Diabetic Foot Care

Anatomy and Physiology

The diabetic foot exhibits multiple structural and functional changes compared to a nondiabetic foot. These modifications encompass musculoskeletal, dermatologic, vascular, and neurological adaptations.

Musculoskeletal Manifestations

Musculoskeletal changes include atrophy of intrinsic musculature, limited joint mobility, alterations in foot type, and the development of ankle equinus. Limited dorsiflexion of the 1st metatarsophalangeal joint (hallux limitus) is frequently observed in patients with diabetes and is often associated with thickening of the Achilles tendon and plantar fascia. This tendon and fascia thickening contributes to increased foot rigidity, greater pes planus, and potential gait instability.

Longstanding diabetes leads to disorganization of the pedal musculature and infiltration with adipose tissue. Atrophy of intrinsic foot muscles relative to extrinsic muscles contributes to deformities, including hammertoes and claw toe deformities.[5]

Hammertoes and claw toes, in combination with hallux limitus, are associated with an elevated risk of ulcer formation. Bus et al demonstrated that plantar pressures at the metatarsal heads increase significantly with the severity of toe deformities. The study further indicated a distal-to-proximal load transfer in affected toes, potentially exacerbated by displacement of the distal fat pad.[6]

Ankle equinus, defined as dorsiflexion less than 5°, is prevalent in patients with diabetes. Searle et al reported that this limitation correlates with increased forefoot pressure and heightened risk of tissue breakdown, both during barefoot ambulation and while wearing shoes.[7]

Dermatologic Changes

Dermatologic integrity is a critical function of human skin. However, chronic diabetes induces multiple alterations that compromise this protective barrier. Autonomic dysfunction associated with diabetes reduces perspiration in the foot, predisposing to fissuring and xerosis.[8]

Repetitive mechanical stress and localized pressure, combined with neuropathy, promote inflammation and ulcer formation. Plantar skin thickness is reduced in patients with type 2 diabetes and neuropathy compared to patients with diabetes without neuropathy, further increasing the risk of ulceration (see Image. Anatomical Model of a Diabetic Foot).[9] Perilesional tissue remains vulnerable to rapid breakdown and recurrent ulceration even after healing.[10]

Vascular Abnormalities

Diabetes also impairs lower extremity perfusion, contributing to delayed wound healing and increased susceptibility to tissue injury. Three primary arteries and their branches perfuse the 6 angiosomes of the foot and ankle. The posterior tibial artery, a branch of the popliteal artery, supplies the plantar surface of the foot. The fibular artery arises from the posterior tibial artery and perfuses the anterolateral ankle and rearfoot. The anterior tibial artery originates from the popliteal artery and continues distally as the dorsalis pedis artery, supplying the anterior ankle and dorsal foot.[11]

Individuals with diabetes are at increased risk of peripheral arterial disease (PAD), characterized by atherosclerotic obstruction of arteries supplying the lower extremities. Over 50% of affected individuals remain asymptomatic. However, some experience intermittent claudication—exercise-induced lower extremity pain relieved by rest—or rest pain, and in severe cases, tissue loss and gangrene.

Neurological Alterations 

The foot receives innervation from 5 principal nerves—tibial, superficial fibular, deep fibular, sural, and saphenous—and their branches. The tibial nerve, a branch of the sciatic nerve, divides into the medial and lateral plantar nerves, which further give rise to the digital nerves. The tibial nerve provides motor innervation to the posterior compartment muscles of the lower leg and sensory innervation to the plantar foot and heel. The superficial fibular nerve originates from the common fibular nerve and branches into the medial and intermediate dorsal cutaneous nerves, innervating the fibularis longus and brevis muscles and providing sensory input to the anterior lower leg and dorsal foot and toes, excluding the 1st webspace.

The deep fibular nerve, also a branch of the common fibular nerve, supplies motor fibers to the anterior compartment muscles and sensory fibers to the 1st webspace. The sural nerve arises from contributions of the tibial and common fibular nerves and provides sensory innervation to the posterolateral lower leg and foot. The saphenous nerve, a branch of the femoral nerve, supplies sensory innervation to the medial distal leg, ankle, and foot.[12][13]

Diabetic neuropathy is a common neurological complication of diabetes, with up to 50% of cases remaining asymptomatic.[14][15] Distal symmetrical polyneuropathy is the most prevalent form and may involve sensory, motor, or mixed nerve fiber dysfunction. Large fiber neuropathy (Aα/β fiber damage) produces painless paresthesia, diminished vibration sense, impaired joint position sense, reduced touch and pressure sensation, and absent or decreased ankle reflexes. Small fiber neuropathy (myelinated Aδ and unmyelinated C fiber damage) manifests as painful, burning sensations with impaired pain and temperature perception.

Peripheral neuropathy typically begins in the distal toes and progresses proximally. In advanced stages, a stocking-glove sensory distribution may develop in the upper extremities. Nocturnal worsening of symptoms is common, and motor involvement can lead to muscle weakness. The pathogenesis involves multiple mechanisms, including chronic hyperglycemia, metabolic alterations, direct axonal injury, and nerve ischemia. However, the precise contribution of each mechanism remains under investigation.[16][17]

A dreaded complication of uncontrolled diabetes and peripheral neuropathy is Charcot neuroarthropathy. This condition likely results from both neurovascular changes, including arteriovenous shunting that increases blood flow and bone resorption, and repetitive microtrauma.[18] These processes lead to joint collapse and severe pedal deformities. The tarsometatarsal joint is most commonly affected, resulting in a rocker-bottom deformity.

Patients with Charcot neuroarthropathy have a 17% annual risk of developing ulceration. The risk of lower extremity amputation in those with ulceration is 12 times higher compared to patients with Charcot neuroarthropathy without ulceration.[19] Early recognition and management improve outcomes. Clinicians should suspect Charcot neuroarthropathy when a patient with diabetes presents with a warm, erythematous, edematous foot and structural abnormalities.

Indications

All patients with diabetes should receive structured education on proper diabetic foot care. Prevention of diabetic foot complications involves identifying at-risk feet, performing daily examination and inspection, providing education to patients, families, and healthcare providers, recommending appropriate shoegear, and initiating timely treatment of preulcerative lesions. Patients at higher risk must be referred to podiatry for specialized management and ongoing monitoring. The ADA recommends the following diabetic foot screening by a qualified medical professional: 

• A thorough foot assessment must be conducted at least once per year to identify factors that increase the risk of ulceration or amputation. The evaluation should include inspection of the skin, identification of structural deformities, neurological testing, and vascular assessment, including palpation of leg and foot pulses.
• Patients with sensory deficits, previous ulceration, or a history of amputation should have their feet examined at every clinical encounter.
• Prior occurrences of ulceration, amputation, Charcot foot, revascularization procedures, cigarette use, retinopathy, and kidney disease must be documented. Current neuropathic symptoms (pain, burning, numbness) and vascular manifestations (leg fatigue, claudication) should be evaluated.
• PAD screening must be performed by assessing lower-extremity pulses, capillary refill, dependent rubor, pallor on elevation, and venous filling time.
• Patients reporting leg fatigue, claudication, rest pain relieved by dependency, or exhibiting diminished or absent pedal pulses should be referred for ankle-brachial index (ABI) with toe pressures and additional vascular evaluation as indicated.
• A podiatrist-led interprofessional team, including other relevant specialists, should manage patients with foot ulcers or high-risk feet (eg, those on dialysis, with Charcot foot, prior ulcers or amputation, or PAD).
• Patients who smoke and have prior lower-extremity complications, loss of protective sensation, structural deformities, or PAD should be given a referral to a foot care specialist for continuous preventive treatment and lifelong monitoring. These patients should also receive education on the benefits of smoking cessation and be referred for counseling as appropriate.
• All patients with diabetes, including those with sensory loss, should receive education on proper foot self-care, including daily inspection and palpation or visual examination using an unbreakable mirror to detect early problems.
• Therapeutic footwear designed for high-risk patients is recommended for individuals with diabetes who have loss of protective sensation, foot deformities, current or prior ulcers, callus formation, poor circulation, or a history of amputation.

Patient education is a mainstay of diabetic foot prevention, enabling daily self-monitoring and early recognition of complications. Ongoing instruction and reinforcement by healthcare teams can substantially reduce morbidity and preserve limb function.

Contraindications

Proper diabetic foot care has no contraindications. Preventive foot care is appropriate for every patient with diabetes and poses minimal risk.

Equipment

A basic diabetic foot examination requires minimal specialized instruments and may be performed by most qualified physicians, including primary care clinicians and podiatrists. Neurological assessment typically includes a Semmes-Weinstein monofilament test (SWMT) for evaluating neuropathy and protective sensation. A 128-Hz tuning fork may be used to assess vibratory sensation, and cotton wool can evaluate tactile sensation. Vascular examination may involve Doppler ultrasonography to assess lower-extremity blood flow.

Caregivers may encounter ulcerations during diabetic foot care. If present and requiring debridement or offloading, instruments such as scalpels, tissue nippers, and offloading padding (eg, felt, foam, or cushion pads) should be available. For advanced wound care, a comprehensive set of products should be accessible, including gauze, cleansing solutions (eg, saline, hydrogen peroxide, acetic acid), topical antimicrobials (eg, povidone-iodine, cadexomer iodine, silver, medical-grade honey), moisture-retentive dressings (eg, films, foams, alginates, hydrogels, hydrocolloids), vacuum-assisted closure devices, and bioengineered dressings.[20]

Personnel

An interprofessional approach to managing the diabetic foot and its potential complications can reduce amputation rates by up to 85%. Key team members include endocrinology, diabetology, vascular surgery, podiatry, orthotics, and prosthetics specialists, wound care nurses, and patient educators. Depending on individual medical conditions and infection status, additional specialties, such as infectious disease, nephrology, cardiology, and dermatology, may also contribute. The primary objectives of interprofessional care are to medically optimize comorbidities, prevent foot complications, and manage existing pedal pathology.

Preparation

Patients with diabetes should remove both shoes and socks prior to examination. Feet should be thoroughly cleaned and dried before any foot assessment or dressing change. Caregivers should wash their hands before and after performing a dressing change for a diabetic foot ulcer. A clean and sanitary environment should be maintained to reduce the likelihood of contamination and infection.

Technique or Treatment

The clinical diabetic foot examination comprises 4 major components: dermatological, vascular, neurological, and musculoskeletal. Each component is explained in detail below.

Dermatological Assessment

The dermatological examination of the diabetic foot should encompass a comprehensive evaluation of the entire foot and ankle, including interdigital spaces and nails. Hyperkeratotic areas should be debrided. Preulcerative and ulcerative lesions require detailed documentation of location, size, depth, wound base characteristics, periwound skin, undermining, sinus tracts, probing to bone, exudate quality, and signs of infection, such as erythema, warmth, malodor, or crepitus.

A temperature difference exceeding 3 °C to 4 °C compared to the contralateral foot may indicate infection or acute Charcot neuroarthropathy. Additionally, a prior history of ulceration, treatments, and preventive interventions should be recorded. Baseline radiographs are recommended for new ulcerations, and serial imaging should be obtained when osteomyelitis is suspected to monitor progression and guide management (see Images. Right Foot Osteomyelitis on Magnetic Resonance Imaging; Right Foot Radiograph After Partial 5th Ray Resection).[21]

Vascular Evaluation

Clinical evaluation of vascularity and PAD begins with a detailed medical history, including PAD risk factors, claudication, rest pain, and prior nonhealing wounds. Dorsalis pedis and posterior tibial artery palpation forms the baseline of diabetic foot exams, while assessment of popliteal and femoral pulses further delineates PAD severity.

A decrease in pedal pulses may prompt evaluation with Doppler ultrasound or additional noninvasive PAD testing. Doppler ultrasound assessment of pedal arteries can help characterize blood flow and detect the severity of PAD. Flow patterns are classified as follows:

• Triphasic: normal
• Biphasic: mild arterial disease
• Monophasic: PAD with some risk of limb ischemia
• Absent: severe PAD, high risk of ischemia and limb loss

Noninvasive vascular tests include ABI, segmental pressures, pulse volume recording, toe pressures, transcutaneous oxygen pressure, and treadmill functional testing. The ADA recommends a screening ABI for individuals with diabetes older than 50 years, repeating every 5 years if normal. A screening ABI should be considered in patients younger than 50 with additional PAD risk factors (eg, smoking, hypertension, hyperlipidemia, diabetes duration >10 years). Any findings suggestive of PAD warrant referral to vascular surgery.[22]

Neurological Examination

The neurological examination of the diabetic foot includes assessment of the Achilles reflex, evaluation using the SWMT, vibratory sensation testing with a 128-Hz tuning fork, and pinprick sensory testing. The Achilles reflex should be assessed on both legs using a reflex hammer. Reflex responses are graded as follows:

• 0+: absent
• 1+: decreased
• 2+: brisk, normal
• 3+: increased
• 4+: increased with clonus

The 5.07/10 g SWMT is commonly used to assess pressure and light-touch sensation. Testing should include the following 10 sites on each foot:

• Distal 1st, 3rd, and 5th toes
• Plantar 1st, 3rd, and 5th metatarsal heads
• Plantar medial and lateral arches
• Plantar heel
• Dorsal 1st interspace

The 128-Hz nongraduated standard tuning fork is used to assess vibratory sensation. An abnormal finding may indicate diabetic neuropathy if the patient cannot perceive vibration. Pinprick testing, performed with a sharp pin device, evaluates the patient’s ability to differentiate between sharp and dull stimuli.[23][24][25]

Musculoskeletal Assessment

Musculoskeletal evaluation should assess lower extremity muscle strength, foot and ankle deformities, and joint range of motion, including flexibility and rigidity, to guide treatment planning. Patients with diabetes face a greater risk of pedal deformities, such as digital contractures and ankle equinus, which elevate the risk of ulceration. For instance, a flexible ankle equinus caused by gastrocnemius tightness can increase plantar foot pressures, leading to tissue breakdown in neuropathic patients. Individuals with pedal deformities should be referred to podiatry or appropriate surgical specialists for further management, as they may benefit from corrective procedures. For example, a digital flexor tenotomy can help prevent distal toe ulceration when tissue compromise is present.[26]

Patient and family education on proper diabetic foot care should be provided and reinforced during each visit.[27] Patients must understand the importance of wearing protective shoes indoors and outdoors, ensuring that footwear fits properly to prevent ulcers. Some patients may require specialized shoegear, which should be evaluated during the diabetic foot examination. Selection of appropriate offloading or protective modalities should be individualized based on biomechanical alterations, pressure points, and existing pathology. Options may include shoe modifications, temporary shoegear, toe spacers, orthoses, and offloading devices such as felt pads and foam to help protect the diabetic foot.[28]

Complications

Inadequate diabetic foot care significantly increases the risk of ulceration, infection, and limb loss. Armstrong and Harkless demonstrated that noncompliant patients, specifically those who missed more than 50% of scheduled appointments within 1 year, are 54 times more likely to develop pedal ulcerations and 20 times more likely to undergo amputation compared to compliant patients.[29] One study reported that individuals with diabetes fear major lower-extremity amputation more than death, foot infection, or end-stage renal disease.[30] Another study found that amputation exerts the largest detrimental effect on quality of life compared to other diabetes-related complications, including stroke, blindness, renal failure, heart failure, and myocardial infarction.[31] Consequently, high-risk limbs require intensive monitoring and management by specialists, such as podiatrists.

Clinical Significance

Proper diabetic foot care is a critical component of diabetes management for limb preservation. Foot ulceration is one of the leading causes of hospitalization and amputation among patients with diabetes. Most diabetic foot complications arise from ischemia, neuropathy, and infection. Patients with diabetes and neuropathy have a 7% to 10% annual risk of developing foot ulceration, which increases to 25% to 30% in individuals with additional risk factors, such as PAD, pedal deformities, or a history of ulceration or amputation. Approximately 85% of diabetes-related lower extremity amputations result from complications of foot ulceration. Risk of amputation rises with age. Patients older than 45 have an 8-fold increased risk of amputation, those older than 65 years a 12-fold risk, and individuals aged 65 to 74 years a 23-fold risk.

Enhancing Healthcare Team Outcomes

Diabetic foot care requires interprofessional collaboration. Patients receiving team-based care demonstrate reduced severity of amputation, shorter hospital stays, lower mortality rates, improved ulcer healing, and enhanced quality of life.[32]

Effective diabetes management is integral to foot care. Beyond routine endocrinology or diabetology oversight, group-based self-management programs improve body weight, fasting blood glucose, waist circumference, diabetic knowledge, and triglyceride levels. Monitoring responsibilities are shared among clinicians, nurses, and pharmacists, with results systematically relayed to the interprofessional team. Interprofessional interventions incorporating peer support have demonstrated superior reductions in HbA1c compared to peer-led groups.[33] Foot care nurses frequently perform assessments and provide patient education, but all team members share responsibility for training, reinforcing self-care, and preventing complications.

Nursing, Allied Health, and Interprofessional Team Interventions

Intensive patient education by the nursing staff, encompassing lifestyle management, podiatric care, routine foot examinations, and callus management, reduces the incidence of diabetic foot ulcerations and lowers amputation rates in high-risk patients. Additionally, such education contributes to improved metabolic parameters, including reductions in plasma glucose, blood pressure, and high-density lipoprotein cholesterol levels.[34]

Nursing, Allied Health, and Interprofessional Team Monitoring

Care of the diabetic foot is an interprofessional responsibility. Holstein et al reported a 75% reduction in major limb amputations in patients with diabetes following the establishment of an interprofessional foot clinic with increased revascularization rates.[35] Primary care physicians and nursing staff play a key role in identifying at-risk feet and providing education on proper care and monitoring. Individuals with elevated risk factors or pedal deformities should receive regular follow-up with podiatry. Development of ulcerations necessitates more frequent surveillance and may require referral to additional specialists, including vascular surgery, infectious disease, plastic surgery, and prosthetics.