#30150: Diabetic Foot Ulcer Prevention and Care

Diabetic neuropathy encompasses a group of nerve disorders caused by chronic hyperglycemia and other metabolic and vascular factors associated with diabetes. Although distal symmetric polyneuropathy (DSPN) is the most common form and is particularly important in the development of diabetic foot complications, diabetes can affect multiple types of nerves. The clinical presentation varies according to the nerves involved and may include sensory loss, pain, weakness, autonomic dysfunction, or focal neurologic deficits.

In more severe forms, neuropathy can cause weakness and stiffness, leading to problems with balance and ambulation [19]. Diabetic neuropathy will eventually result in a loss of protective sensation (LOPS), which leaves the foot vulnerable to injury and ulceration [16]. Unfortunately, mild neuropathy is missed in an estimated 60% of cases, and severe forms are not detected in about 30% of patients [19]. This underdiagnosis can result in the condition progressing unchecked, leading to irreversible nerve damage [19].

Focal and Multifocal Neuropathies

Diabetes can also cause focal or multifocal nerve disorders. Diabetic amyotrophy (diabetic lumbosacral radiculoplexus neuropathy) typically presents with acute or subacute pain and weakness involving the hip, thigh, or buttock and may be followed by muscle wasting. Entrapment neuropathies, such as carpal tunnel syndrome, are also more common in people with diabetes. Less commonly, diabetes may cause isolated cranial or peripheral nerve palsies. The usual pattern for multifocal or diffuse neuropathy is that it begins in the toes, progressing up the leg; it what has been described as a stocking pattern of sensory loss [21].

Motor Neuropathy

Motor neuropathy causes problems with ambulation, and over an extended period of time, patients with motor neuropathy can lose up to half of the muscle volume of their feet [18]. Common signs and symptoms include progressive muscle weakness, visible muscle atrophy, loss of deep tendon reflexes (e.g., Achilles reflex), poor balance, foot drop, and foot deformities (e.g., claw toes).

Autonomic Neuropathy

Diabetic autonomic neuropathy affects nerves that regulate involuntary functions, including cardiovascular, gastrointestinal, genitourinary, and sudomotor functions. In the feet, autonomic dysfunction can reduce sweating and lead to dry, cracked skin, which increases susceptibility to skin breakdown and infection. Autonomic neuropathy may therefore contribute indirectly to diabetic foot ulcer development, particularly when combined with sensory neuropathy [18].

Distal Symmetric Polyneuropathy (DSPN)

Distal symmetric polyneuropathy (DSPN) is the most common diabetic neuropathy and typically develops gradually in a length-dependent, symmetric pattern, initially affecting the toes and feet before progressing proximally. Patients may experience numbness, tingling, burning, or electric or shooting pain. However, some patients have predominantly sensory loss without pain and may be unaware of injuries to their feet [22,23].

As the neuropathy progresses, loss of protective sensation becomes particularly important in relation to diabetic foot ulcers. Patients may not perceive pressure, friction, thermal injury, or minor trauma, allowing repetitive injury to continue without recognition. Motor involvement can also contribute to muscle weakness and foot deformities, altering pressure distribution across the foot and further increasing ulcer risk [23].

The diagnosis of diabetic neuropathy is primarily clinical, based on the patient's history, symptoms, and neurologic examination. Because diabetic neuropathy can present in different forms and may be asymptomatic, routine assessment is important, particularly for individuals at increased risk for diabetic foot complications. The evaluation should also consider other potential causes of neuropathy, because not all peripheral nerve dysfunction in a person with diabetes is attributable to diabetes.

The assessment begins with a detailed history of neurologic symptoms and their progression. Patients should be asked about numbness, tingling, burning, electric or shooting pain, sensitivity to touch, weakness, balance problems, and changes in gait. Particular attention should be given to symptoms involving the feet and lower extremities and whether they are symmetric and progressively extend from the toes proximally, a pattern characteristic of DSPN. A history of foot injuries, falls, burns, blisters, or wounds that the patient did not initially notice can provide an important indication of loss of protective sensation.

In addition, sensory, motor, and reflex function should be assessed. In patients with suspected DSPN, examination commonly includes assessment of [24]:

Loss of protective sensation is particularly important when evaluating the risk of diabetic foot ulceration. The 10-g monofilament test is commonly used to identify patients with clinically significant sensory loss. However, monofilament testing should generally be performed in combination with another assessment of sensory function, rather than being used as the sole diagnostic test [24].

Certain findings should prompt consideration of diagnoses other than typical diabetic DSPN. These include marked asymmetry, rapid progression, prominent motor weakness, acute onset, an unusual distribution of symptoms, or significant systemic features. In such cases, additional neurologic evaluation and diagnostic testing may be warranted.

Treatment of diabetic neuropathy focuses on preventing or slowing further nerve damage, managing symptoms, and addressing complications that may increase the risk of injury, particularly to the feet. Optimal glycemic management is an important component of treatment. Evidence from the Diabetes Control and Complications Trial (DCCT) demonstrated that intensive insulin therapy reduced the risk of developing diabetic neuropathy and slowed its progression in people with type 1 diabetes [21]. However, glycemic optimization does not reliably reverse established neuropathy, and treatment should therefore also address neuropathic symptoms and modifiable risk factors.

Correctly Fitting Shoes

It is estimated that up to 80% of diabetic foot ulcers are related to pressure from poorly fitting footwear [16]. As such, correctly fitting shoes are a mainstay in the prevention of foot injury for patients with diabetes and peripheral neuropathy [22]. Shoes should fit comfortably and should be correctly sized. Unwittingly, many individuals with peripheral neuropathy wear shoes that are too tight, because the reduced sensory function requires that footwear squeeze the feet before it is felt. Shoes should have an ample toe box that does not press down on the toes or squeeze them together from side to side [18].

According to the American Diabetes Association, the use of specialized therapeutic footwear is recommended for people with diabetes at high risk for ulceration, including those with loss of protective sensation, foot deformities, ulcers, callous formation, poor peripheral circulation, or history of amputation.

(https://diabetesjournals.org/care/article/49/Supplement_1/S261/163919/12-Retinopathy-Neuropathy-and-Foot-Care-Standards Last Accessed: August 21, 2026)

Strength of Recommendation: B (Evidence from randomized controlled trials with an identified flaw that may limit validity of the results Supportive evidence from well-conducted cohort studies.)

Shoe inserts are frequently prescribed to counteract shear and friction caused by the foot sliding against the sole of the shoe [22]. Reducing pressure on the plantar surfaces of the feet and under the metatarsal heads is of prime importance [16].

When deciding on appropriate footwear, the patient's lifestyle (e.g., occupation, sports activities, general environment/climate) should be taken into consideration. If shoes are not practical, they will not be worn, no matter how much benefit they provide. Often overlooked, it is also important to consider the cosmetic appeal/acceptability of the footwear. Patients may refuse to wear anything that draws attention to the need for adaptive footwear. It is important not to lose sight of the therapeutic value of feeling good about one's appearance and the relevance it has in the lives of those coping with a chronic disease.

Alcohol Use and Smoking

Alcohol and tobacco use are important modifiable factors in the management of diabetic neuropathy. Chronic heavy alcohol consumption can independently cause peripheral neuropathy, worsen glycemic control, and contribute to nutritional deficiencies that may further impair nerve function. Smoking promotes vascular dysfunction and is strongly associated with peripheral arterial disease, impaired wound healing, and an increased risk of diabetic foot complications. Patients with diabetic neuropathy should be counseled to avoid or substantially reduce heavy alcohol use and to stop smoking as part of a comprehensive treatment plan that includes glycemic management, symptom control, and preventive foot care [14,23].

Pain Management

For patients with painful diabetic neuropathy, pharmacologic therapy can reduce pain and improve quality of life, although available treatments generally do not restore normal nerve function. Recommended options include pregabalin, duloxetine, or gabapentin, while other medications, including certain tricyclic antidepressants, may be considered in selected patients. Treatment should be individualized based on symptom severity, comorbidities, potential adverse effects, drug interactions, and patient preferences. Opioids are generally not recommended for the routine treatment of painful diabetic neuropathy because of their limited long-term benefit and risks associated with chronic use [21].

Pulsed electromagnetic field (PEMF) therapy is a noninvasive modality that has been investigated as an adjunctive treatment for painful diabetic peripheral neuropathy. Some clinical trials have reported reductions in neuropathic pain, including a randomized, sham-controlled trial demonstrating approximately a 30% reduction in pain among patients receiving active treatment [14]. However, evidence remains limited, and systematic reviews have not established consistent benefits across peripheral neuropathies [14].

When tissue perfusion is inadequate, the foot may become cool, pale with elevation, or exhibit dependent rubor, and wounds may heal poorly. However, PAD may be asymptomatic, and the absence of classic intermittent claudication does not exclude the disease.

Although claudication and resting pain are classic symptoms of peripheral arterial disease, they may be missing in the patient with diabetes who has sensory neuropathy [16]. If these symptoms are present, they are indicative of the need for aggressive re-vascularization [16]. However, in more than 60% of lower extremity amputations there is no attempt at re-vascularization prior to the amputation [26].

Individuals with diabetes and PAD are at much higher risk of developing serious foot ulcerations and infections [21]. If both neuropathy, and PAD are present in the patient with diabetes then the risk of ulceration, infection and amputation are even higher [21]. Diabetic foot ulcers—like all wounds—require oxygen and leukocytes to heal. In the presence of poor circulation there is impaired delivery of oxygen and leukocytes to the wound [25]. This in turn, not only prevents healing, it also promotes the growth of anaerobic organisms, which are difficult to eradicate from the wound and increases the likelihood of amputation [25].

If ischemia is present on noninvasive testing, the patient will need an arteriography study done by endovascular surgeon or by an interventional radiologist [16]. During this procedure, detailed views of the circulation to the foot can be obtained [16]. Compromised circulation can be corrected by a revascularization procedure, and studies demonstrated that these procedures have good success rate among patients with diabetes [16].

One cause of circulatory compromise is blockage in an artery. Angioplasty accompanied by stent placement may be warranted to ensure that the artery remains open [18].

The early symptoms of a Charcot foot are not always easily detected [16]. The condition may start with mild swelling, erythema, and an elevation of the skin temperature in the affected foot and ankle [16]. Charcot foot can also have a gradual onset, and it is a condition that must be watched closely for in all people with diabetes. Left untreated, it can cause permanent foot deformities, which in turn leads to an abnormal distribution of pressure on the plantar surface of the foot [30].

An acute Charcot foot can be mistaken for cellulitis, acute gouty arthritis, or thrombophlebitis [16,29]. A hot, red, swollen foot in a person with diabetes and peripheral neuropathy should be presumed to have acute Charcot arthropathy until it has been appropriately evaluated. The absence of significant pain does not exclude a serious underlying process. Persistent erythema, systemic symptoms, an open wound, elevated inflammatory markers, or other evidence of infection should increase concern for cellulitis or osteomyelitis. If swelling and redness abates with elevation of the affected extremity, Charcot foot is more likely than infection.

A patient with diabetes and a red, hot foot should have x-ray studies ordered to evaluate for possible changes in the underlying structures [21]. A positive Charcot deformity can be seen on x-ray as multiple fractures of the small bones of the foot [21].

Early recognition and treatment of Charcot arthropathy is the key to minimizing foot deformity, and disfiguration [21]. Treatment of this condition aims at decreasing or, if possible, eliminating weight bearing on the affected foot. Careful attention to providing proper footwear is essential because of the altered shape of the foot [21]. Put simply, shoe shape should match foot shape.

In some instances, a total contact cast may be applied to the affected extremity to achieve complete non-weight bearing [28]. This is a hard cast that will incorporate the patient's toes and end just below the patient's knee.

The feet should be carefully examined for deformities (i.e., any alterations in the normal shape of the foot) and callous formation [18,21]. Charcot foot can usually be identified by its shape, frequently with medial protrusion and a flat foot. Other deformities to look for are hammertoes (i.e., toes pulled out of their normal positions, usually due to motor neuropathy), claw toes, and bunions [32]. Corns are often noted developing over prominent toe joints; however, they can also occur between the toes (referred to as soft corns or kissing corns). These corns are the result of the bones in adjacent toes rubbing against each other [18]. Shoes that cramp toes tightly together can aggravate corns and can lead to skin breakdown, ulcer formation, and subsequent infection [18].

Skin inspection of both feet should include noting skin color, particularly unilateral redness, may indicate the beginning of Charcot arthropathy. Skin thickness, dryness, and cracking should also be noted [16].

It is important to remember to check between the patient's toes and under the metatarsal heads [18]. Patients with diabetes and peripheral neuropathy often lose the protective fat pads over the boney prominences in their feet [18]. They are also at increased risk for fungal infections, and tinea pedis (athlete's foot) is a common problem. Fissures and cracks in the interdigital spaces are another common problem and should be carefully checked [21].

The importance of keeping the spaces between the toes clean and dry should be stressed to the patient. If a build-up of moisture in these areas is a concern for the patient, small strips of lamb's wool may be placed between the toes and change daily, although pressure and shear should be cautioned against. Because fungal infections are contagious, advise patients not to share nail clippers with other members of their household [18].

Patients with diabetes frequently have problems with ingrown toenails. In the absence of peripheral neuropathy, this is a painful condition, but a lack of pain sensation can result in the condition becoming more severe before treatment is sought and infection is a concern. Patients with diabetes and an ingrown toenail should see a podiatrist to correct the problem rather than attempting to address it themselves [30].

Calluses should be checked for hemorrhaging [16]. Calluses and corns should be carefully paired back or removed to reduce pressure on the underlying tissue. However, the patient should be warned not to attempt to do this at home. Instead, callus and corn removal should be done by a podiatrist during a diabetic foot examination. The podiatrist may also recommend that the patient use a silicone rubber splint to provide cushioning underneath cramped toe joints as a preventive measure.

Checking for loss of protective sensation is a cornerstone of the diabetic foot exam. The most common tests used in this assessment are [16]:

At least two of these tests should be routinely done during a diabetic foot screening [16].

Monofilament Testing

The American Diabetes Association recommends that all people with diabetes should have annual 10-g monofilament testing to identify feet at risk for ulceration and amputation.

(https://diabetesjournals.org/care/article/49/Supplement_1/S261/163919/12-Retinopathy-Neuropathy-and-Foot-Care-Standards Last Accessed: August 21, 2026)

Strength of Recommendation: B (Evidence from randomized controlled trials with an identified flaw that may limit validity of the results Supportive evidence from well-conducted cohort studies.)

The 10-g Semmes-Weinstein monofilament test is a widely recommended clinical tool for detecting loss of protective sensation and identifying patients at increased risk for diabetic foot ulceration [24]. Studies have proven that loss of pressure sensation using a 10-gauge monofilament is indicative of high risk for ulcer development [16]. It is a non-invasive test, simple to learn, and easily implemented.

To begin, the patient removes their shoes and socks and is seated in a comfortable position, with their legs and feet extended. The test is explained to the patient, and the monofilament is applied to the back of their hand or arm, so that they are aware of how the sensation feels. The patient is then asked to close their eyes, and the examiner is careful not to touch the patient's foot with his/her hand. The patient is asked to say "yes" whenever they feel the pressure of the monofilament on their foot.

In general, ten sites on the patient's foot are tested [21]:

During the test, enough force is applied to the monofilament to cause the wire to bend into a c-shape [21]. The normal response time is less than three seconds; greater than three seconds is considered a delayed response indicating some degree of neuropathy. A negative response (i.e., failure to sense the filament) at any of the test sites identifies loss of protective sensation in that area and suggests increased risk for ulceration [32].

128-Hz Tuning Fork Test

Another frequently done test to evaluation sensation is the 128-Hz tuning fork. This simple and inexpensive test checks for vibratory sensation, and it is done over the tips of the hallux [16]. The result is considered abnormal if the patient is unaware of the vibratory stimulation from the tuning fork while the person performing the test can detect it [24]. This test assesses early sensory loss, but it does not evaluate the degree of sensory loss present [24].

As discussed, peripheral vascular disease is a major contributory factor to diabetic foot ulcers and can contribute to impaired wound healing. Adequate circulation to the feet should be assessed during every diabetic foot examination [18].

During the examination, the femoral, popliteal, and dorsalis pedis and posterior tibial artery pulses should be palpated [16]. Normally, clearly palpable posterior tibialis and dorsalis pedal pulses are a positive indication of adequate circulation [16].

In all patients where foot pulses are not palpable, non-invasive testing should be ordered to further evaluate circulation [16]. An ankle-brachial index is an indirect measurement of arterial circulation to the feet. It is often recommended as a baseline test for people with diabetes older than 50 years of age [18]. Normal results are in the range of 0.9 to 1.1 [31]. A frequent occurrence in patients with diabetes are noncompressible arteries and ankle-brachial index readings of 1.2 and higher [31].

Diabetic foot education should begin with the following instructions to patients [18,34,35]:

Advise the patient to make these simple steps part of their daily routine, similar to showering or brushing their teeth.

Off–loading can be achieved by applying either a removable or nonremovable device to the extremity [39]. Frequently used methods to off-load the diabetic foot are [21]:

Reducing pressure and shear forces at the ulcer site allows tissue to heal and helps prevent continued trauma to the wound. There is some evidence that off-loading with nonremovable devices achieves a higher level of healing than with removable devices [39]. Current guidelines recommend a nonremovable knee-high offloading device as the first-choice treatment for a neuropathic plantar forefoot or midfoot ulcer in a person with diabetes. A total contact cast (TCC) or a nonremovable knee-high walker may be used, with the choice based on available resources, clinician expertise, patient-specific factors, and acceptability.

Total Contact Casting

A TCC is a customized, minimally padded cast that closely conforms to the contours of the foot and lower leg. By redistributing plantar pressure and limiting movement of the foot, it substantially reduces mechanical stress on the ulcer. TCC has been extensively studied and remains an effective method for promoting healing of appropriately selected diabetic plantar foot ulcers. Importantly, the effectiveness of a TCC depends on appropriate patient selection, skilled application, and close monitoring for cast-related complications [16,40].

Patients receiving a TCC require regular follow-up to assess the ulcer, surrounding skin, edema, and overall tolerance of the cast. The cast may need to be changed or reapplied as edema decreases or if complications develop. Close monitoring is particularly important because patients with peripheral neuropathy may not recognize pressure-related injury or other complications.

Nonremovable Knee-High Walkers and Instant Total Contact Casts

A nonremovable knee-high walker provides another evidence-supported option for offloading a neuropathic plantar ulcer. A removable cast walker can also be converted into an instant total contact cast (iTCC) by securing the device so that the patient cannot readily remove it. This approach combines the pressure redistribution of a knee-high walker with the adherence advantage of a nonremovable device [41].

One important advantage of nonremovable devices is that they enforce adherence. With a removable device, patients may remove the device for convenience or during ambulation, thereby reducing the amount of time the ulcer is actually offloaded. Current evidence and guidelines therefore favor nonremovable knee-high devices over removable devices when they are tolerated and not contraindicated [16,41].

Removable Cast Walkers

When a nonremovable knee-high device is contraindicated or not tolerated, a removable knee-high or ankle-high offloading device may be used as a second-choice approach. Patients should be instructed to wear the device during all weight-bearing activities, because inconsistent use can substantially reduce its effectiveness [16].

Removable devices offer practical advantages, including the ability to remove them for wound care, bathing, and examination. However, these advantages must be balanced against the potential for inconsistent adherence.

Other Offloading Approaches

When a nonremovable or removable knee-high device cannot be used or is unavailable, other approaches may be considered depending on the location and characteristics of the ulcer. These may include appropriately fitted footwear combined with felted foam or other pressure-relieving interventions. For selected ulcers that do not heal with conservative offloading, surgical offloading procedures may also be considered.

Wound healing typically proceeds in well-defined stages; however, patients with diabetic foot ulcers are at increased risk for developing chronic wounds, which stall in the inflammatory phase of wound healing and are unable to progress any further [16]. Growth factors are necessary component of wound healing, and research findings show that patients with diabetes and ulcers produce fewer growth factors than those without diabetes.

An unexplained increase in blood glucose may sometimes accompany infection and can be an important clinical clue in a person with diabetes [25]. Infection and other acute illnesses can cause hyperglycemia through increased insulin resistance and the release of counter-regulatory hormones. However, elevated blood glucose is nonspecific and should not be used alone to diagnose a diabetic foot infection. Because peripheral neuropathy may reduce pain and other inflammatory symptoms, clinicians should carefully examine the foot for local signs of infection, including new or increasing swelling, erythema, warmth, tenderness, induration, or purulent drainage [16].

In a person with suspected soft tissue diabetic foot infection, the International Working Group on the Diabetic Foot (IWGDF) and the Infectious Diseases Society of America (IDSA) recommends considering a sample for culture to determine the causative micro-organisms, preferably by aseptically collecting a tissue specimen (by curettage or biopsy) from the wound.

(https://www.idsociety.org/practice-guideline/diabetic-foot-infections/ Last Accessed: August 21, 2026)

Strength of Recommendation/Level of Evidence: Conditional/moderate

Deeper infections, defined as those down to and including the bone, pose a serious risk of limb amputation, and hospitalization is required for these patients, with immediate surgical debridement, drainage of the wound, and the commencement of IV antibiotics [25]. To determine the causative organism(s) in diabetic wounds, deep tissue cultures should be performed, rather than swabbing the wound surface [25]. Tissue cultures should be obtained after debridement has been done and tested for both aerobic and anaerobic organisms [31]. Any individual who presents with a diabetic foot ulcer that extends down to bone should be evaluated immediately for possible osteomyelitis.

However, a positive wound culture alone does not establish infection because diabetic foot ulcers are frequently colonized by bacteria. Culture results should be interpreted in conjunction with the clinical findings and used to help guide antimicrobial therapy.

Management of a diabetic foot infection should be based on the clinical severity, depth and extent of infection, presence of ischemia or necrosis, suspected or confirmed osteomyelitis, previous antimicrobial exposure, and patient-specific factors. Depending on the severity and complexity of the infection, management may involve primary care, podiatry, wound care, infectious disease, vascular surgery, and other surgical specialists [33].

Antibiotics should not be used to treat a clinically uninfected diabetic foot ulcer or simply to promote wound healing [31]. Instead, antibiotic therapy should be reserved for wounds with clinical evidence of infection.

Mild infections can often be managed with oral antibiotics on an outpatient basis, provided the patient is clinically stable and there are no factors requiring hospitalization or surgical management [31]. Antibiotic selection should be based on the severity and likely pathogens, previous microbiologic results, recent antibiotic exposure, allergies, renal function, local resistance patterns, and other patient-specific considerations. Empiric treatment of a mild infection in a patient who has not recently received antibiotics generally does not need to provide broad-spectrum coverage for multiple resistant or unusual organisms.

For moderate or severe infections, deeper infection, extensive tissue involvement, significant ischemia, or suspected osteomyelitis, more extensive evaluation and treatment may be necessary. As noted, hospitalization and intravenous antibiotics may be appropriate in selected patients.

Osteomyelitis should be considered when infection is deep, prolonged, recurrent, or associated with exposed or palpable bone. Initial evaluation may include a probe-to-bone test, plain radiographs, and inflammatory markers such as ESR and CRP. MRI may be appropriate when the diagnosis remains uncertain after clinical examination, plain radiographs, and laboratory testing. When osteomyelitis is suspected, obtaining an appropriately collected bone specimen for culture may be necessary to guide treatment.

Some diabetic foot infections require surgical as well as antimicrobial treatment. Surgical intervention may be necessary to drain an abscess, remove necrotic or infected tissue, excise infected bone, or control a rapidly progressing infection. Urgent surgical consultation should be obtained for conditions such as necrotizing infection, deep abscess, compartment syndrome, extensive gangrene, or severe ischemia [31]. Early surgical intervention may also be appropriate for selected moderate or severe infections to remove infected and necrotic tissue and control the source of infection.

The extent of surgery depends on the location and severity of infection and the amount of viable tissue that can be preserved. Procedures may range from incision and drainage or limited debridement to removal of infected bone or partial foot amputation. Major lower-extremity amputation is generally reserved for situations in which infection, ischemia, or extensive tissue destruction cannot be adequately controlled while preserving a functional limb.

One of the advanced modalities used in the treatment of diabetic foot ulcer is hyperbaric oxygen therapy. Because all wounds require oxygen to heal, the therapeutic value of hyperbaric oxygen therapy is to increase the amount of oxygen available to the wound bed. Hyperbaric oxygen therapy is administered in a specially designed pressurized chamber. During the treatment, the patient breathes 100% oxygen, which results in increased oxygen delivery to the wound bed. This stimulates collagen growth and the proliferation of fibroblasts [38]. Evidence supporting the use of this modality is limited, and it is generally considered an adjunctive treatment of non-healing foot ulcers.

Negative pressure wound therapy also provides beneficial therapy for wound healing, and granulation tissue formation, by removing fluid from the wound bed, decreasing edema, and stimulating small blood vessels to dilate which increases local wound circulation [14]. Current evidence suggests that negative pressure wound therapy may improve healing outcomes in certain diabetic foot wounds, particularly postoperative wounds, but its use should be individualized according to wound characteristics and patient needs.

Cellular and tissue-based products (CTPs), sometimes referred to as skin substitutes, are a heterogeneous group of advanced wound-care products that may provide structural or biologic support to selected chronic wounds. Products used in diabetic foot ulcers include cellular and acellular products derived from human or animal tissue, among other materials. Because these products differ substantially in composition, mechanism, and evidence of effectiveness, results from one product or product category should not be generalized to all CTPs [44].

CTPs should not replace the fundamental components of diabetic foot-ulcer management. Before considering an advanced wound therapy, clinicians should ensure that the wound is appropriately prepared, including adequate debridement of nonviable tissue and callus, appropriate management of infection, adequate offloading, and assessment and management of peripheral arterial disease when present.

Some CTPs have demonstrated potential benefits in clinical studies, but the evidence is heterogeneous and generally of low certainty. The IWGDF therefore recommends against routine use of cellular or acellular skin substitutes as adjunctive therapy for diabetic foot ulcers [44]. Selected products, including certain placental-derived products, may be considered when appropriate standard care has failed and the necessary expertise and resources are available.

The decision to use a CTP should be individualized according to the characteristics of the ulcer, vascular status, infection status, response to standard care, available evidence for the specific product, and applicable regulatory and reimbursement requirements.