Diabetic Foot

A spectrum of foot complications occurring in patients with diabetes mellitus, arising from a combination of peripheral neuropathy, peripheral arterial disease and impaired immune function.

These encompass ulceration, infection, Charcot neuroarthropathy and, in severe cases, the risk of amputation. They represent a major cause of hospitalisation and disability in the diabetic population.

The central clinical principle is that prevention through regular foot surveillance and early, aggressive multidisciplinary management of any identified problem substantially reduces the risk of progression to limb threatening complications.

Pathophysiology

• Peripheral sensory neuropathy causes loss of protective sensation. Repetitive trauma or pressure that would normally provoke a protective response goes unrecognised and unaddressed, leading to progressive tissue breakdown and ulceration.
• Motor neuropathy contributes to intrinsic foot muscle wasting and altered foot architecture, further concentrating pressure over specific bony prominences.
• Autonomic neuropathy reduces sweating, producing dry, cracked skin that is more vulnerable to breakdown and infection.
• Peripheral arterial disease, common in the diabetic population, impairs tissue perfusion and wound healing capacity.
• Neuropathy combined with vascular disease (neuroischaemic ulceration) carries a particularly poor prognosis, compounding reduced protective sensation with impaired healing capacity.
• Hyperglycaemia itself impairs neutrophil function and overall immune response, increasing susceptibility to infection and facilitating its rapid spread once established, explaining the potential for a seemingly minor foot lesion to progress rapidly to severe, limb threatening infection if not promptly recognised and treated.

• Foot ulceration typically develops at sites of repetitive pressure or friction: the plantar surface over the metatarsal heads, the heel, or areas of bony deformity.
• It is often painless given the underlying neuropathy, so the ulcer may be advanced by the time the patient notices it.
• This reinforces the importance of regular, proactive foot inspection rather than reliance on patient reported symptoms.
• Signs of infection complicating an ulcer include increasing erythema, warmth and swelling extending beyond the wound margin, purulent discharge, and malodour.
• In more severe or deep infection, systemic features including fever may occur.
• Systemic features may be blunted or absent even in significant infection, given the impaired inflammatory response associated with diabetes. A normal temperature or white cell count should never be used to exclude significant infection in this population.
• Charcot neuroarthropathy presents with a warm, swollen, erythematous foot, often with minimal or no pain despite significant clinical findings, given the underlying neuropathy.
• It is frequently misdiagnosed initially as cellulitis or gout. This is a serious diagnostic pitfall, given the very different management implications.
• If the diagnosis is missed and the foot is not appropriately offloaded, there is a risk of progressive, irreversible bony destruction and deformity.
• Peripheral arterial disease should be actively assessed through palpation of pedal pulses and, where indicated, formal vascular assessment.
• Signs of critical limb ischaemia (rest pain, non healing ulceration, gangrene) require urgent vascular surgical involvement, given the time critical nature of limb salvage in this context.

• Full foot examination should be performed regularly in every patient with diabetes as part of routine structured diabetic review.
• It covers sensation (using a 10 gram monofilament and, where available, vibration perception testing), pedal pulses, skin integrity, foot deformity, and any existing ulceration.
• Risk stratification guides the frequency of subsequent surveillance.
• Any identified ulcer requires assessment of depth, size, and the presence of infection or ischaemia.
• Probing to bone is an important component of this assessment: a positive probe to bone test has reasonable predictive value for underlying osteomyelitis.
• Plain radiography assesses for bony involvement, gas in the soft tissue, or foreign material.
• Magnetic resonance imaging is the investigation of choice where osteomyelitis is suspected but not confirmed on plain radiography.
• Bone biopsy, where feasible, provides the definitive microbiological diagnosis to guide targeted antibiotic therapy.
• Superficial wound swabs are of limited reliability for this purpose, as frequent surface colonisation does not reflect the true deep pathogen.
• Vascular assessment, including ankle brachial pressure index, and referral to vascular surgery are indicated where peripheral arterial disease is suspected or confirmed, given the direct relevance to healing potential and the management approach required.
• Ankle brachial pressure index can be falsely elevated in diabetic patients because of arterial calcification, so toe brachial pressure index or formal vascular imaging may be required for accurate assessment.
• Charcot neuroarthropathy is diagnosed from the characteristic clinical picture in a patient with significant peripheral neuropathy.
• Plain radiography supports the diagnosis, though changes may be subtle or absent in the earliest, acute phase.
• Where diagnostic uncertainty persists, magnetic resonance imaging can identify the earliest bone marrow oedema changes before overt radiographic bony destruction becomes apparent.

• Offloading of the affected area is fundamental to ulcer healing, because healing cannot occur while pressure continues to be applied to the ulcerated site, regardless of any other treatment provided.
• Options are total contact casting (considered the reference standard for plantar forefoot and midfoot ulceration), removable cast walkers, or specialist footwear.
• Wound debridement of any necrotic tissue or callus, together with appropriate moist wound dressing selection according to the specific wound characteristics, supports the local wound healing process, following similar general principles to chronic wound management.
• Antibiotic therapy is reserved for clinically infected ulcers, rather than given for colonisation or uncomplicated, non infected ulceration.
• Mild infection is managed with oral antibiotics covering Staphylococcus aureus and Streptococcus species for one to two weeks:
  • flucloxacillin 500 mg to 1 g four times daily
  • co amoxiclav 625 mg three times daily where broader cover including some Gram negative and anaerobic activity is warranted
• More severe or deep infection requires intravenous therapy with broader spectrum cover, such as piperacillin with tazobactam 4.5 g intravenously three times daily.
• Where osteomyelitis is confirmed, a substantially more prolonged course is needed, as detailed under that specific condition.
• Severe infection, including evidence of deep space involvement, extensive necrosis, gas in the tissues, or systemic sepsis, requires urgent surgical debridement, sometimes extensive, alongside broad spectrum intravenous antibiotic therapy.
• Amputation, ranging from minor digital amputation to major limb amputation, is required in a proportion of severe cases where limb salvage is not achievable or where delay would pose unacceptable risk to the patient's life.
• Optimisation of glycaemic control is an essential component of full management alongside local wound and infection control measures.
• Peripheral arterial disease, where present, needs aggressive management. This includes revascularisation by angioplasty or surgical bypass, which can be essential to achieve adequate perfusion for wound healing in ischaemic ulceration.
• Charcot neuroarthropathy is managed with strict, prolonged immobilisation and complete offloading (typically with total contact casting) of the affected foot during the acute phase.
• Offloading continues until clinical and radiographic signs of the acute inflammatory process have resolved, which can take many months. Transition to specialist protective footwear follows.
• Surgical intervention is reserved for significant resulting deformity causing recurrent ulceration or instability not manageable with footwear alone.
• Multidisciplinary foot care is the most effective overall approach to both prevention and management, given the complex, multifactorial nature of the underlying pathophysiology.
• It involves diabetology, podiatry, vascular surgery, orthopaedic or plastic surgery, and tissue viability specialists, working within a structured diabetic foot service.
• Coordinated, proactive, specialist multidisciplinary care has demonstrated substantial benefit in reducing amputation rates and improving overall outcomes.