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Diabetic foot ulcer

61 citationsUpdated Sep 2026

Overview

Diabetic foot ulcers are the most common medical complication for which patients with diabetes seek treatment, affecting approximately 12% of this population [4]. These ulcers are responsible for approximately 85% of lower extremity amputations in patients with diabetes mellitus [4]. The clinical burden is substantial, with over 70,000 lower extremity amputations performed yearly in the United States due to foot morbidity [6] and more than 80,000 diabetes-related amputations annually [61]. Approximately 40% of non-trauma related amputations in British hospitals are for complications of diabetes [19]. The long-term prognosis following amputation is poor; the mortality rate within the first two years following transtibial amputation is one-third [6], the 5-year mortality rate after leg amputation is approximately 66% [61], and approximately 30% of amputees undergo amputation of the contralateral limb within 3 years [61].

Pathophysiology involves a critical triad of sensory neuropathy, trauma, and foot deformity, which was present in 63% of patients with lower extremity ulcers in one study [39]. Sensory neuropathy is the most prevalent nerve dysfunction, affecting as many as 70% of patients [39], while motor loss may lead to claw toes and high arches that predispose to plantar ulceration [19]. Inflammatory responses to microbial invasion may be diminished, often resulting in absent clinical signs of infection [1]. Factors associated with the inability of a diabetic foot ulcer to heal include persistently uncontrolled hyperglycemia, inability to unload the affected area effectively, diminished circulation, infection, and poor nutrition [4].

Management requires a multisystem approach addressing the nervous, vascular, skeletal, immune, and integumentary systems through a multidisciplinary team [5]. Optimal management includes clinical awareness, adequate blood glucose control, periodic foot inspection, custom therapeutic footwear, offloading in high-risk patients, local wound care, and diagnosis and control of osteomyelitis and ischaemia [12]. Multidisciplinary foot care programs, along with comprehensive patient education, can reduce lower extremity amputation rates as much as 45% to 60% [61]. Regular attendance at an appropriate clinic, full compliance with medication, and checks for early signs of vascular or neurological abnormality are recommended for prevention [19].

Anatomy & Pathophysiology

Epidemiology and Burden

Diabetic foot morbidity carries a significant mortality burden, with a one-third mortality rate within the first two years following transtibial amputation [6]. In the United States, this condition leads to over 100,000 lower extremity amputations and early deaths annually [46]. The prevalence of diabetes is substantial, affecting 30.3 million Americans (9.4% of the population) in 2015, with a prevalence of 25.2% among those aged 65 years and older [42]. Globally, the Global Burden of Disease Study of 2015 estimated that diabetes affects 435 million people, a number expected to rise to 642 million by 2040 [42]. In 2010, 73,000 nontraumatic lower-limb amputations were performed in adults aged 20 years and older with a diagnosis of diabetes [42].

The economic and clinical impact is profound. Up to 25% of annual expenditures on diabetic care are directly attributable to foot ulcers and their complications, including infection and amputation [42]. A diabetic patient has a lifetime risk of developing a diabetic foot ulcer of 15%, with an annual incidence of 2% [42]. Foot problems are the most common cause for hospitalization in diabetics, accounting for 20% or more of all inpatient days in this population [43]. More than half of all nontraumatic amputations are performed on diabetics [43], and one report showed a 68% incidence of foot disorders in a large diabetic clinic [43].

Medicare patients with a diabetic foot ulcer are seen by a health care provider an average of 14 times per year and have 1.5 hospitalizations each year at a reimbursed cost of $33,000 annually [42]. Patients with a lower extremity amputation incur over $52,000 in reimbursed costs for Medicare services each year [42].

Neuropathy

Diabetic neuropathy manifests in the somatic and/or autonomic parts of the peripheral nervous system [39]. At the time of diagnosis, 10% of patients with diabetes mellitus have some form of sensory, motor, or autonomic dysfunction [39]. Neuropathy develops in 50% of patients within 25 years of diagnosis [39], and studies estimate that as many as 65% of people with type 1 or 2 diabetes have evidence of peripheral neuropathy [60]. The presence of peripheral neuropathy is the most predictive factor for the development of diabetic foot ulcers and is an independent predictor of ulcers [60]. The length of time a patient has had diabetes and the level of metabolic control are the main predictors for the development, progression, and extent of neuropathy [60].

No single etiologic pathway has been confirmed as responsible for all diabetic neuropathy [39]. Metabolic factors, including glycosylation of proteins, reduced availability of nerve growth factors, and immunologic factors, combined with microvascular insufficiency likely result in the final common pathway of neuropathic changes [39]. With high levels of blood glucose, hemoglobin and proteins become glycosylated and form end products that precipitate in the walls of small peripheral vessels and nerve tissue [60]. Metabolic causes of neuropathy include accumulation of sorbitol, enzyme deficiencies, and increased oxygen-free radical activity [60]. Examination of nerves in diabetic patients has shown multifocal ischemic proximal nerve lesions and epineural vessel atherosclerosis [60].

Sensory neuropathy is the most prevalent and obvious nerve dysfunction, affecting as many as 70% of patients [39]. Protective sensation is indicated by the ability to perceive a 5.07 (10 g) Semmes-Weinstein monofilament applied perpendicular to the skin [39]. Loss of protective sensation, defined as the inability to perceive the 5.07 Semmes-Weinstein monofilament, is the most common cause of plantar foot ulcers and is associated with a 30% risk of development of an ulcer [28]. This loss blunts the patient’s awareness of foot problems and delays the request for care because of the absence of pain [60].

Autonomic neuropathy occurs when the autonomic system cannot control blood vessel tone and sweat glands in the foot [39]. Sweat gland dysfunction allows the skin to dry out and crack, allowing the ingress of microbes [39]. The absence of skin oils released by autonomic signals leads to increased susceptibility to fissuring of the skin from mild trauma [60]. Standing foot pressure can be as high as 400 kPa, necessitating fine regulation of blood vessels to ensure adequate oxygenation and avoid local anoxia [39].

Motor neuropathy leads to muscle imbalance and joint contractures around the toes [60]. Weak intrinsic muscles become overpowered by stronger extrinsic muscles, leading to the development of hammer toes, claw toes, and distal migration of the fat pad [60]. Loss of intrinsic function, as seen in diabetic neuropathy, predictably leads to claw toes [73]. Muscle contractures of the gastrosoleus complex increase the force load transmitted to the forefoot [60]. Increased stiffness and tone in extrinsic foot muscles, Achilles tendon, and plantar fascia may contribute to abnormal foot loading patterns, potentially increasing the risk of ulcer recurrence [23]. Skin compromise occurs secondary to pressure placed on the dorsal surface as toes contact the toe box of the shoe and increased pressure beneath the metatarsal heads [39]. No proven method exists to reverse peripheral neuropathy associated with diabetes [2, 39].

Vascular Pathophysiology

Peripheral vascular disease is present in 60% to 70% of patients who have had diabetes for more than 10 years [28]. Peripheral arterial disease increases susceptibility to ischemic ulcers and compounds the effect of diabetes [60]. Diabetic patients with peripheral arterial disease are nine times more likely to develop a foot ulcer [60]. Hyperglycemia can damage vascular endothelium, which is a precursor to atherosclerosis and leads to diminished extremity blood flow and limited healing potential [43]. Elevated blood glucose levels over a long period lead to glycation of the body’s proteins, commonly measured by hemoglobin A1c [43]. Glucose covalently binds to lysine in proteins in a reversible process [43]. The addition of glucose molecules changes the flexibility of tissues, especially fibrous tissue, making tissues such as skin less able to handle sheer stresses [43]. Diabetic patients have glycation of arterial vessel walls, thickening of basement membranes, and reduced endothelial nitric oxide activity [60].

Specific hemodynamic thresholds are necessary for ulcer healing. An ABI of at least 0.45 and toe pressures greater than 40 mm Hg are necessary to heal an ulcer in the diabetic foot [4]. Transcutaneous oxygen values for the toes greater than 40 mm Hg have been found to be predictive of healing [28]. If the ischemic index (brachial artery blood pressure divided by dorsalis pedis and posterior tibial artery blood pressure) is 0.45 or greater, there is a 90% chance that a foot ulcer will heal [43]. Ultrasound examinations of Achilles tendons have shown disorganized tendon fibers and calcification in 75% of diabetic patients without foot problems [60]. A study examining peak midfoot joint pressures in diabetic and nondiabetic cadaver feet during simulated walking showed 46% higher dynamic pressures in the first metatarsocuneiform, medial and middle naviculocuneiform, and the first intercuneiform joints in specimens from diabetic patients [60].

Infection and Immunity

The identification and diagnosis of diabetic foot ulcer infections remains a complex problem because inflammatory responses to microbial invasion may be diminished in persons with diabetes [1]. Diminished inflammatory responses often result in absent clinical signs of infection in persons with diabetes [1]. Diabetes impairs the immune system because of alterations in the chemotaxis abilities of polymorphonuclear cells and cell wall abnormalities that make patients susceptible to secondary infections [60].

The most common pathogens in diabetic foot infections are aerobic gram-positive cocci, especially Staphylococcus aureus [4]. Deep cultures and bacterial biopsy are sometimes necessary to make a diagnosis of diabetic foot infection [4]. Superficial wound culture does not identify the organism responsible for the infection and should not be performed [57]. Culture of a deep surgical specimen or bone biopsy of exposed bone provides the most accurate result for identifying the causative organism [57]. Contiguous osteomyelitis is present in 67% of foot ulcerations that reach bone [57].

Charcot Arthropathy Pathophysiology

Up to 7.5% of patients with diabetes and neuropathy have Charcot arthropathy of the foot and ankle [48]. Of patients with Charcot arthropathy, 9% to 35% have bilateral involvement [48]. The midtarsal joints are the most commonly affected in Charcot arthropathy, followed by the MTP and ankle joints [19].

Classification: * Type 1: Involves the midfoot and accounts for approximately 60% of cases [48]. * Type 2: Involves the hindfoot and accounts for 30% to 35% of cases [48]. * Type 3: Involves the ankle or calcaneal tuberosity and accounts for the remaining 5% to 10% of cases [48].

The pathophysiology involves both neurotraumatic and neurovascular mechanisms. The neurotraumatic theory attributes bony destruction to the loss of pain sensation and proprioception, combined with repetitive and mechanical trauma to the foot [48]. It suggests that microtrauma in insensate joints causes progressive bony destruction with repeated partial healing [64]. The neurovascular theory suggests that joint destruction is secondary to an autonomic stimulated vascular reflex causing hyperemia and periarticular osteopenia with contributory trauma [48]. It posits that nerve damage results in increased local vascularity, precipitating osteoclastic activation with secondary osteopenia, fractures, and deformity [64].

Trauma, often trivial, initiates a cytokine-mediated inflammatory process in patients with long-standing peripheral neuropathy [92]. This pathway is characterized by acute and chronic inflammation, osteoclastic bone resorption, and mechanical bony failure (eg, fracture) [92]. There is associated activation of pro-inflammatory cytokines with resulting increased vascularity and activation of the receptor activator kappa beta (RANK)–RANK ligand (RANKL) axis in Charcot foot [64]. Activation of the RANK–RANKL axis results in osteoclastic activation and bone loss [64]. Hyperglycaemia in diabetic patients has been shown to increase levels of advanced glycosylation end products (AGEs) [64]. AGEs are able to upregulate the RANK–RANKL pathway by interacting with their receptor, the RANK receptor, especially after a fracture or repetitive trauma [64]. TNF-alpha and IL-1B lead to increased levels of NF-KB, which is responsible for increased osteoclast production and loss of bone in Charcot arthropathy [28].

An impaired healing response following the inflammatory process leads to a resultant deformity in Charcot foot [92]. Motor imbalance between relatively weakened ankle dorsiflexors and overpowering plantar flexors leads to a relative dynamic ankle equinus loading during terminal stance phase of gait [92]. Loading of prepositioned dynamic equinus osteoporotic bone creates a bending moment akin to a “stress fracture” [92]. The patient continues to load the bone because of the loss of protective sensation, leading to mechanical failure of the bone [92]. Autonomic peripheral neuropathy is expressed as loss of autonomic vascular tone, with resulting venous swelling [92]. Swollen tissues have less resistance to repetitive trauma, making tissue breakdown overlying bony deformity more likely [92]. Increasing cumulative glycemic burden is positively associated with diabetic foot ulcer, while it is not associated with Charcot arthropathy [21].

Soft Tissue and Biomechanical Changes

A histologic examination of the plantar skin of diabetic and nondiabetic patients showed significantly thicker elastic septae and dermal layers in diabetic tissue [60]. Thicker elastic septae and dermal layers in diabetic tissue may play a role in the biomechanical changes leading to ulcer formation [60]. Adverse plantar pressure patterns are associated with redistribution of joint moments and a consequent reduced capacity to control forward velocity at heel strike in diabetic polyneuropathy [89]. Individuals with either partial foot amputation due to peripheral neuropathy or peripheral neuropathy alone showed similar alterations in the sagittal plane kinematics and moments of the lower limb joints [82].

Classification

Wagner-Meggitt: The Wagner ulcer classification system and the Brodsky depth-ischemia classification are commonly used for classifying diabetic foot ulcers [4]. The Meggitt-Wagner grading system is a validated tool that can be used to both risk stratify and determine treatment strategy for diabetic foot ulcers [40]. In this system, grade 0 patients have either had a previous foot ulcer or infection or are "at risk" to develop an ulcer or infection [40]. Grade I is defined as a superficial ulcer, and grade II as a deep wound without abscess or bony involvement [40]. Grade III ulcers are defined by the presence of an abscess or osteomyelitis [40].

Ischemia-Based: An ischemia-based classification for diabetic foot ulcers includes grade A (normal vascularity), grade B (ischemia without gangrene), grade C (partial forefoot gangrene), and grade D (complete foot gangrene) [28, 29].

Eichenholtz: The classic classification system for Charcot arthropathy is that of Eichenholtz [48]. Stage 0 is the acute inflammatory phase characterized by a swollen, erythematous, warm, and hyperemic foot with radiographs revealing periarticular soft-tissue changes [48]. Stages 1 to 4 are characterized by soft tissue stabilization, subsiding swelling, improving skin color, and potential development of deformity and instability [48]. Stage 4 is the consolidation phase where foot stability may increase via arthrodesis or fibrous union [48].

Brodsky: Brodsky created an anatomic-based classification system for the Charcot foot [48]. Type 1 involves the midfoot and accounts for approximately 60% of Charcot arthropathy [48]. Type 2 involves the hindfoot and accounts for 30% to 35% of Charcot arthropathy [48]. Type 3 involves the ankle or calcaneal tuberosity and accounts for the remaining 5% to 10% of Charcot arthropathy [48].

WIfI: The Wound, Ischemia, and foot Infection (WIfI) clinical stage classification system is used to classify limb threat in diabetic foot ulcers [55].

Clinical Presentation

Epidemiology and Risk Factors

Diabetic foot ulcers carry a significant burden, with an annual incidence of 2% [42]. The mortality rate within the first two years following transtibial amputation in patients with diabetes is one-third [6]. Problems are more common in patients diagnosed with diabetes for more than a decade or those with poor glycaemic control [19]. The critical triad of sensory neuropathy, trauma, and foot deformity is present in 63% of patients with lower extremity ulcers [39] and in two-thirds of patients at risk for progression to ulceration [54]. Inappropriate footwear is the most common cause of trauma leading to ulceration [54]. Sensory neuropathy affects as many as 70% of patients with diabetes, while pain is associated with 25% to 33% of neuropathies [39]. Motor neuropathy leads to claw toes from intrinsic muscle weakness and equinus contracture of the Achilles tendon [39].

Histologic examination reveals that plantar skin in diabetic patients has significantly thicker elastic septae and dermal layers compared to nondiabetic tissue [60]. Peak midfoot joint pressures are 46% higher in diabetic cadaver feet during simulated walking [60]. Standing foot pressure can reach 400 kPa, necessitating fine regulation of blood vessels to ensure adequate oxygenation [39]. In patients with peripheral vascular disease, atherosclerosis affects mainly the medium-sized vessels below the knee [19], which can lead to falsely elevated ankle brachial indices [28, 29].

Clinical Evaluation

A comprehensive evaluation includes the foot and ankle, paying special attention to tobacco use, prior treatments, medical comorbidities, and Achilles tendon tightness [4]. Examination of the lower extremity vascular system involves assessing dorsalis pedis and tibialis pulses and examining skin condition, noting the absence of hair on the feet and toes [4]. Weight-bearing AP, lateral, and oblique radiographs of the foot and ankle are obtained for evaluation [4]. MRI can help differentiate conditions but may not distinguish between Charcot arthropathy and infection with high specificity [4].

The physical examination begins with inspection of the shoe for internal and external wear patterns [43]. The leg and foot are inspected for overall skin appearance, hair growth, perfusion, pulses, and color [43]. Any bony prominences are recognized as areas of potential skin breakdown [43]. The most common bony prominences are located at the apex of deformities such as under the metatarsal heads, on the dorsum of the proximal interphalangeal joints, under the medial sesamoid, at the base of the fifth metatarsal, under the medial arch in the Charcot foot, and over the medial eminence of the hallux [43]. Neurologic examination tests for protective sensation, defined by the patient’s ability to feel the 10-g Semmes-Weinstein monofilament, as well as motor function [43].

Ulcers are carefully documented and evaluated for evidence of infection in adjacent soft tissues [43]. Wounds are measured for length, width, and depth, in addition to documenting their location [43]. Open wounds are probed with a sterile Q-tip or other appropriate instrument to evaluate the extent of involvement of deeper structures, such as tendons, joints, and bone [43]. Vascular evaluation is essential to ensure adequate perfusion for healing [43]. Patients with palpable pedal pulses and normal capillary filling have adequate blood supply and usually do not require further vascular evaluation [43]. The ischemic index is obtained by dividing the brachial artery blood pressure by that in the dorsalis pedis and posterior tibial arteries, measured by Doppler ultrasound with a calf cuff [43]. If the ischemic index is 0.45 or greater, there is a 90% chance that a foot ulcer will heal [43]. Lower ischemic indices indicate the need for further vascular evaluation [43]. Glucose assessment is ideally evaluated with A1c measurement, which indicates past 3 months of glucose control [28, 29].

Diagnosis of Infection and Osteomyelitis

The identification and diagnosis of diabetic foot ulcer infections remains complex because inflammatory responses to microbial invasion may be diminished in persons with diabetes, often resulting in absent clinical signs of infection [1]. The most accurate test to identify a deep infection and the need for surgical intervention is the “probe-to-bone” test [93]. A positive probe-to-bone test virtually assures deep infection and the need for surgery [93], while a negative probe-to-bone test does not rule out deep infection [93]. A positive probe to bone test usually indicates the presence of osteomyelitis [43]. Bony destruction with a break in the cortex is a late finding on plain radiographs, making them very difficult to interpret for osteomyelitis [93]. Radionucleotide imaging with or without labels has a high false-positive and false-negative rate for diagnosing deep infection [93]. MRI also has a high false-positive and false-negative rate for diagnosing deep infection in the diabetic foot [93]. Consequently, the diagnosis of deep infection and the need for surgery is primarily a clinical decision [93].

Diabetic patients with an abscess often present with clinical signs of sepsis characterized by fever, chills, hypotension, and hyperglycemia [93]. A foot abscess and sepsis is often the first sign that the patient is diabetic [93]. Long-standing diabetics might have noticed prodromal elevated blood glucose or difficulty controlling blood glucose when presenting with infection [93]. It is highly unusual for a diabetic foot abscess to develop in the absence of an ulcer, open wound, infected ingrown toenail, or skin crack between toes [93]. Hematogenous source of infection is rare in diabetic foot abscesses [93]. In patients with diabetes, blood glucose levels usually fluctuate during a substantial infection; therefore, normal blood glucose levels should discount infection in the differential diagnosis [48]. The mean fold change in the M1/M2 score at 4 weeks was 90 times higher for nonhealing ulcers compared with healing ulcers [37].

Charcot Arthropathy

Early Charcot arthropathy often is confused with infection, despite the lack of a substantially elevated white blood cell count or fever [48]. Patients with Charcot arthropathy complain of swelling, warmth, redness, and deformity [28, 29]. Pain is present in up to 50% of patients with Charcot arthropathy [28, 29]. The midfoot is most commonly affected in Charcot arthropathy, followed by the ankle and then the hindfoot [28, 29].

Classification Systems

The Meggitt-Wagner grading system is a validated tool used to risk stratify and determine treatment strategy [40]. Wagner Grade 0: Patients have either had a previous foot ulcer or infection or are “at risk” to develop an ulcer or infection [40]. Wagner Grade I: Defined as a superficial ulcer [40]. Wagner Grade II: Defined as a deep wound without abscess or bony involvement [40]. Wagner Grade III: Defined by the presence of an abscess or osteomyelitis [40]. Wagner-Meggitt Grade III: Defined by deep wound or abscess [93]. Wagner-Meggitt Grade IV: Has bony involvement, such as osteomyelitis [93].

An alternative depth-based classification system guides management: Depth Grade 0: Involves an extra-depth shoe and pressure relief insoles [28, 29]. Depth Grade 1: Involves no bony involvement and is superficial, managed with in-office débridement and total contact cast (TCC) [28, 29]. Depth Grade 2: Involves a deep ulcer with soft tissue exposure, managed with operative débridement to healthy tissue followed by dressing changes/TCC [28, 29]. Depth Grade 3: Involves an extensive ulcer with osteomyelitis or abscess and exposed bone, managed with surgical débridement of bone/soft tissue followed by dressing changes/TCC [28, 29].

An ischemia-based classification system categorizes vascular status: Grade A: Indicates normal vascularity [28, 29]. Grade B: Indicates ischemia without gangrene [28, 29]. Grade C: Indicates partial forefoot gangrene [28, 29]. Grade D: Indicates complete foot gangrene [28, 29].

Charcot arthropathy is classified by location and stage: Brodsky Type 1: Involves the midfoot and accounts for approximately 60% of cases [48]. Brodsky Type 2: Involves the hindfoot and accounts for 30% to 35% of cases [48]. Brodsky Type 3: Involves the ankle or calcaneal tuberosity and accounts for the remaining 5% to 10% of cases [48].

Eichenholtz Stage 0 (acute): Characterized by hyperemia of the foot with increased warmth and swelling; radiographs can show fracture or joint subluxation [48]. Eichenholtz Stages 1 to 4: Characterized by soft tissues stabilizing and swelling subsiding, with skin color improving; the foot may develop deformity and instability [48]. Eichenholtz Stage 4 (consolidation): Characterized by foot stability increasing via arthrodesis or fibrous union [48].

Investigations

Clinical Evaluation

The initial assessment of a diabetic foot ulcer requires evaluation of ulcer depth, presence of infection, nonviable tissue such as gangrene, and pressure at the ulcer site [4]. Regular examination for early signs of neuropathy should include testing skin sensibility with Semmes–Weinstein hairs and vibration sense with a biothesiometer [19]. The presence of ulcers necessitates differentiation between vascular, neuropathic, or combined causes [19]. Osteomyelitis is present in 67% of foot ulcerations that reach bone [57].

Imaging

MRI: MRI can help differentiate between soft-tissue infection and osteomyelitis, though it may not distinguish between Charcot arthropathy and infection with high specificity [4]. The sensitivity of MRI for osteomyelitis approaches 100%, but reported specificity is less [58]. In neuropathic patients, the specificity of MR signal abnormalities is reduced, and MRI has a high false-positive rate for osteomyelitis, particularly with concurrent Charcot arthropathy [57, 58]. Consequently, the current workup of osteomyelitis in the diabetic foot often involves a combination of scintigraphy, MRI, laboratory data, and especially physical examination [58]. The addition of contrast-enhanced sequences is helpful in defining nonenhancing fluid collections or abscesses and devascularized or gangrenous tissue [58].

Bone scan: Labeled WBC scan or dual-image technetium/indium (Tc/In) scan is more sensitive and specific for osteomyelitis than isolated Tc scan [57].

Microbiology and Laboratory

The most common pathogens are aerobic gram-positive cocci, especially Staphylococcus aureus; gram-negative rods may be present in patients with chronic wounds or those recently treated with antibiotics [4]. Deep cultures and bacterial biopsy are sometimes necessary to make a diagnosis [4]. Culture of a deep surgical specimen or bone biopsy of exposed bone provides the most accurate result [57]. However, information gained from biopsy of bone may not be the gold standard that it is believed to be [65].

Treatment

General Principles and Multidisciplinary Care

Management of foot problems in diabetic patients requires a multisystem approach addressing the nervous, vascular, skeletal, immune, and integumentary systems through a multidisciplinary team to prevent ulceration, infection, and amputation [5]. The orthopedic surgeon should play a central role in this multidisciplinary management by providing a biomechanical perspective to avoid complications recurrence [11]. Scheduling interventional surgery and debridement are key points in complicated diabetic foot ulcer cases, and multidisciplinary collaboration in treatment is significantly important [17]. The American Diabetes Association reports that multidisciplinary foot care programs, along with comprehensive patient education, can reduce lower extremity amputation rates as much as 45% to 60% [61].

The desired optimal clinical outcome of any patient with diabetic foot morbidity is an ulcer- and infection-free limb that can be managed longitudinally with commercially available depth-inlay therapeutic footwear and custom accommodative foot orthoses/insoles [41]. A proactive program combining foot-specific patient education, ongoing clinical monitoring, and accommodative footwear can be very successful in decreasing the incidence of diabetic foot ulceration, infection, and amputation [41]. Foot-specific patient education includes instruction on daily foot inspection, appropriate footwear, and instruction on nail and callus care [41]. No proven method exists to reverse peripheral neuropathy, and treatment focuses on symptom management, protection from mechanical trauma, and off-loading pressure to prevent ulceration and amputation [2].

Non-Operative

Wound dressings should provide a moist environment, absorb exudates, act as a barrier, off-load pressure, and provide antibiosis when required [4]. "Offloading" the wound is accomplished by distributing weight-bearing pressure over a large surface area with either a healing shoe, custom orthotic, commercially available fracture foot with pressure-dissipating insole, or a total contact cast [41]. Plastazote (closed cell—cross linked polyethylene) is often used to line the shoe and offload prominent areas [28]. Plastazote is lightweight, can absorb shock, and is able to be soft and compliant [28].

Total contact casts (TCCs) should be changed every 2 to 4 weeks until erythema and edema have resolved and the temperature of the affected limb has decreased and becomes similar to that of the contralateral limb [4]. Radiographs should be repeated every 4 to 6 weeks for patients in TCC, or more often if an acute change occurs [4]. The total-contact cast provided safe, reliable, and cost-effective treatment for patients who had neuropathic ulcers of the foot [59]. Advantages of the pneumatic walking brace include permitting more frequent wound surveillance, allowing several types of dressings, and ease of application [4]. Severe foot deformity makes using a pneumatic walking brace difficult, and patient compliance may be suboptimal [4].

Patients with grade I and II wounds are managed as outpatients with local débridement, empiric oral first-generation cephalosporin antibiotic therapy, and either a commercially available offloading device or total contact cast [40]. Once resolved, patients with grade I or II ulcers are managed longitudinally with ongoing patient education, periodic monitoring, and therapeutic footwear [40]. The Medicare Therapeutic Shoe Bill of 1993 provides one pair of appropriate depth-inlay shoes and three insoles per year for Medicare-entitled individuals [41]. The Medicare Therapeutic Shoe Bill was signed into law in 1998 after studies showed potential net Medicare savings by preventing diabetic foot complications [4]. Medicare pays 80% of the cost for therapeutic shoes, with 20% charged to the approved patient or their supplemental insurance [4].

Extracorporeal shock wave therapy combined with standard care resulted in a higher rate of complete wound closure (53.33% vs 33.33%) and shorter healing times (60.8 vs 82.2 days) compared to standard care alone in patients with neuropathic diabetic foot ulcers [16]. Autologous platelet-rich plasma (Au-PRP) therapy has been shown to facilitate the process of wound healing and represents a viable and secure therapeutic alternative for individuals with diabetic foot ulcers [66]. Application of a simple skin stretching system and negative pressure wound therapy (NPWT) is an effective and safe approach to complex diabetic foot wounds [20].

Protected weightbearing in an orthopedic device can reduce the risk for complications in acute Charcot neuroarthropathy of the foot and ankle [44]. Acute Charcot arthropathy may be treated or resolved with a total contact cast for 4 to 6 weeks [28]. Initial treatment of Charcot arthropathy is non-weight-bearing status with a total contact cast [28].

Operative

Indications: Grade III ulcers, defined by the presence of an abscess or osteomyelitis, require a minimum of surgical débridement, culture-specific antibiotic therapy, and longitudinal care [40]. Drainage of deep infections is often necessary to prevent tissue necrosis, rid the area of infection, and achieve wound healing without tension [4]. Débridement of infected tissue with use of negative-pressure dressings is recommended when infection prevents healing with conservative management [28].

Surgical Approach / Technique: Before antibiotic treatment is begun for osteomyelitis, specimens for culture should be obtained by biopsy, ulcer curettage, or aspiration, rather than by wound swab [4]. Osteectomy or realignment arthrodesis may be needed to remove the internal pressure caused by bony prominences [4]. Treatment often requires Achilles lengthening to prevent recurrence of forefoot/midfoot ulceration [28]. Toe deformities often require joint resection or amputation [28]. Dorsal toe ulcers are best served with flexor tenotomies [28]. Plantar hallux IP joint ulcers for which contact casting has failed should be treated with a Keller arthroplasty [28].

Implant Selection: Use of an intramedullary rod for tibiotalocalcaneal arthrodesis affords internal stability and can be left indefinitely, in contrast to a multiplanar external fixator [28]. Even with radiographic evidence of nonunion after tibiotalocalcaneal arthrodesis, many patients can be pain-free [28]. Unstable or unbraceable deformities should be addressed with a tibiotalocalcaneal arthrodesis to afford a braceable/plantigrade foot while reducing risk of ulceration [28].

Adjuncts: Internal partial forefoot amputation (IPFA) is a valuable treatment of chronic ulcers of the forefoot, although new ulceration is a frequent event following this type of surgery [7]. Proximal tibial cortex transverse distraction substantially facilitated healing and limb salvage and decreased the recurrence of severe and recalcitrant diabetic foot ulcers compared with standard surgical therapy [9]. Tibial periosteal distraction (TPD) surgery technique is a simple procedure that significantly increases the efficacy and reduces the complications of moderate diabetic foot ulcer patients, which could accelerate the formation of collateral circulation [22]. Periosteal distraction-related treatments for diabetic foot ulcers should not be interpreted as evidence that periosteal distraction alone has an independent effect, and robust limb salvage endpoints remain insufficiently reported [49]. Application of antibiotic bone cement can effectively decrease the frequency of debridement procedures and shorten the healing duration in patients with infected diabetic foot ulcers [67]. Different flap techniques can obtain better clinical efficacy in repairing diabetic foot defects [68].

Other Considerations: Surgical management of Charcot foot remains controversial in the acute phase, with superconstruct techniques and retrograde intramedullary nailing providing successful fixation [25]. At follow-up after treatment of resistant ulcers on the plantar surface of the great toe, no obvious functional impairment of gait was evident, and each patient had regained his or her original functional status [24].

Amputation Considerations

After amputation of a leg, the 5-year mortality rate is approximately 66% [61]. First ray amputations can increase load to the adjacent rays and can weaken ankle dorsiflexion by losing the anterior tibialis insertion, resulting in pronation of the foot [61]. The patient requires less energy for ambulation after a TMA than after a transtibial amputation, and a TMA leaves a patient with a distal weight-bearing residual limb [61]. Careful patient selection for TMA is required, including an assessment of muscle balance to determine the need for Achilles tendon lengthening and/or tendon transfer [61].

Chopart amputation retains the tibiotalar joint and a functional residual limb, in contrast to a more proximal amputation [61]. Achilles tendon lengthening is usually necessary for Chopart amputation, as well as transfer of the extensors to the dorsal talus to prevent equinovarus deformity [61]. The Syme amputation can be performed in two stages approximately 6 weeks apart; however, most surgeons use the single-stage technique because the results are essentially the same, but the cost and the risk of perioperative complications are lower with only one procedure [61]. Successful healing was reported in 84.5% of patients treated with single-stage Syme amputation [61]. Heel pad migration after a Syme amputation can be avoided by anchoring the heel pad to the distal tibia [61].

Complications

Infection and Osteomyelitis: Diabetic foot infections are usually polymicrobial [4]. Autonomic neuropathy causes dry skin and dermal cracks, which may serve as portals of entry for infection [43]. Additionally, reactive hyperemia, which normally helps to clear infections, is blunted by autonomic neuropathy [43]. The presence of infection may be a reason why ulcers do not heal with conservative management [28].

Ulcer Recurrence and Non-Healing: Loss of protective sensation is associated with a 30% risk of development of a plantar foot ulcer [28].

Amputation and Limb Loss: In a cohort of patients undergoing Chopart amputation for diabetic foot infection, 94% developed postoperative wound complications [32]. In the same cohort, only 44% successfully ambulated with a prosthesis [32].

Charcot Arthropathy: The midtarsal joints are the most commonly affected in Charcot arthropathy, followed by the metatarsophalangeal and ankle joints [19]. A minor provocative incident, such as a twisting injury or a fracture, leads to a painless progressive collapse of the joint in Charcot arthropathy [19]. Fragmentation to consolidation in Charcot arthropathy may take 6 to 18 months [28]. Hyperglycaemia in diabetic patients increases levels of advanced glycosylation end products (AGEs), which may upregulate the RANK–RANKL pathway and contribute to Charcot development [64]. Arthrodesis for neuropathic joint disease has a very poor union rate [19].

Surgical and Procedural Complications: Postoperative infection rates in foot and ankle surgery are a concern in patients with diabetes mellitus [47]. Neurocutaneous flaps for diabetic lower limb reconstruction might be associated with longer healing time and additional revision surgeries [34]. Most patients preferred to undergo multiple procedures to salvage the limb from diabetic foot infection even if it ultimately concluded with a below-knee amputation [15].

Recovery

Factors Associated with Wound Healing and Non-Healing: Several clinical factors are associated with the inability of a diabetic foot ulcer to heal. These include persistently uncontrolled hyperglycemia [4], ineffective unloading of the affected area [4], diminished circulation [4], infection [4], and poor nutrition [4]. Specific perfusion thresholds are necessary for ulcer healing in the diabetic foot: an ankle-brachial index (ABI) of at least 0.45 is required [4], and toe pressures greater than 40 mm Hg are necessary [4].

Off-Loading and Mechanical Management: Radiographs should be repeated every 4 to 6 weeks, or more often if an acute change occurs [4]. A prefabricated pneumatic walking brace can be used to reduce forefoot and midfoot plantar pressure as an alternative to total contact casting (TCC) [4]. In patients with diabetes and previous forefoot ulcerations, a rigid outsole causes changes in the subphases of the stance phase and improves spatiotemporal parameters compared to semirigid soles and barefoot conditions [26].

Wound Care and Adjunctive Therapies: Wound dressings should provide a moist environment, absorb exudates, act as a barrier, off-load pressure, and provide antibiosis when occasionally required [4].

Surgical Interventions and Outcomes: In a cohort of patients undergoing Chopart amputation for diabetic foot infection, only 44% successfully ambulated with a prosthesis, while the remainder required revision amputations [32]. Neurocutaneous flaps are specially indicated for larger and more distally located defects, although they might be associated with longer healing time and additional revision surgeries [34]. Following treatment of resistant ulcers on the plantar surface of the great toe, no obvious functional impairment of gait was evident at follow-up, and each patient had regained his or her original functional status [24]. Most free toe transfers caused no obvious side effects on the function of the foot, with 86% of patients recovering completely within 6 months [69].

Prognosis and Complications: There is a one-third mortality rate within the first two years following transtibial amputation [6]. The identification and diagnosis of diabetic foot ulcer (DFU) infections remains a complex problem because inflammatory responses to microbial invasion may be diminished in persons with diabetes, often resulting in absent clinical signs of infection [1].

Key Evidence

  • [L5] The identification and diagnosis of diabetic foot ulcer (DFU) infections remains a complex problem because inflammatory responses to microbial invasion may be diminished in persons with diabetes, often resulting in absent clinical signs of infection. [1] (10.1177/1099800408319056)
  • [L3] A high frequency of foot ulcers must be anticipated and addressed as part of the treatment approach. [3] (10.1097/corr.0000000000002546)
  • [L5] Management of foot problems in diabetic patients requires a multisystem approach addressing the nervous, vascular, skeletal, immune, and integumentary systems through a multidisciplinary team to prevent ulceration, infection, and amputation. [5] (10.5435/00124635-199507000-00004)
  • [L4] IPFA is a valuable treatment of chronic ulcers of the forefoot, although new ulceration is a frequent event following this type of surgery. [7] (10.1007/s00402-020-03441-3)
  • [L5] Patient outcomes have not been objectively assessed for the purpose of this paper; however, it is the author’s experience that tendoscopic peroneus longus to brevis transfer for the treatment of recurrent diabetic foot ulcers secondary to medial forefoot overload is a successful procedure with a low complication profile. [8] (10.1016/j.eats.2024.103372)
  • [L2] Proximal tibial cortex transverse distraction substantially facilitated healing and limb salvage and decreased the recurrence of severe and recalcitrant diabetic foot ulcers compared with standard surgical therapy. [9] (10.1097/corr.0000000000001075)
  • [Paper] Management of diabetic foot remains multidisciplinary, but the orthopedic surgeon should play a central role by providing a biomechanical perspective to avoid complications recurrence. [11] (10.1016/j.otsr.2011.03.001)
  • [L5] Optimal management of patients with diabetic foot ulcers must include clinical awareness, adequate blood glucose control, periodic foot inspection, custom therapeutic footwear, offloading in high-risk patients, local wound care, diagnosis and control of osteomyelitis and ischaemia. [12] (10.1302/2058-5241.3.180010)
  • [L1] Based on our experience with the patients in the present study, we believe that AF represents a useful and safe option for the treatment of chronic diabetic foot ulcers. [13] (10.3389/fpubh.2022.1025391)
  • [L4] Primary wound closure following limited amputation of the foot in patients with diabetes is a safe and effective technique when associated with appropriate antibiotic treatment. [14] (10.1302/0301-620x.95b8.31280)
  • [L4] Most patients preferred to undergo multiple procedures to salvage the limb from diabetic foot infection even if it ultimately concluded with a BKA. [15] (10.1302/0301-620x.99b11.bjj-2016-0793.r2)
  • [L2] Extracorporeal shock wave therapy combined with standard care resulted in a higher rate of complete wound closure (53.33% vs 33.33%) and shorter healing times (60.8 vs 82.2 days) compared to standard care alone in patients with neuropathic diabetic foot ulcers. [16] (10.1186/1471-2474-10-54)
  • [Case_report] Scheduling interventional surgery and debridement are the key point in a complicated diabetic foot ulcers case, and multidisciplinary collaboration in treatment of diabetic foot is significantly important. [17] (10.1186/s12891-019-2522-3)
  • [L4] Application of the simple skin stretching system and NPWT is an effective and safe approach to complex diabetic foot wounds. [20] (10.1186/s13018-021-02405-6)
  • [L3] Increasing cumulative glycemic burden is positively associated with diabetic foot ulcer, while it is not associated with Charcot arthropathy. [21] (10.1186/s13018-016-0474-y)
  • [L4] TPD surgery technique is a simple procedure that significantly increases the efficacy and reduces the complications of moderate diabetic foot ulcer patients, which could accelerate the formation of collateral circulation. [22] (10.1186/s13018-024-05375-7)
  • [L3] The increased stiffness and tone in these structures may contribute to abnormal foot loading patterns, potentially increasing the risk of ulcer recurrence. [23] (10.1186/s12891-025-08791-w)
  • [L4] At followup no obvious functional impairment of gait was evident, and each patient had regained his or her original functional status. [24] (10.2106/00004623-198264060-00017)
  • [L5] The review highlights that total-contact casts are the benchmark for off-loading, advanced imaging modalities offer advantages for diagnosis, and surgical management of Charcot foot remains controversial in the acute phase with superconstruct techniques and retrograde intramedullary nailing providing successful fixation. [25] (10.1302/2058-5241.3.170073)
  • [L4] A rigid outsole causes changes in the subphases of the stance phase and improves spatiotemporal parameters compared to semirigid soles and barefoot conditions in patients with diabetes and previous forefoot ulcerations. [26] (10.3390/jcm9040907)
  • [L4] Topical hyperbaric oxygen combined with a low power laser or topical hyperbaric oxygen alone are attractive modalities which should be considered in the treatment of chronic diabetic foot ulcers. [30] (10.1007/s004020050217)
  • [L4] In this patient cohort, 94% of patients developed postoperative wound complications, and only 44% successfully ambulated with a prosthesis, while the remainder required revision amputations. [32] (10.5435/jaaos-d-19-00757)
  • [L3] Reverse neurocutaneous and propeller flaps may provide stable reconstruction of diabetic lower limb defects; neurocutaneous flaps are specially indicated for larger and more distally located defects, although they might be associated with longer healing time and additional revision surgeries. [34] (10.1016/j.injury.2020.03.014)
  • [L5] This CORR Insights commentary discusses the need to identify patients whose goals match limb salvage requirements and highlights the novel concept of using proximal tibial cortex transverse distraction to enhance blood flow for healing severe diabetic foot ulcers. [36] (10.1097/corr.0000000000001146)
  • [L4] The mean fold change in the M1/M2 score at 4 weeks was 90 times higher for nonhealing ulcers compared with healing ulcers. [37] (10.1038/jid.2015.30)
  • [L3] Protected weightbearing in an orthopedic device can reduce the risk for complications in acute CN of the foot and ankle. [44] (10.1186/s12891-016-1357-4)
  • [L1] These findings should not be interpreted as evidence that PD alone has an independent efect, and robust limbsalvage endpoints remain insuficiently reported. [49] (10.1186/s13018-026-06920-2)
  • [L5] [54] (10.1097/01.blo.0000181497.42117.fa)
  • [L3] [55] (10.1186/s13018-026-06933-x)
  • [L4] The total-contact cast provided safe, reliable, and cost-effective treatment for patients who had neuropathic ulcers of the foot. [59] (10.2106/00004623-199274020-00012)
  • [L5] [64] (10.1302/2058-5241.3.180003)
  • [L5] Information gained from biopsy of bone may not be the gold standard that it is believed to be, and in the absence of a gold standard, the surgical treatment of infection in patients with morbid diabetes is best provided by a multidisciplinary team. [65] (10.2106/jbjs.18.00593)
  • [L1] Au-PRP therapy has been shown to facilitate the process of wound healing and represents a viable and secure therapeutic alternative for individuals with DFU. [66] (10.1186/s13018-023-03854-x)
  • [L3] It can effectively decrease the frequency of debridement procedures and shorten the healing duration in patients with infected DFU. [67] (10.1186/s12891-023-06244-w)
  • [L3] Different flap techniques can obtain better clinical efficacy in repairing DFD wounds. [68] (10.1186/s13018-024-05122-y)
  • [L4] Most free toe transfers caused no obvious side effects on the function of the foot, with 86% of patients recovering completely within 6 months. [69] (10.1054/jhsb.2000.0397)
  • [L3] Individuals with either partial foot amputation due to peripheral neuropathy or peripheral neuropathy alone showed similar alterations in the sagittal plane kinematics and moments of the lower limb joints. [82] (10.1186/s13018-025-06376-w)
  • [L3] The results of this study suggest that adverse plantar pressure patterns are associated with redistribution of joint moments, and a consequent reduced capacity to control forward velocity at heel strike. [89] (10.1186/1471-2474-10-16)

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a. for the avoidance of doubt, Section 2(a)(1) grants You the right to extract, reuse, reproduce, and Share all or a substantial portion of the contents of the database for NonCommercial purposes only;

b. if You include all or a substantial portion of the database contents in a database in which You have Sui Generis Database Rights, then the database in which You have Sui Generis Database Rights (but not its individual contents) is Adapted Material; and

c. You must comply with the conditions in Section 3(a) if You Share all or a substantial portion of the contents of the database.

For the avoidance of doubt, this Section 4 supplements and does not replace Your obligations under this Public License where the Licensed Rights include other Copyright and Similar Rights.

Section 5 -- Disclaimer of Warranties and Limitation of Liability.

a. UNLESS OTHERWISE SEPARATELY UNDERTAKEN BY THE LICENSOR, TO THE EXTENT POSSIBLE, THE LICENSOR OFFERS THE LICENSED MATERIAL AS-IS AND AS-AVAILABLE, AND MAKES NO REPRESENTATIONS OR WARRANTIES OF ANY KIND CONCERNING THE LICENSED MATERIAL, WHETHER EXPRESS, IMPLIED, STATUTORY, OR OTHER. THIS INCLUDES, WITHOUT LIMITATION, WARRANTIES OF TITLE, MERCHANTABILITY, FITNESS FOR A PARTICULAR PURPOSE, NON-INFRINGEMENT, ABSENCE OF LATENT OR OTHER DEFECTS, ACCURACY, OR THE PRESENCE OR ABSENCE OF ERRORS, WHETHER OR NOT KNOWN OR DISCOVERABLE. WHERE DISCLAIMERS OF WARRANTIES ARE NOT ALLOWED IN FULL OR IN PART, THIS DISCLAIMER MAY NOT APPLY TO YOU.

b. TO THE EXTENT POSSIBLE, IN NO EVENT WILL THE LICENSOR BE LIABLE TO YOU ON ANY LEGAL THEORY (INCLUDING, WITHOUT LIMITATION, NEGLIGENCE) OR OTHERWISE FOR ANY DIRECT, SPECIAL, INDIRECT, INCIDENTAL, CONSEQUENTIAL, PUNITIVE, EXEMPLARY, OR OTHER LOSSES, COSTS, EXPENSES, OR DAMAGES ARISING OUT OF THIS PUBLIC LICENSE OR USE OF THE LICENSED MATERIAL, EVEN IF THE LICENSOR HAS BEEN ADVISED OF THE POSSIBILITY OF SUCH LOSSES, COSTS, EXPENSES, OR DAMAGES. WHERE A LIMITATION OF LIABILITY IS NOT ALLOWED IN FULL OR IN PART, THIS LIMITATION MAY NOT APPLY TO YOU.

c. The disclaimer of warranties and limitation of liability provided above shall be interpreted in a manner that, to the extent possible, most closely approximates an absolute disclaimer and waiver of all liability.

Section 6 -- Term and Termination.

a. This Public License applies for the term of the Copyright and Similar Rights licensed here. However, if You fail to comply with this Public License, then Your rights under this Public License terminate automatically.

b. Where Your right to use the Licensed Material has terminated under Section 6(a), it reinstates:

1. automatically as of the date the violation is cured, provided it is cured within 30 days of Your discovery of the violation; or

2. upon express reinstatement by the Licensor.

For the avoidance of doubt, this Section 6(b) does not affect any right the Licensor may have to seek remedies for Your violations of this Public License.

c. For the avoidance of doubt, the Licensor may also offer the Licensed Material under separate terms or conditions or stop distributing the Licensed Material at any time; however, doing so will not terminate this Public License.

d. Sections 1, 5, 6, 7, and 8 survive termination of this Public License.

Section 7 -- Other Terms and Conditions.

a. The Licensor shall not be bound by any additional or different terms or conditions communicated by You unless expressly agreed.

b. Any arrangements, understandings, or agreements regarding the Licensed Material not stated herein are separate from and independent of the terms and conditions of this Public License.

Section 8 -- Interpretation.

a. For the avoidance of doubt, this Public License does not, and shall not be interpreted to, reduce, limit, restrict, or impose conditions on any use of the Licensed Material that could lawfully be made without permission under this Public License.

b. To the extent possible, if any provision of this Public License is deemed unenforceable, it shall be automatically reformed to the minimum extent necessary to make it enforceable. If the provision cannot be reformed, it shall be severed from this Public License without affecting the enforceability of the remaining terms and conditions.

c. No term or condition of this Public License will be waived and no failure to comply consented to unless expressly agreed to by the Licensor.

d. Nothing in this Public License constitutes or may be interpreted as a limitation upon, or waiver of, any privileges and immunities that apply to the Licensor or You, including from the legal processes of any jurisdiction or authority.

Creative Commons is not a party to its public licenses. Notwithstanding, Creative Commons may elect to apply one of its public licenses to material it publishes and in those instances will be considered the “Licensor.” The text of the Creative Commons public licenses is dedicated to the public domain under the CC0 Public Domain Dedication. Except for the limited purpose of indicating that material is shared under a Creative Commons public license or as otherwise permitted by the Creative Commons policies published at creativecommons.org/policies, Creative Commons does not authorize the use of the trademark "Creative Commons" or any other trademark or logo of Creative Commons without its prior written consent including, without limitation, in connection with any unauthorized modifications to any of its public licenses or any other arrangements, understandings, or agreements concerning use of licensed material. For the avoidance of doubt, this paragraph does not form part of the public licenses.

Creative Commons may be contacted at creativecommons.org.