Diabetic trophic ulcers: treatment and prevention

Diabetic plantar ulcers are one of the most common and severe late complications of diabetes. They arise from a combination of peripheral neuropathy (loss of sensation, foot deformity) and ischemia (damage to the arteries of the lower leg and foot), and often become infected. The key to healing is offloading, prompt wound debridement, infection control, and restoration of blood flow—and these measures only work together. Current clinical guidelines emphasize that a properly selected offloading device is the "gold standard" for neuropathic plantar ulcers, and that ischemia and infection should be assessed in every patient from the first visit. [1]

Without active management, ulcers lead to infections, hospitalizations, and amputations, increasing mortality and reducing quality of life. According to international reviews, a history of ulcers is the strongest predictor of recurrent wounds and amputations; approximately 40% of patients experience recurrence within 1 year of healing. Therefore, treatment goals extend beyond wound closure and include recurrence prevention, footwear selection, and patient education. [2]

In everyday practice, errors are often associated with late recognition of infection, underestimation of ischemia, and the use of regular footwear instead of specialized unloading. Current standards (ADA 2025; IWGDF/IDSA 2023) offer step-by-step algorithms: stratify infection, select patients for hospitalization, choose empirical antibiotics based on the severity and source of infection, and, if osteomyelitis is suspected, promptly use imaging and (when possible) bone biopsy. [3]

Another pillar is vascular management. A patient with chronic limb ischemia and ulceration (the term "chronic limb-threatening ischemia") requires early evaluation for revascularization (endovascular or bypass) as indicated. The decision is made based on the wound profile, the degree of ischemia, and the severity of infection according to the WIfI (Wound-Ischemia-foot Infection) system, which improves the prognosis for limb preservation. [4]

Code according to ICD-10 and ICD-11

There is no separate "single" code for "diabetic foot ulcer": ICD-10 codes for both diabetes with ulcer and ulcer location/severity. Recommended combinations: E10.621/E11.621 ("diabetes mellitus type 1 or 2 with foot ulcer") plus one of the codes from the L97.- range ("chronic ulcer of the lower limb, not associated with pressure"), specifying the location (foot, ankle, shin) and degree (with/without necrosis). For neuropathy, angiopathy, or osteomyelitis, the corresponding complication codes are added based on the clinical situation. [5]

ICD-11 uses post-coordination: the basic condition BD54 "Diabetic foot ulcer" (within the section on lower limb wounds) is combined with codes for diabetes (5A10 - type 1 diabetes or 5A11 - type 2 diabetes) and, if necessary, with codes for neuropathy (8C03.0), autonomic neuropathy (8D88.1), and codes for infection or ischemia. This approach more accurately reflects the pathogenesis and complications and is recommended by ICD-11 coding guidelines. [6]

Table 1. Practice of coding diabetic ulcers

System	Basic code	Add-ons/clusters	Comment
ICD-10	E10.621 / E11.621	L97.- (localization/severity), if necessary M86.- (osteomyelitis), I70.2- (peripheral atherosclerosis)	E10/E11.621 is placed before L97. - according to the "code first" rules
ICD-11	BD54	5A10/5A11 (+ codes for neuropathy, infection, ischemia, osteomyelitis)	Post-coordination is essential for a complete picture

Epidemiology

Over the course of their lifetime, trophic ulcers develop in 19-34% of people with diabetes. Their occurrence is a powerful predictor of hospitalizations, amputations, and mortality. The risk increases with age, the duration of diabetes, and the accumulation of comorbidities. Recent publications emphasize that the disease burden continues to increase due to the increasing life expectancy with diabetes. [7]

Recurrences are extremely common: among healed wounds, approximately 40% recur within 1 year, and according to some reviews, up to 60% within 3 years. This justifies a lifelong preventive program: shoes, insoles, support devices, nail and skin control, and self-care training. [8]

A significant proportion of ulcers become infected: estimates vary, but it is often stated that up to 60% of ulcers become infected at some point, with chronic and recurrent ulcers becoming infected more frequently. Infection is the main trigger for amputations, so repeated trauma and prolonged healing are critical to outcome. [9]

Mortality after ulcer onset is high: in some series, ≈10% in the first year, and the need for major amputation increases mortality even further. At the population level, multidisciplinary teams (endocrinologist, vascular surgeon, podiatrist/orthopedist, infectious disease specialist, diabetes nurse) reduce the risk of amputation and mortality. [10]

Table 2. Epidemiological landmarks

Indicator	Ratings
Lifetime risk of ulcers	19-34%
Recurrence 1 year after healing	≈40%
Infection during the course of the ulcer	up to 60%
Mortality within 1 year from ulcer onset	≈10%

Reasons

Ulcer formation in diabetes is caused by mechanical tissue overload, accompanied by loss of protective sensitivity (peripheral neuropathy), foot deformities, and dry skin. Constant pressure and friction in areas of increased stress (most often under the metatarsal heads) lead to calluses, then to hidden subcutaneous damage, and finally to open ulcers. Therefore, unloading is a key treatment tool. [11]

The second driver is ischemia due to atherosclerotic lesions of the arteries of the leg and foot. Poor perfusion slows granulation formation, impairs antibiotic delivery, and increases the risk of necrosis. If ischemia is present, early vascular assessment with a plan for revascularization is indicated; otherwise, conservative therapy is ineffective. [12]

Infection often occurs secondarily, especially in chronic, deep, or subcalcaneal (under the callus) ulcers. Infection can extend to joints and bone (osteomyelitis), and in severe cases, lead to sepsis. According to the IWGDF/IDSA, antibiotic therapy is indicated only if there are signs of infection, and its duration depends on the depth of the lesion and the presence of osteomyelitis. [13]

Contributing factors include glycemic decompensation, smoking, renal failure, previous ulcers and amputations, and inappropriate footwear. Correcting these factors is a necessary part of the etiotropic approach; otherwise, the wound will recur. [14]

Risk factors

Strong risk factors include a history of ulceration or amputation, peripheral neuropathy, foot deformities (claw toes, hammer toes, Charcot arthropathy), peripheral arterial disease, and poor vision/self-care. The more factors, the higher the risk of recurrence. [15]

A recent meta-analysis of recurrence identified additional predictors: male gender, smoking, living alone, plantar location, retinopathy, nephropathy, neuropathy, foot deformity, and peripheral arterial disease. These features help prioritize prevention. [16]

For infections/osteomyelitis, the risks include a long-standing, non-healing ulcer, large size and depth, location over a bone or joint, and visible bone on probing. Such findings increase the likelihood of osteomyelitis and require enhanced diagnostic testing. [17]

Finally, systemic factors (chronic kidney disease, cardiovascular disease), decompensated diabetes, and inadequate education shorten the path from callus to ulcer and from ulcer to infection. Educational programs and preventative footwear are as important as dressings. [18]

Table 3. What increases the risk of ulcers and their recurrence

Factor group	Examples
Local	Neuropathy, deformity, calluses/corns, dry skin
Vascular	Peripheral arterial disease, low perfusion
Systemic	Nephropathy, retinopathy, prolonged decompensation
Behavioral	Smoking, inappropriate footwear, poor grooming habits

Pathogenesis

The pathogenesis is multifactorial. Neuropathy deprives the foot of pain feedback, alters gait, and increases local pressure; autonomic neuropathy impairs sweating, increasing dryness and brittleness of the skin. This sets the stage for microtrauma and hidden internal hemorrhages under the calluses. [19]

Mechanical stress is the primary immediate driver of ulcer formation. According to the IWGDF, reducing pressure under the affected area with a permanent knee unloading device (total contact cast or equivalent) is the most powerful way to accelerate the healing of neuropathic plantar ulcers. [20]

Ischemia reduces the flow of oxygen and nutrients, inhibits granulation and epithelialization, and increases the risk of necrosis and infectious complications. Therefore, when signs of ischemia are detected, the algorithm always includes an early vascular consultation and a revascularization plan. [21]

Infection perpetuates a "vicious cycle": inflammation destroys tissue, increasing oxygen demand, while ischemia fails to meet it; abscesses, phlegmon, and osteomyelitis develop. Proper stratification of infection according to the IWGDF/IDSA determines the indications for hospitalization, the choice of antibiotics, and the extent of surgery. [22]

Symptoms

Most neuropathic ulcers are painless due to decreased sensitivity. The patient may notice a oozing sore under the callus, an unpleasant odor, or marks on the toe. Signs of inflammation—redness, swelling, warmth, pain—may be diminished with neuropathy, so it's important to examine the feet daily. [23]

Infections are characterized by increasing exudate, foul odor, pus, swelling, and redness. Systemic signs (fever, weakness) are common in moderate to severe infections; such patients require urgent evaluation and often hospitalization. [24]

Ischemic ulcers are often painful, localized on the toe tips and lateral margin of the foot, bleed poorly during debridement, and granulate slowly. They are accompanied by cold feet, weak arterial pulsation, and intermittent claudication. [25]

Osteomyelitis can be suspected based on the depth of the wound, its location above the bone, a positive bone probe test, lack of healing for >6 weeks with adequate unloading and care, and changes on an X-ray or magnetic resonance imaging. [26]

Classification, forms and stages

There are several classifications, and they are used in parallel. Wagner is a simple classification based on depth: from 0 (intact skin) to 5 (healing of the entire foot). Its convenience lies in its "quick" description of depth, but it does not take infection and ischemia into account separately. [27]

The University of Texas (UT) is adding a "depth x infection/ischemia" matrix: grading 0-3 by depth and AD stages based on the presence of infection and ischemia. This system is better at predicting amputations because it takes into account critical risk components. [28]

The IWGDF/IDSA-PEDIS scale is used for infection: 1 - no infection, 2 - mild, 3 - moderate, 4 - severe (with systemic reaction). This scale standardizes the choice of antibiotics and indications for hospitalization. [29]

To assess limb risk and plan revascularization, the WIfI (Wound-Ischemia-foot Infection) score is used: separate gradations for each axis (0-3) predict the risk of amputation and the likelihood of limb salvage. WIfI is a "bridge" between surgeons, vascular specialists, and wound care specialists. [30]

Table 4. “Working set” of classifications

System	What does it evaluate?	When to use
Wagner	Depth/gangrene (0-5)	Quick Depth Description
UT (Texas)	Depth × infection/ischemia	Amputation prognosis/choice of tactics
IWGDF/IDSA (PEDIS)	Severity of infection (1-4)	Antibiotic/hospitalization decision
WIfI (SVS)	Wound, ischemia, infection (0-3 on each axis)	Revascularization plan/limb threat assessment

Complications and consequences

The most common complications are soft tissue infections, abscesses, cellulitis, osteomyelitis, and sepsis. Deep and chronic ulcers, ischemia, and delayed presentation increase the risk. IWGDF/IDSA recommend antibiotics for 1–2 weeks for clinical signs of infection (soft tissue), extended to 3–4 weeks in cases of slow response or severe ischemia; for osteomyelitis, up to 6 weeks; or up to 3 weeks after minor amputation with positive resection margins. [31]

Amputations remain common outcomes of uncontrolled infection and ischemia. Multidisciplinary teams, early offloading and revascularization, and early infection detection protocols reduce the risk of major amputations. Recurrent ulcers after healing are the main driver of new hospitalizations. [32]

The consequences for quality of life are significant: pain (including neuropathic pain), limited mobility, loss of employment, and depression. At the population level, ulcers contribute significantly to healthcare system costs, justifying prevention and early intervention programs. [33]

When to see a doctor

Seek immediate medical attention if a wound, blister, bloody spot under a callus, crack, or foul odor is detected. A diabetic patient should not "monitor" the ulcer at home for more than 1-2 days – early examination and rest are critical for prognosis. [34]

Signs of infection require immediate evaluation: increasing pain (even with neuropathy), redness, swelling, pus, fever, and streaks along the lymphatic vessels. In cases of moderate/severe infection and the presence of severe comorbidities, hospitalization is indicated. [35]

If signs of ischemia are present (pain at rest, coldness, pallor/cyanosis of the fingers, weak pulse), a vascular consultation is necessary to decide on revascularization. Delays worsen the chances of limb preservation. [36]

If the ulcer has not decreased by ≥50% in 4-6 weeks with adequate unloading and care, the tactics need to be reviewed: exclude ischemia, latent bone infection, discuss advanced interventions. [37]

Diagnostics

Step 1. Screening of every patient with diabetes. Inspection of feet and footwear at each visit; testing of sensitivity (10 g monofilament) and vibration (128 Hz tuning fork); assessment of deformities, calluses, and cracks. This allows for the early detection of pre-ulcerative conditions. [38]

Step 2. Infection assessment. Stratify according to IWGDF/IDSA (1-4): mild - local signs, moderate - deep/widespread changes, severe - systemic reaction. Decide on hospitalization and initial empirical therapy; antibiotics are not indicated if there are no signs of infection. [39]

Step 3. Ischemia assessment. Ankle-brachial index, finger tonometry, and transcutaneous oximetry are used when available; if chronic limb-threatening ischemia is suspected, vascular imaging and consideration of revascularization are performed. The WIfI is used for prognosis. [40]

Step 4. Exclusion of osteomyelitis. The "bone probe" is a simple test: pooled sensitivity ≈0.87, specificity ≈0.83 in a meta-analysis; X-ray is the first step (but changes may be delayed by 10-14 days), magnetic resonance imaging is the most accurate method available; if possible, a bone biopsy for verification and microbiology. The combination of "X-ray + bone probe" increases accuracy. [41]

Step 5. Basic tests and "get ready." Complete blood count, inflammation markers (C-reactive protein), glycosylated hemoglobin, kidney and liver profile; in case of infection, take a deep swab after cleaning the wound (not a surface swab) before starting antibiotics. Next comes an individualized treatment plan. [42]

Table 5. Minimum diagnostic kit for foot ulcer

Block	What are we doing?	For what
Examination + neuro	Monofilament, tuning fork, deformations, footwear	Identify neuropathy and pressure points
Infection	IWGDF/IDSA stratification, depth seeding	Decide on antibiotics/hospitalization
Ischemia	Ankle-brachial index, finger pressures, WIfI	Plan revascularization
Osteomyelitis	Bone probe, X-ray → magnetic resonance imaging; biopsy	Confirm/rule out bone infection
Overall rating	Glycated hemoglobin, inflammatory markers, organ function	Assess the background and risks of therapy

Differential diagnosis

Neuropathic vs. ischemic ulcers. Neuropathic ulcers are usually painless, located on the sole under pressure zones, surrounded by calluses and hyperkeratosis, with warm skin and preserved pulse. Ischemic ulcers are painful, located distally (toe tips, lateral margin), with cool skin and weakened pulse. Sometimes a mixed ulcer is encountered, and management should consider both components. [43]

Infection vs. colonization. The presence of bacteria does not equal infection: we focus on clinical signs (pus, erythema, swelling, pain, warmth), the depth of the lesion, and systemic symptoms. Antibiotics do not accelerate healing for a "clean" uninfected ulcer and are not indicated. [44]

Osteomyelitis vs. soft tissue infection. A positive bone probe test, failure to heal for >6 weeks, and changes on magnetic resonance imaging (MRI) support the diagnosis of osteomyelitis; when in doubt, consider the combination of clinical presentation, imaging, and, when possible, bone biopsy. [45]

Other ulcers. Venous (medial malleolus, hyperpigmentation), arterial (distal areas, "stamped" edges), pressure/bedsores (over bony prominences in sedentary individuals), vasculitis, and tumors are considered based on clinical presentation and instrumental diagnostic data. The correct ulcer type changes the treatment strategy. [46]

Treatment

Offloading is the foundation. For neuropathic plantar ulcers, the first choice is a permanent knee offloading device: a total contact cast or a permanent knee walker (modified to a permanent one). If there are contraindications/intolerances, removable walkers (preferably knee walkers) are used, and if these are unavailable, felt foam with appropriate footwear is used as a third line. Offloading is also effective for mild infection or mild ischemia, but in moderate-to-severe conditions, infection/blood flow stabilization is first recommended. [47]

Surgical correction of overload. For recurrent ulcers over the metatarsal heads after failure of conservative unloading, a metatarsal osteotomy is possible; for ulcers on the toes due to flexion deformity, a flexor tenotomy is recommended (for toes 2-5, this is a "strong" recommendation). Such minimally invasive interventions reduce local pressure and the risk of recurrence. [48]

Wound care and debridement. Regular gentle/sharp debridement removes necrotic tissue and calluses, reduces bioburden, and relieves pressure at the edges. Moist wound healing is promoted (with appropriate dressings based on the wound phase and amount of exudate), and maceration and infection are controlled. The IWGDF 2023 Guidelines for "Healing Accelerators" emphasize that no dressing alone can replace offloading, debridement, and background control. [49]

Antibiotics - only in case of infection. For mild soft tissue infection - 1-2 weeks; for moderate/severe and after adequate debridement - usually 10-14 days; for osteomyelitis without bone resection - ≈6 weeks, and after "minor" amputation with positive margins - up to 3 weeks. Start empirically based on local microbial profiles and severity, then de-escalate based on culture. [50]

Diagnosis and treatment of osteomyelitis. If there is a high suspicion, magnetic resonance imaging is performed; if possible, a bedside percutaneous bone biopsy is safe and improves targeted therapy. Osteomyelitis remission is assessed at least 6 months after discontinuing antibiotics. Surgical bone debridement accelerates infection control, reducing the duration of antibiotic therapy. [51]

Revascularization in ischemia. In chronic limb-threatening ischemia, the choice between endovascular and bypass reconstruction is determined by anatomy, risk, and WIfI profile: with high anatomical complexity and acceptable risk, a vein bypass is often preferred, while with less complex anatomy and high surgical risk, an endovascular approach is preferred. All patients are prescribed "best medical treatment" (antithrombotics, statins, blood pressure and glycemic control, smoking cessation). [52]

Negative pressure wound therapy (NPWT). In patients with post-surgical debridement and significant exudate, NPWT may accelerate healing and reduce the risk of amputation, according to systematic reviews, although the quality of evidence is low. This method should be considered as an adjuvant to basic therapy (offloading, debridement, infection/blood flow control). [53]

Hyperbaric oxygen therapy (HBO). In the IWGDF 2023-2024 guidelines, HBO may be considered as an adjunct for neuroischemic/ischemic ulcers when standard therapy is ineffective, particularly for Wagner II-IV. Moderate-quality evidence suggests an improved likelihood of healing, but the decision is made on an individual basis, taking into account availability and contraindications. [54]

Biocoatings/cellular tissues and "accelerators." Tissue-cell equivalents, growth factors, platelet-rich plasma, etc. may be considered for ulcers that do not improve by ≥50% within 4-6 weeks with adequate background therapy. The IWGDF emphasizes that their use should be followed by optimization of offloading, debridement, infection control, and blood flow; otherwise, there will be no effect. [55]

Education, footwear, and recurrence prevention. After healing, consider custom-fitted insoles and orthopedic shoes, regular checkups, skin and nail care, and avoiding barefoot walking. The goal is to reduce recurrent stress and prevent the very likely recurrence. Programs involving a multidisciplinary team reduce the risk of recurrent ulcers and amputations. [56]

Table 6. Treatment options and their role

Intervention	Role	Key Notes
Non-removable TCC / "non-removable" walker	First line for neuropathic plantar ulcers	The most powerful relief effect
Removable walker / felted foam	Alternatives in case of contraindications/unavailability	Requires high commitment
Antibiotics	Only in case of infection	1-2 weeks skin/soft tissue; up to 6 weeks for osteomyelitis
Revascularization	In case of ischemia	Choice by anatomy and risk (GVG, WIfI)
NPWT	Adjuvant	May speed up healing after debridement
LPG	Adjuvant for neuroischemic ulcers	Consider if basic therapy is ineffective
Overload surgery	Relapse prevention	Tenotomies, osteotomies according to indications

Prevention

Prevention begins with daily self-examination: check the soles and spaces between the toes, use a mirror or have a loved one help you, and immediately report any skin damage to your doctor. Proper hygiene, neat nail trimming, callus control, and avoiding self-debridement are important. [57]

Footwear and insoles are key: soft, seamless materials, sufficient toe space, and custom-fitted insoles to redistribute pressure; for high-risk individuals, preventative relief solutions. Footwear should be regularly inspected for foreign bodies and wear. [58]

Glycemic control, smoking cessation, and correction of dyslipidemia and blood pressure reduce the risk of recurrence and amputation. Frequent visits and inclusion in multidisciplinary programs are recommended for patients with neuropathy and/or a history of ulcers. [59]

After healing, follow-up during the first year is critical: visits every 1-3 months, re-fitting of insoles/shoes, and training in recognizing "hot spots." This is the time of greatest risk of relapse. [60]

Forecast

The prognosis is determined by the three "I's": infection, ischemia, and the intensity of unloading. With early treatment, adequate unloading, and the absence of ischemia, most neuropathic ulcers heal. With ischemia without revascularization and inadequate unloading, the risk of chronicity, infection, and amputation is significantly higher. [61]

Once healing has occurred, prevention is paramount: without it, the risk of recurrence is high within the first year. Education, footwear, and team management improve long-term outcomes and reduce mortality. [62]

In osteomyelitis, remission is assessed at least 6 months after the end of antibiotic treatment; with timely bone debridement and optimization of blood flow, the chances are higher. The choice of tactics should be individualized, with priority given to limb preservation. [63]

FAQ

Is it true that every ulcer should be treated immediately with antibiotics? No. Antibiotics are only indicated if there are clinical signs of infection. For a "clean" ulcer, antibiotics do not speed healing and are unnecessary. [64]

What's the most important thing for healing a neuropathic plantar ulcer? Offloading. According to the IWGDF, a permanent knee offloading device (total contact cast or equivalent) is the first choice. Dressings and "accelerators" only work in conjunction with offloading. [65]

How do you know if you have osteomyelitis? Suspect it if there is a deep ulcer over the bone, no progression for more than 6 weeks, or a positive bone probe test. Magnetic resonance imaging and, if possible, a bone biopsy are optimal for confirmation. [66]

When is revascularization needed? When there are signs of ischemia and a non-healing ulcer. The decision is made by vascular specialists based on the WIfI and global vascular guidelines; the strategy (endovascular or bypass) depends on anatomy and risk. [67]

Additional table: step-by-step plan for the initial appointment

Table 7. Five steps for managing diabetic ulcers at the doctor’s office

Step	Action	Tools
1	Confirm the ulcer type and assess the pressure	Inspection, monofilament, shoe inspection
2	Stratify the infection	IWGDF/IDSA; decide on antibiotics/hospitalization
3	Assess ischemia	Ankle-brachial index, finger pressures; WIfI
4	Rule out osteomyelitis	Bone probe, X-ray → magnetic resonance imaging; if possible, biopsy
5	Start treatment	Unloading (first line), debridement, wound care; in case of ischemia - vascular routing