Introduction

Diabetic foot ulcers (DFUs) are one of the most common and serious complications of diabetes mellitus and are a major cause of hospitalization, lower-extremity amputation, disability, and mortality. They result from the interaction of peripheral neuropathy, peripheral arterial disease (ischaemia), repetitive trauma, and infection, leading to skin breakdown and impaired wound healing. Secondary infection commonly involves Staphylococcus aureus, streptococci, Enterobacterales (coliforms), and anaerobic bacteria, and may progress to cellulitis, abscess formation, gangrene, osteomyelitis, or sepsis if not promptly treated.

Early recognition, multidisciplinary management, optimal glycaemic control, pressure off-loading, appropriate antibiotic therapy, and timely surgical intervention are essential to improve limb salvage and reduce mortality.

Epidemiology

• Affects approximately 15–25% of patients with diabetes during their lifetime.

• The leading cause of non-traumatic lower limb amputation worldwide.

• More common in patients with long-standing diabetes.

• Frequently associated with peripheral neuropathy and peripheral arterial disease.

• High recurrence rate after ulcer healing.

Etiology

Diabetic foot ulcers develop due to the combined effects of:

• Peripheral sensory neuropathy

• Peripheral motor neuropathy

• Peripheral autonomic neuropathy

• Peripheral arterial disease

• Repetitive mechanical trauma

• Foot deformities

• Poor glycaemic control

• Secondary bacterial infection

Common causative organisms include:

• Staphylococcus aureus

• β-haemolytic streptococci

• Enterobacterales (coliform bacteria)

• Pseudomonas aeruginosa (selected chronic wounds)

• Anaerobic bacteria in deep or necrotic infections

Risk factors

• Long-standing diabetes mellitus

• Poor glycaemic control

• Peripheral neuropathy

• Peripheral arterial disease

• Previous foot ulcer

• Previous lower-limb amputation

• Foot deformities

• Charcot foot

• Chronic kidney disease

• Cigarette smoking

• Visual impairment

• Inappropriate footwear

• Limited joint mobility

Pathophysiology

Diabetic foot ulceration develops through the interaction of neuropathy, ischaemia, and infection. Peripheral sensory neuropathy results in loss of protective sensation, allowing repeated minor trauma to go unnoticed. Motor neuropathy causes muscle imbalance and foot deformities, creating areas of abnormally high plantar pressure that predispose to skin breakdown. Autonomic neuropathy reduces sweating, producing dry, cracked skin that is more susceptible to ulceration. Peripheral arterial disease impairs tissue perfusion and oxygen delivery, delaying wound healing and reducing host defence. Once the skin barrier is disrupted, bacteria colonize and infect the wound. In severe cases, infection spreads into deeper tissues causing cellulitis, abscess formation, osteomyelitis, gangrene, and systemic sepsis.

Classification

According to Wagner's classification

Clinical note

• Grades 1–3 are classified as non-gangrenous ulcers.

• Grades 4–5 are classified as gangrenous ulcers.

Clinical presentation

The three principal mechanisms leading to tissue necrosis are:

• Peripheral neuropathy

• Infection

• Ischaemia

Patient may present with:

• Foot ulcer

• Purulent discharge

• Foot swelling

• Local warmth

• Erythema

• Foul-smelling wound

• Pain (may be absent because of neuropathy)

• Loss of protective sensation

• Foot deformity

• Callus formation

• Black discoloration indicating gangrene

• Fever in severe infection

• Difficulty walking

• Signs of systemic sepsis in advanced disease

Diagnostic criteria

A diabetic foot ulcer is diagnosed in a patient with diabetes who has:

• A full-thickness break in the skin below the malleoli

• Clinical evidence of neuropathy and/or peripheral arterial disease

• Assessment of infection using clinical signs (erythema, warmth, swelling, tenderness, purulent discharge)

• Ulcer classification using the Wagner grading system

• Evaluation for underlying osteomyelitis and limb ischaemia where indicated

Investigations

Laboratory investigations

• Complete blood count

• C-reactive protein

• Erythrocyte sedimentation rate

• Blood glucose

• HbA1c

• Renal function tests

• Serum electrolytes

• Blood cultures (if systemic infection is suspected)

• Deep tissue or wound culture and sensitivity after debridement

Imaging

Plain X-ray

Useful for detecting:

• Osteomyelitis

• Foreign bodies

• Gas in soft tissues

• Charcot arthropathy

MRI

Most sensitive investigation for:

• Early osteomyelitis

• Deep abscess

• Extent of soft tissue infection

Duplex Doppler ultrasound

Assessment of peripheral arterial disease.

CT angiography or conventional angiography

When vascular intervention is being considered.

Differential diagnosis

• Venous leg ulcer

• Arterial ulcer

• Pressure ulcer

• Vasculitic ulcer

• Charcot neuroarthropathy

• Osteomyelitis without ulcer

• Malignant ulcer (Marjolin ulcer)

Management

Treatment aims to:

• Control infection

• Achieve optimal glycaemic control

• Promote wound healing

• Relieve pressure

• Restore tissue perfusion where possible

• Prevent amputation

• Reduce recurrence

Non-pharmacological management

• Optimise metabolic (glycaemic) control

• Pressure off-loading with non-weight bearing where appropriate

• Smoking cessation

• Regular wound care and dressing changes

• Frequent removal of callus and excess keratin

• Adequate drainage of infected wounds

• Appropriate footwear

• Nutritional optimisation

• Patient education on daily foot inspection

• Management of peripheral arterial disease

• Multidisciplinary diabetic foot care

Pharmacological treatment

Empirical antibiotic therapy

Ceftriaxone

• 1–2 g intravenously once daily for 7–10 days

AND

Metronidazole

• 500 mg intravenously every 8 hours for 7–10 days

Treatment guided by culture and sensitivity

Piperacillin–tazobactam

• 4.5 g intravenously every 6–8 hours for 7–10 days (severe or complicated infections)

OR

Meropenem

• 1 g intravenously every 8 hours for 7–10 days

Surgical management

Surgical treatment depends on the severity of infection and Wagner grade.

Procedures may include:

• Surgical debridement of necrotic tissue

• Drainage of abscesses

• Minor amputations (toe or ray amputation)

• Major amputations where limb salvage is not feasible according to Wagner classification

• Revascularization procedures for patients with critical limb ischaemia when appropriate

Rehabilitation

• Pressure redistribution

• Gradual mobilisation

• Protective footwear

• Custom orthoses

• Physiotherapy

• Gait training following amputation where required

• Patient education to prevent recurrence

Monitoring and follow-up

Patients should be reviewed regularly to assess:

• Ulcer size and depth

• Presence of infection

• Glycaemic control

• Vascular status

• Neurological status

• Response to antibiotic therapy

• Wound healing progress

• Need for further debridement or vascular intervention

Patients with severe infection, gangrene, limb ischaemia, or suspected osteomyelitis should be referred urgently to specialist diabetic foot services.

Complications

• Cellulitis

• Deep soft tissue abscess

• Osteomyelitis

• Septic arthritis

• Necrotizing soft tissue infection

• Gangrene

• Sepsis

• Lower limb amputation

• Recurrent ulceration

• Disability

• Death

Prevention

• Good glycaemic control

• Daily foot inspection

• Appropriate footwear

• Smoking cessation

• Annual comprehensive foot examination

• Prompt treatment of minor foot injuries

• Regular podiatric care

• Management of peripheral arterial disease

• Patient education regarding foot hygiene and early presentation

Prognosis

The prognosis depends on ulcer severity, adequacy of vascular supply, glycaemic control, and promptness of treatment. Superficial ulcers treated early usually heal successfully with appropriate wound care and pressure off-loading. Deep infection, peripheral arterial disease, osteomyelitis, and gangrene substantially increase the risk of limb loss and mortality. Multidisciplinary diabetic foot care has been shown to significantly reduce major amputations and improve long-term outcomes.