Diabetic foot complications are a major source of morbidity and disability among people with diabetes. Peripheral neuropathy, peripheral arterial disease, foot deformities, and other diabetes-related complications can increase the risk of skin breakdown and impair the body's ability to heal once an ulcer develops. Diabetic foot ulcers may become infected, progress to deeper tissue involvement or osteomyelitis, and in severe cases contribute to lower-extremity amputation. Importantly, many diabetic foot ulcers are preventable through early identification of risk factors, appropriate foot surveillance, patient education, pressure reduction and offloading, and timely management of wounds and infections.

Diabetic foot ulcers are a common and potentially serious complication of diabetes, arising from a combination of neurologic, vascular, and musculoskeletal abnormalities that impair the foot's ability to withstand and recover from repetitive stress or injury. Several factors substantially increase the risk of ulceration, particularly peripheral neuropathy, peripheral vascular disease, and Charcot foot. Less common factors include peripheral arterial disease, foot deformity, history of foot ulcerations, past amputation, poor vision, renal disease, and suboptimal glucose control [16]. Peripheral vascular disease can reduce tissue perfusion and impair wound healing, while Charcot foot causes progressive bone and joint destruction, deformity, and abnormal pressure distribution that can increase the risk of skin breakdown. Recognizing these risk factors is essential for identifying patients who require closer surveillance and implementing preventive interventions before an ulcer develops.

Diabetic foot ulcers are a common and potentially serious complication of diabetes, arising from a combination of neurologic, vascular, and musculoskeletal abnormalities that impair the foot's ability to withstand and recover from repetitive stress or injury. Several factors substantially increase the risk of ulceration, particularly peripheral neuropathy, peripheral vascular disease, and Charcot foot. Less common factors include peripheral arterial disease, foot deformity, history of foot ulcerations, past amputation, poor vision, renal disease, and suboptimal glucose control [16]. Peripheral vascular disease can reduce tissue perfusion and impair wound healing, while Charcot foot causes progressive bone and joint destruction, deformity, and abnormal pressure distribution that can increase the risk of skin breakdown. Recognizing these risk factors is essential for identifying patients who require closer surveillance and implementing preventive interventions before an ulcer develops.

Neuropathy is one of the most common causes of diabetic foot ulceration [16]. It can diminish protective sensation and alter foot biomechanics, allowing repetitive trauma or minor injuries to go unnoticed. Patients with diabetes and neuropathy have a sevenfold increase risk of developing foot wounds compared with people with diabetes who are free from neuropathy [16]. More than 60% of those diagnosed with diabetes will go on to develop neuropathy [17]. It is especially prevalent in those who have had diabetes for more than 10 years and have poorly controlled blood glucose levels [18].

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.

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).

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].

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].

Neuropathy and PAD can produce different, but overlapping, foot findings. Autonomic neuropathy may cause reduced sweating and dry, cracked skin, whereas peripheral arterial disease may produce cool skin, diminished pulses, pallor with elevation, and dependent rubor. Because these conditions frequently coexist, a comprehensive diabetic foot examination should assess both neurologic and vascular status.

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.

The most important member of the team is the patient, and the goal of care is to empower them to take charge of their own foot health. Family members and the patient's support system will also play an important role, especially if the patient is unable to perform routine foot care and daily foot inspections.

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].

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].

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

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

The two most important components in healing diabetic foot ulcers are adequate circulation and pressure relief. The first and possibly most important approach in the treatment of diabetic foot ulcers is off-loading [22,39]. This results in pressure being dispersed over a wider area of the foot and reduces the burden of mechanical stress on the wound, which is essential for healing [16].

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.

The IWGDF/IDSA classification categorizes infection according to its severity [31]. A mild infection involves at least two local signs of inflammation with erythema extending no more than 2 cm beyond the wound margin and no systemic manifestations. A moderate infection involves deeper tissues and/or erythema extending 2 cm or more beyond the wound margin, without systemic inflammatory response. Severe infection is characterized by local infection accompanied by systemic manifestations of infection.

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.

Re-occurrence of diabetic foot ulcers is a major problem, with approximately 40% of patients who have successfully healed a diabetic foot ulcer experience another ulcer within one year, increasing to approximately 65% within three years [16,44]. The use of custom-made footwear appears to play a protective role in preventing additional ulceration [16]. After a diabetic foot ulcer has healed, the patient should not go back to wearing the shoes (or similar shoes) that they were wearing at the time the ulcer developed. Regular shoes are not made to accommodate irregularities in foot shape and at-risk pressure points.