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EMERGENCY

Diabetic Foot Ulcer

High EvidenceUpdated: 2025-12-24

On This Page

Red Flags

  • Deep Abscess / Plantar Sepsis
  • Gas Gangrene (Necrotising Fasciitis)
  • Wet Gangrene (Ischaemia + Infection)
  • Systemic Sepsis (Silent in diabetics)
  • Probe-to-Bone Positive (Osteomyelitis)
Overview

Diabetic Foot Ulcer

1. Clinical Overview

Summary

A Diabetic Foot Ulcer (DFU) is a full-thickness wound below the ankle in a patient with diabetes, resulting from the complex interplay of Neuropathy (loss of protective sensation), Ischaemia (Peripheral Arterial Disease), and Deformity (Motor neuropathy). It is the leading cause of non-traumatic lower limb amputation globally. Management requires a multidisciplinary "High Risk Foot Team" approach. The cornerstone of treatment is Offloading (Total Contact Cast), Infection Control, Revascularisation if ischaemic, and Excision of osteomyelitic bone. The risk of death following a major diabetic amputation is higher than that of many cancers (50% at 5 years).

Key Facts

  • Lifetime Risk: 25% of diabetics will develop a foot ulcer.
  • Amputation: 85% of amputations are preceded by a DFU.
  • The Triad: Neuropathy + Deformity + Trauma = Ulcer.
  • Osteomyelitis: If you can probe bone with a metal instrument, osteomyelitis is present until proven otherwise (Probe-to-Bone positive).
  • Ischaemia: Often macrovascular ("Tibial vessel disease") with calcification (Monckeberg's medial sclerosis).
  • Gold Standard: Total Contact Cast (TCC) for offloading neuropathic ulcers.

Clinical Pearls

"Probe to Bone": Use a sterile metal probe. If you hit something hard and gritty at the base of the ulcer, the Positive Predictive Value for Osteomyelitis is >90%.

"Assume Sepsis": Diabetics are often immunosuppressed. They may have a foot full of pus (deep plantar abscess) but have NO fever, NO tachycardia, and normal CRP. Pain or unexplained hyperglycaemia might be the only sign.

"Don't Trust the ABPI": In diabetics, vessel walls are calcified (stiff pipes). The cuff cannot compress them, giving falsely elevated readings (>1.3). You MUST use Toe Pressures (TBPI) or Waveforms.

"It's not the sugar, it's the shoe": Most ulcers are caused by repetitive trauma from ill-fitting shoewear on a numb, deformed foot.


2. Epidemiology

Incidence

  • Global Burden: Every 20 seconds, a limb is lost to diabetes somewhere in the world.
  • Prevalence: 4-10% of diabetics have an active ulcer.
  • Mortality: 5-year mortality after DFU is 40%; after Major Amputation is 50-70%.

Risk Factors (The "Foot at Risk")

  • History of Ulcer: Strongest predictor of recurrence.
  • Neuropathy: Loss of 10g monofilament sensation.
  • PVD: Absent pulses.
  • Deformity: Hammer toes, Charcot foot.
  • Poor Glycaemic Control: HbA1c >7%.
  • Smoking.

3. Pathophysiology

1. Neuropathy (The Driver)

Diabetes damages nerves in three ways:

  • Sensory: Loss of pain/temperature/proprioception. Patient steps on a tack/stone and keeps walking. "Painless trauma".
  • Motor: Atrophy of intrinsic foot muscles (Lumbricals/Interossei). leads to "Intrinsic Minus" foot -> Claw toes -> Prominent metatarsal heads -> High pressure points.
  • Autonomic: Loss of sweating (Anhidrosis). Skin becomes dry/cracked (fissures). AV shunting (warm, distended veins but shunted blood bypasses tissue).

2. Ischaemia (The Healer blocker)

  • Macrovascular: Atherosclerosis of Tibial/Peroneal arteries. Often multisegmental.
  • Microvascular: Capillary basement membrane thickening. Impairs diffusion (but rarely the primary cause of ulceration).

3. Infection (The Destroyer)

  • Hyperglycaemia impairs neutrophil function (chemotaxis/phagocytosis).
  • Rich environment for bacteria.
  • Polymicrobial (Staph, Strep, Gram negs, Anaerobes).

4. Clinical Presentation

Types of Ulcer

  1. Neuropathic Ulcer:
    • Site: Plantar surface (Metatarsal heads, Heel, Tops of claw toes).
    • Appearance: Punched out, deep, surrounded by thick callus ("Hyperkeratotic rim").
    • Pain: Painless.
    • Pulses: Palpable (often bounding due to autonomic shunting).
  2. Neuro-Ischaemic Ulcer:
    • Site: Margins of foot, Digits.
    • Appearance: Sloughy base, irregular edges, scant callus.
    • Pain: May be painful (if some nerve function left) or painless.
    • Pulses: Absent. Foot is cool.

Signs of Infection


Local
Redness (Cellulitis >2cm), Warmth, Swelling, Purulence, Odour.
Systemic
Fever, Tachycardia, Hypotension, Confusion (Sepsis). Remember these may be absent!
5. Clinical Examination

The "3-Minute Foot Exam"

  1. Look: Skin breaks? Callus? Deformity (Claw toes)? Colour?
  2. Feel: Temperature (Hot = Charcot or Infection; Cold = Ischaemia). Pulses (DP/PT).
  3. Test:
    • Monofilament (10g): Test 10 sites. Failure to feel = Loss of Protective Sensation (LOPS).
    • Probe: Sterile probe into any ulcer.

6. Investigations

Bedside

  • ABPI: Unreliable >1.3.
  • Toe Brachial Pressure Index (TBPI): >0.7 is normal. <0.3 is critical ischaemia.
  • Transcutaneous O2 (TcPO2): Predicts healing potential. >30mmHg required relative healing.

Imaging

  • X-ray: Look for Osteomyelitis (Erosion, periosteal reaction), Gas in soft tissue, Charcot deformity.
  • MRI: Most sensitive for Osteomyelitis (90%).
  • Bone Scan: Useful if MRI impossible.

Microbiology

  • Deep Tissue Sample: Gold standard. Curette the base after cleaning.
  • Swab: Generally useless (picks up colonisers). Only swab if pus is expressing.

7. Classifications

Wagner Classification (Old but common)

  • Grade 0: Intact skin (High risk).
  • Grade 1: Superficial ulcer.
  • Grade 2: Deep ulcer (to tendon/bone).
  • Grade 3: Deep ulcer + Abscess/Osteomyelitis.
  • Grade 4: Forefoot Gangrene.
  • Grade 5: Whole foot Gangrene.

University of Texas (Modern)

Matrix of Depth (0-3) vs Infection/Ischaemia (A-D). Better prognostic value.


8. Management Algorithm
          DIABETIC FOOT ULCER
                   ↓
┌─────────────────────────────────────────┐
│        ASSESS: VIP (Vascular,           │
│        Infection, Pressure)             │
└─────────────────────────────────────────┘
        ↙          ↓            ↘
   ISCHAEMIC?    INFECTED?     NEUROPATHIC?
      │            │              │
      ↓            ↓              ↓
┌───────────┐ ┌───────────┐ ┌────────────────┐
│ RE-VASC   │ │ ANTIBIOTIC│ │ OFFLOADING     │
│ - Angio   │ │ - Debride │ │ - TCC (Cast)   │
│ - Bypass  │ │ - Drain   │ │ - Reduct. Shoe │
│           │ │ - Amputat │ │ - Callus cut   │
└───────────┘ └───────────┘ └────────────────┘

1. Infection Management (Source Control)

  • "Time is Tissue".
  • Deep Abscess: Needs urgent surgical drainage (Incision & Drainage).
  • Osteomyelitis:
    • Medical: 6 weeks IV/Oral antibiotics (high bone penetration e.g., Doxycycline, Ciprofloxacin, Rifampicin).
    • Surgical: Resection of infected bone (e.g., digit amputation, metatarsal head resection).

2. Vascular Management

  • If pulses absent or TBPI <0.5 -> Urgent Vascular Referral.
  • Angioplasty (Balloon) is commonest intervention for tibial vessels.

3. Pressure Management (Offloading)

  • Total Contact Cast (TCC): Gold standard. Forces compliance. Distributes pressure over whole leg. 90% healing rate in 6-8 weeks.
  • Removable Walker (Moonboot): Patient can take it off (Poor compliance).
  • Felt Padding: Temporary.

9. Surgical Atlas: Amputations

Often the most effective way to restore function and remove infection.

1. Ray Amputation

  • Removing a toe and its metatarsal.
  • Indication: Osteomyelitis of MTPJ or Metatarsal Head.
  • Leaves a narrower functional foot.

2. Transmetatarsal Amputation (TMA)

  • Removing all toes and metatarsal heads.
  • Indication: Gangrene of multiple toes / forefoot.
  • Preserves the heel/ankle for walking. Requires Achilles Lengthening to prevent equinus.

3. Major Amputation (BKA/AKA)

  • Below Knee (Transtibial): Preserves knee joint. Energy expenditure for walking is much lower than AKA.
  • Above Knee (Transfemoral): For extensive gangrene. Rehabilitation is harder.

10. Technical Appendix: Charcot Neuroarthropathy

A separate topic, but linked.

  • Definition: Acute inflammatory destruction of bone/joints in neuropathic foot.
  • Presentation: Resembles Cellulitis (Red, Hot, Swollen).
  • Distinction: Elevate the leg. Charcot redness fades; Cellulitis stays red.
  • Treatment: STRICT IMMOBILISATION (Cast) until cooling occurs.

11. Evidence and Guidelines

Key Guidelines

  1. IWGDF Guidelines (International Working Group on the Diabetic Foot): The global bible.
  2. NICE NG19: Diabetic foot problems.

Key Trials

  1. Eurodiale Study: Large cohort. Showed infection + ischaemia = worst prognosis.
  2. TCC Evidence: Multiple RCTs confirm TCC is superior to removable devices for healing.

12. Patient/Layperson Explanation

What is a Diabetic Foot Ulcer?

It is a wound on the foot of someone with diabetes. Because diabetes damages the nerves, you might not feel pain when you get a blister or stone in your shoe. This turns into a deep sore.

Why is it dangerous?

Because the blood supply is often poor, these wounds heal very slowly. Germs (bacteria) can get in and spread to the bone. If not treated quickly, this can lead to gangrene and amputation.

What is the treatment?

  1. Take the pressure off: You may need a special cast or boot. You cannot walk on the wound.
  2. Clean it: A specialist will remove dead skin (callus).
  3. Blood flow: We check if you need a procedure to open blocked arteries.
  4. Antibiotics: If there is infection.

How do I prevent it?

  • Check your feet EVERY DAY (use a mirror for the bottom).
  • Never walk barefoot.
  • Get your feet checked by a podiatrist regularly.
  • Keep your blood sugar controlled.

13. References
  1. Schaper NC, et al. IWGDF Guidelines on the prevention and management of diabetic foot disease. Diabetes Metab Res Rev. 2020.
  2. Armstrong DG, et al. Diabetic Foot Ulcers and Their Recurrence. N Engl J Med. 2017.

(End of File)

Last updated: 2025-12-24

At a Glance

EvidenceHigh
Last Updated2025-12-24
Emergency Protocol

Red Flags

  • Deep Abscess / Plantar Sepsis
  • Gas Gangrene (Necrotising Fasciitis)
  • Wet Gangrene (Ischaemia + Infection)
  • Systemic Sepsis (Silent in diabetics)
  • Probe-to-Bone Positive (Osteomyelitis)

Clinical Pearls

  • **"Probe to Bone"**: Use a sterile metal probe. If you hit something hard and gritty at the base of the ulcer, the Positive Predictive Value for Osteomyelitis is &gt;90%.
  • **"It's not the sugar, it's the shoe"**: Most ulcers are caused by repetitive trauma from ill-fitting shoewear on a numb, deformed foot.
  • Prominent metatarsal heads -
  • High pressure points.
  • Urgent Vascular Referral.

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines