a significantly lower risk for amputation. However, the absolute risk reduction for amputation was small. Based upon four trials that directly compared products, no specific type of skin graft or skin substitute was superior to another.

The use of skin substitutes and skin grafts are shown in these case examples:

●The figure shows the management of a patient with diabetes and a chronic sinus draining from the plantar aspect of the foot that was present for over nine months. Following debridement, the wound was dressed and treated with a matrix wound dressing to provide an appropriate wound bed for subsequent skin grafting (picture 1). After two weeks, the overlying silicone layer was removed, and a skin graft was placed (picture 2).

●The figure shows the management of a patient with diabetes and a foot infection (picture 3). Following incision and drainage of the ankle joint and debridement of necrotic skin, the postsurgical wound was managed with wound dressings, followed by skin grafting.

Follow-up

Frequency — The follow-up frequency should be tailored to each patient's specific needs and circumstances. However, in most instances where the wound is stable, weekly visits are common. For patients who require inpatient hospitalization, daily wound assessments are standard. In the outpatient care setting:

●For noninfected, nonischemic ulcers, initial follow-up can be weekly or biweekly, then less frequently as healing progresses.

●For infected or ischemic ulcers, more frequent follow-up (two to three times per week) is needed initially to monitor for complications and assess response to treatment or to determine when transition to an acute care setting may be necessary [126].

●Heel ulcers often require more frequent follow-ups due to their slower healing rate and increased risk of complications [127].

●Digital ulcers require close monitoring due to the risk of infection and ischemia spreading to the rest of the foot. Primary care clinician and outpatient wound care team follow-up may be weekly or biweekly initially, then less frequent as the ulcer heals.

The patient's overall health and social situation, including poor glycemic control, multiple comorbidities, or limited mobility, may indicate the need for more frequent follow-up. Communication is important among the team members to ensure continuity of care and coordinate follow-up appointments [128]. Patients should be empowered to monitor their ulcers at home and report any changes (increased pain, redness, drainage) promptly.

Reducing the risk of recurrence — The weight-bearing nature of the foot increases the risk for wound recurrence after closure/coverage, particularly when a skin graft is used since these are insensate. The wound care plan should address durability and the demands of ambulation. The patient will also require long-term use of a custom shoe with an accommodative orthotic. Bracing with an ankle-foot orthosis may also be necessary to reduce the risk of recurrence [129]. (See "Management of diabetic foot ulcers".)

Special attention should also be given to identifying and correcting any underlying bony deformities or biomechanical instability causing areas of focal pressure or shear stress as the source of delayed wound healing. Correction may require adjunctive surgery (eg, Achilles tendon lengthening to offload the plantar forefoot, free or pedicled flap to provide tissue durability) or more complex bony reconstruction/realignment. (See "Management of diabetic foot ulcers".)

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Diabetes mellitus in adults" and "Society guideline links: Open wound management".)

SUMMARY AND RECOMMENDATIONS

●Approach based on wound classification – Diabetic foot ulcers should be classified upon initial presentation, and with each follow-up visit, a standardized system should be used to document the examination and treatment plan and to follow the progress of healing. We use the wound, ischemia, and foot infection (WIfI) system (figure 1 and table 1), which classifies the affected limb based on the presence and severity of the wound, infection, and ischemia. WIfI limb staging is predictive of the one-year amputation risk and can also help set realistic expectations for healing. (See 'Approach by wound classification' above.)

•Noninfected, nonischemic wounds – Patients with uncomplicated low-grade superficial diabetic foot wounds (no infection, no ischemia; WIfI limb stage 1) have a low risk for complications and can often be managed in the office setting (eg, primary care, wound clinic). Consider referral to a wound care specialist or vascular surgeon for any wound that does not show signs of improvement within two to four weeks or becomes complicated (eg, signs of infection or ischemia, deeper involvement).

•Ischemic, noninfected wounds – Diabetic foot wounds that are ischemic (toe pressures reduced [TcPO₂] <60 mmHg) but not infected (WIfI limb stage 2 through 4) should be kept dry. Debridement is limited to avoid worsening ischemia or introducing infection. Early referral to a vascular specialist is appropriate to evaluate for possible revascularization. Vascular evaluation can usually be undertaken in the outpatient setting. With severe ischemia (TcPO₂ <40 mmHg), wound healing cannot be expected until revascularization has occurred.

•Infected, nonischemic wounds – Wound infection is treated aggressively. Inpatient hospitalization is often necessary for more severe or extensive diabetic foot infections (WIfI limb stage 3 or 4) to initiate intravenous antibiotics and perform operative debridement.

•Infected, ischemic wounds – Infected and ischemic (TcPO₂ <60 mmHg) wounds often present with higher grades of foot infection (WIfI limb stage 3 or 4) and are at high risk for amputation. The combination of infection and ischemia often indicates a need for hospitalization to initiate intravenous antibiotics and expedite vascular evaluation for possible revascularization.

●Wound care – Appropriate local wound care (debridement and dressings) tailored to the characteristics of the wound is essential. For any diabetic foot ulcer related to pressure (see 'Anatomic location of the ulcer' above), mechanical offloading should be implemented to relieve pressure at the ulcer site and promote healing. (See "Management of diabetic foot ulcers".)

•Debridement – As with any wound, diabetic foot ulcers should be debrided to remove infected or necrotic tissue, with a preference for sharp surgical debridement when possible. If a clinician with clinical expertise in sharp debridement is not available, we suggest autolytic debridement with hydrogels. Alternatively, the patient can be referred to a facility with appropriate expertise in the management of diabetic wounds. (See 'Debridement' above.)

•Dressings – After debridement, ulcers should be kept clean and moist but free of excess fluids (table 3). Dressings are selected based on the ulcer or postsurgical wound characteristics, such as the extent of exudate, desiccation, or necrotic tissue (table 2). Some dressings simply provide protection, whereas others promote wound hydration or prevent excessive moisture. Wet-to-dry saline dressings are frequently used but can remove both nonviable and viable tissue and may result in a dry wound. Other dressings are impregnated with antimicrobial agents to prevent infection and enhance ulcer healing.

-For diabetic foot ulcers that are slow to heal with standard treatment or have not responded within 30 days, negative pressure wound therapy (NPWT) is an alternative option, provided any infection is controlled and ischemia has been excluded or is not completely correctable. (See 'Role of negative pressure wound therapy' above.)

-To manage extensive open wounds following debridement for infection or necrosis, or partial foot amputation, we recommend NPWT (Grade 1B). Following surgery, NPWT increases the percentage of patients with healed wounds and decreases the length of hospitalization, complications, and costs. All necrotic tissue or infected bone (osteomyelitis) must first be removed from the wound prior to using NPWT. (See 'Dressings and other treatments' above and 'Role of negative pressure wound therapy' above.)

•Use of growth factors – For wounds that are slow to heal or have not responded despite standard treatment within 30 days, we suggest a trial of a topical growth factor prior to the use of other adjuncts, provided any infection is controlled and ischemia has been excluded or is not completely correctable (Grade 2C). High cost often limits the use of topical growth factors.

●Reducing the risk of recurrence – Once a patient has healed an ulcer, they remain at very high risk for re-ulceration. Proper foot care and measures to limit excess pressure (ie, mechanical offloading) are important. Therefore, people with healed ulcers should not be considered cured but rather "in remission," a term that better communicates the lifetime of visits (often bimonthly) needed to reduce the risk of recurrence. The goals of long-term surveillance and care are to maximize ulcer-free, hospital-free, and activity-rich days. (See 'Reducing the risk of recurrence' above and "Management of diabetic foot ulcers".)