Lucan · Conditions

Diabetic foot disease

Australian guidance: Australian Guidelines for Diabetes-Related Foot Disease (Diabetes Feet Australia 2021)

1. Definition and epidemiology

Diabetic foot disease (DFD) encompasses the spectrum of foot complications arising in people with diabetes mellitus, including peripheral neuropathy, peripheral artery disease (PAD), foot deformity, ulceration, infection, and amputation. In Australia, an estimated 50,000 people are living with a diabetes-related foot ulcer (DFU) at any given time, generating approximately 28,000 hospital admissions, 4,500 amputations, and 1,700 deaths each year, at a cost exceeding $AU1.6 billion annually. Aboriginal and Torres Strait Islander peoples face a 3 to 6-fold increased risk of developing DFU and requiring amputation compared with the broader Australian population, making DFD a key target of the Closing the Gap agenda.

2. Pathophysiology

The core pathological triad in DFD is peripheral sensorimotor neuropathy, peripheral artery disease, and impaired immune response, all amplified by chronic hyperglycaemia (Robbins Ch 24). Advanced glycation end-products accumulate in vascular walls and connective tissues, promoting atherosclerosis and reducing vessel compliance. Schwann cell and axonal damage from metabolic and ischaemic injury leads to loss of protective sensation, which eliminates the normal pain-withdrawal reflex. Without this protective feedback, repetitive mechanical plantar pressure accumulates during weight-bearing activity, producing high plantar tissue stress that causes subcutaneous tissue damage and ulceration. Autonomic neuropathy impairs sweating, leading to dry and fissured skin that breaches the epidermal barrier. Concurrent PAD reduces perfusion to the point where even minor wounds cannot heal, and impaired leucocyte chemotaxis and phagocytosis permit rapid bacterial proliferation. Once a wound is established, deep tissue infection can spread rapidly along fascial planes to bone, producing osteomyelitis.

3. Clinical presentation and diagnostic criteria

Patients typically present with a foot wound or pre-ulcerative sign (callus, blister, fissure, haematoma, or erythema) detected incidentally on examination, or with an established ulcer that may be painless due to neuropathy. History should document duration of diabetes, glycaemic control, prior ulceration or amputation, renal function (end-stage renal disease substantially increases risk), and footwear habits. Examination assesses loss of protective sensation using a 10 g monofilament, peripheral pulses, foot deformity including prominent metatarsal heads and Charcot joint changes, and wound characteristics. A diabetes-related foot infection is defined as any infection in tissue distal to the malleolus accompanied by local or systemic signs of inflammation; colonisation of a wound without inflammatory signs does not constitute infection. The IWGDF/IDSA classification grades infection from 1 (uninfected) through 4 (severe, with systemic signs), and this scheme is the AU standard for severity stratification.

4. Investigations and AU-specific cutoffs

Initial investigations target the three pathophysiological pillars. Loss of protective sensation is confirmed with a 10 g Semmes-Weinstein monofilament at specified plantar sites. Vascular assessment uses ankle-brachial index (ABI), with values below 0.9 indicating PAD and values above 1.3 suggesting non-compressible vessels requiring toe-brachial index or waveform analysis instead. For suspected osteomyelitis, the 2021 AU Infection Guideline recommends a combination of the probe-to-bone test, erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) or procalcitonin, and plain X-rays as the initial diagnostic approach. Where plain X-ray and clinical findings are consistent with osteomyelitis, no further imaging is required. When the diagnosis remains uncertain, MRI is the preferred advanced modality; 18F-FDG PET/CT or leucocyte scintigraphy are alternatives. Wound culture should be obtained by aseptic tissue curettage or biopsy from the ulcer bed rather than superficial swab, as swab cultures over-represent colonising flora. Inflammatory biomarkers including CRP and ESR support infection diagnosis when clinical findings are equivocal, with procalcitonin as an adjunct. Blood glucose, HbA1c, renal function, and full blood count complete the initial workup.

5. Management

Management follows a multidisciplinary framework spanning prevention, wound care, offloading, infection control, and vascular restoration.

Prevention: The 2021 AU Prevention Guideline recommends annual foot examination for all people with diabetes to detect early signs of neuropathy or PAD (IWGDF risk 0). Those classified at increased risk (IWGDF risk 1 to 3) require reassessment every 6 to 12 months for risk 1, every 3 to 6 months for risk 2, and every 1 to 3 months for risk 3. All at-risk patients should be instructed not to walk barefoot or in thin-soled slippers indoors or outdoors, to inspect feet daily, wash feet carefully with thorough drying between the toes, use emollients on dry skin, and trim nails straight across. Pre-ulcerative signs including callus, ingrown toenails, and tinea pedis should be treated promptly. Patients at moderate or high risk should receive structured foot self-care education and integrated foot care, including professional podiatry, appropriate footwear, and education, provided every 1 to 3 months.

Offloading: For a neuropathic plantar forefoot or midfoot ulcer, AU guidelines recommend a non-removable knee-high offloading device (total contact cast or non-removable knee-high walker) as first-line treatment; a removable knee-high device is second line when non-removable devices are contraindicated or not tolerated; a removable ankle-high device is third line; and medical grade footwear is last resort. Felted foam added to the chosen device or footwear further reduces plantar pressure and is recommended in combination. If offloading device options fail to heal a plantar ulcer, surgical options including Achilles tendon lengthening, Gastrocnemius recession, or metatarsal head resection may be considered.

Wound care: Local wound management includes sharp debridement to remove non-viable tissue, appropriate wound dressings, and optimisation of glycaemic control, nutrition, and hydration. Negative pressure wound therapy and other adjuncts are not routinely used for the purpose of treating infection.

Vascular referral: All patients with evidence of PAD and a non-healing ulcer should be referred urgently to vascular surgery for revascularisation assessment.

Infection: Mild (grade 2) infections in the community setting are treated with oral antibiotics targeting aerobic Gram-positive cocci, principally beta-haemolytic streptococci and Staphylococcus aureus, for 1 to 2 weeks. Moderate (grade 3) infections that are complex or associated with significant comorbidities warrant hospitalisation. Severe (grade 4) infections require urgent hospitalisation, parenteral antibiotics, and urgent surgical consultation.

6. Pharmacology and AU PBS notes

For mild soft tissue infection, oral flucloxacillin (500 mg four times daily) is the AU first-line agent targeting MSSA; amoxicillin-clavulanate (875/125 mg twice daily) is used when polymicrobial or anaerobic coverage is needed. Cefalexin (500 mg four times daily) is an alternative in penicillin-tolerant patients. Doxycycline (100 mg twice daily) or trimethoprim-sulfamethoxazole covers skin flora in penicillin allergy. For moderate to severe infections requiring parenteral therapy, piperacillin-tazobactam or a carbapenem covers Gram-negative and anaerobic organisms; vancomycin or daptomycin is added when methicillin-resistant Staphylococcus aureus (MRSA) is suspected based on prior colonisation or local epidemiology. Linezolid is effective for Gram-positive infections and allows oral step-down from day 5 to 7. Duration for soft tissue infection is 1 to 2 weeks; uncomplicated forefoot osteomyelitis managed conservatively after complete bone clearance may require only a few days, while culture-positive stump-residual osteomyelitis warrants up to 6 weeks. Antibiotic selection should align with local susceptibility patterns from PathWest and state health laboratory networks. Empiric Pseudomonas aeruginosa cover is not routine but is considered in tropical and subtropical Australian regions at moderate to severe infection grades. No PBS streamlined codes govern DFD antibiotic choice; selection follows Therapeutic Guidelines: Antibiotic for AU-specific dosing and duration.

7. Complications and monitoring

The major complications of DFD are lower limb amputation, recurrent ulceration, osteomyelitis, sepsis, and death. Ulcer recurrence rates are high, with approximately 40% recurring within one year and 65% within three years of healing. Annual foot review for all patients with diabetes is the AU surveillance baseline, with frequency escalated according to IWGDF risk category as outlined above. After ulcer healing, ongoing podiatric care, therapeutic footwear review, and self-monitoring of plantar foot skin temperature (where validated systems become available) are recommended to prevent recurrence. Glycaemic, lipid, and blood pressure targets should be optimised at each review. Renal function monitoring is important as end-stage renal disease is an independent risk factor for DFU and amputation. HbA1c target in people with DFD should be contextualised to individual frailty and hypoglycaemia risk. Patients with a healed plantar ulcer (IWGDF risk 3) should receive integrated foot care including professional podiatry, medical grade footwear with a demonstrated plantar pressure relieving effect, and structured self-care education reviewed every 1 to 3 months. Charcot neuroarthropathy must be considered in any patient with a hot swollen foot; prompt offloading prevents progressive deformity.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.