Diabetic Ulcers
Diabetic foot ulcers (DFUs) are among the most serious, costly and feared long-term complications of diabetes. They are the leading cause of hospital admission and of non-traumatic lower-limb amputation. A foot ulcer signals a chain-reaction breakdown of the skin’s mechanical protection, the microcirculation and local immunity.
How the ulcer develops at the cell and tissue level:
- Peripheral neuropathy:
- Sensory nerves: Chronic high blood sugar causes sorbitol to build up and nerve fibers to degenerate, leading to loss of protective sensation (LOPS). Patients no longer feel pain, heat or repeated minor trauma (such as stubbing a toe or wearing tight shoes).
- Motor nerves: Increased tone and wasting of the small foot muscles distort the foot’s bony structure (hammer toes, claw toes, Charcot foot). This changes how the foot meets the ground and creates points of very high pressure on the sole.
- Autonomic nerves: Reduced or absent sweating (anhidrosis) leaves the skin of the feet dry and rough and strips its natural lipid layer, producing fissures that let microbes in.
- Peripheral artery disease (PAD) and microangiopathy:
- Atherosclerosis progresses quickly in the medium and small arteries below the knee (anterior and posterior tibial arteries), sharply reducing blood supply to the foot.
- Thickened capillary basement membranes hinder the delivery of oxygen, nutrients and immune cells to injured tissue.
- Disrupted healing and persistent chronic inflammation:
- High glucose generates advanced glycation end products (AGEs), which keep macrophages in a pro-inflammatory M1 state, increase release of protein-degrading matrix metalloproteinases (MMPs) and reduce tissue growth factors (PDGF, VEGF).
- As a result, new collagen is broken down as soon as it is made, and the wound stays stuck in a chronic inflammatory phase instead of moving on to proliferation and scar formation.
At Haute-Derma, we manage diabetic foot ulcers on multidisciplinary principles: accurate assessment and grading, pressure off-loading, conservative surgical debridement, modern biological wound cleansing and optimization of whole-body metabolic control.
Clinical Features and the Wagner Classification
A diabetic foot ulcer can start as a blister, a small crack or a callus with bleeding underneath:
- Most Common Sites:
- The main weight-bearing areas of the sole: the metatarsal heads (especially the 1st and 5th), the heel and the underside of the big toe.
- Friction points: the tops of deformed toes and the outer edge of the foot from tight shoes.
- Clinical Features:
- The edge is usually thickened and hyperkeratotic, surrounded by a hard rim of callus.
- The base may show red granulation tissue (if blood supply is good) or gray/black necrotic tissue with foul-smelling mucopurulent discharge (if secondarily infected).
- Usually painless (neuropathic ulcers), or severely painful at rest (ischemic ulcers).
Wagner Ulcer Classification System
| Wagner Grade | Clinical Features and Extent of Damage |
|---|---|
| Grade 0 | No open ulcer. Intact but high-risk skin (thick callus, foot deformity, dryness). |
| Grade 1 | Superficial ulcer limited to the epidermis and dermis, not reaching subcutaneous tissue. |
| Grade 2 | Deep ulcer through subcutaneous tissue exposing tendon, muscle or joint capsule, without deep abscess or bone infection. |
| Grade 3 | Deep ulcer with deep tissue abscess, osteomyelitis or septic arthritis. |
| Grade 4 | Localized gangrene (usually of the forefoot or heel). |
| Grade 5 | Gangrene of the whole foot; limb-sparing treatment is no longer possible. |
Telling Common Types of Foot Ulcer Apart
| Neuropathic Ulcer | Ischemic Ulcer | Venous Stasis Ulcer |
|---|---|---|
| Sole of the foot, pressure points (metatarsal heads, heel) | Toe tips, outer edge of the foot, heel | Ankle and lower leg (gaiter zone) |
| Painless, or numbness and tingling | Severe pain, worse when the leg is raised or at rest, eased by hanging the leg down | Dull ache and heaviness, eased by raising the leg |
| Pulses easily felt | Weak or absent pulses | Pulses present (unless arterial disease coexists) |
| Warm, dry skin with thick callus around the ulcer | Cold, pale or dusky purple skin, hair loss, shiny skin | Gray-brown hardened discoloration (hemosiderin), lower-leg swelling |
| Bright red granulation tissue, moderate discharge | Pale, gray/black necrotic base, very little discharge | Shallow base, heavily exuding granulation tissue |
Management and Treatment at Haute-Derma
Haute-Derma’s approach to diabetic foot ulcers follows the international TIME model (Tissue – Infection – Moisture – Edge):
Initial Assessment and Screening
- Nerve function and protective sensation: A 10 g Semmes-Weinstein monofilament test at 10 standard sites on the foot, plus a 128 Hz tuning fork to check vibration sense.
- Peripheral blood flow: We feel the dorsalis pedis and posterior tibial pulses and measure the ankle-brachial index (ABI). If the ABI is below 0.8, a Doppler ultrasound is arranged to look for arterial narrowing or blockage.
- Screening for osteomyelitis: A probe-to-bone test. If a sterile metal probe touches hard bone at the base of the ulcer, the likelihood of bone infection exceeds 85%, and an X-ray or MRI of the foot is needed.
- Systemic laboratory tests: HbA1c, complete blood count, CRP, erythrocyte sedimentation rate (ESR) and a wound culture with antibiotic sensitivities.
Specialist Treatment Plan
- Off-loading – the deciding factor: All mechanical pressure must be taken off the ulcer using dedicated devices: custom orthopedic shoes or sandals, a removable walker or a non-removable total contact cast (TCC).
- Standardized surgical debridement: Thorough removal of necrotic tissue, slough, bacteria and the hard callus around the ulcer frees the body’s own growth factors and moves the wound from chronic inflammation back into an active healing phase.
- Moist wound healing and advanced dressings:
- Dressings are chosen according to how much the wound is draining:
- Heavy drainage or infection: Gel-forming alginate dressings or antimicrobial silver foam dressings.
- Moderate or light drainage: Moisture-retaining hydrocolloid or hydrogel dressings, which speed autolytic breakdown of dead tissue.
- Dressings are chosen according to how much the wound is draining:
- Whole-body optimization and blood sugar control:
- Close collaboration with endocrinologists to adjust insulin and bring HbA1c below the 7.0% target.
- Systemic antibiotics guided by culture results for Wagner grade 2 ulcers with soft-tissue infection, or grade 3 and above.
What to Avoid with a Diabetic Foot Ulcer
- Do not soak the feet in hot water (above 37–40 °C) or in herbal or leaf preparations of unknown origin: Without temperature sensation, patients cannot judge how hot the water is and can suffer deep burns. Non-sterile water can also carry bacteria deep into the ulcer bed and cause sepsis.
- Do not keep walking and loading the foot without an off-loading device: Walking on the ulcer crushes newly formed tissue, undoes the debridement and drives bacteria deeper toward tendon and bone.
- No aggressive or extensive debridement of severely ischemic ulcers (ABI below 0.5) before blood flow has been restored: Debriding tissue that has no blood supply makes the ulcer spread rapidly and turn into irreversible dry gangrene.
- Do not sprinkle antibiotic powders, apply traditional remedies or plasters, or use corticosteroid creams on the ulcer: Dry antibiotic powder forms a crust that seals the wound and lets anaerobic bacteria flourish underneath; corticosteroids suppress healing and raise the risk of spreading infection.
