Diabetic Foot Disease: Ulceration, Infection and the Charcot Foot

Introduction

Diabetic foot disease is the commonest cause of hospital admission in people with diabetes and the leading cause of non-traumatic lower limb amputation in the UK. More than 7,000 diabetes-related amputations are performed in England each year, and foot complications account for roughly 1% of total NHS expenditure - more than is spent on breast, prostate and lung cancer combined.²

Up to a quarter of people with diabetes will develop a foot ulcer at some point, and around 80% of amputations are preceded by an ulcer. That statistic is the reason this topic matters: the pathway to amputation runs through a preventable, detectable and treatable lesion, and the interventions that interrupt it are unglamorous and cheap.

How the foot is lost

1. Peripheral neuropathy removes the warning. Sensory loss means injury goes unnoticed; motor neuropathy wastes the small muscles of the foot, clawing the toes and displacing the fat pads so that pressure is concentrated under the metatarsal heads; autonomic neuropathy abolishes sweating, leaving dry, cracked skin that fissures.
2. Peripheral arterial disease removes the ability to heal. Diabetic arterial disease is characteristically distal, diffuse and involves the tibial and peroneal vessels, which is why it is often not amenable to simple bypass.
3. Repetitive trauma - an ill-fitting shoe, a stone, a hot water bottle, a barefoot step onto a drawing pin - produces callus and then tissue breakdown at a site the patient cannot feel
4. Impaired immunity and hyperglycaemia allow infection to establish quickly and spread along tendon sheaths and fascial planes
5. Infection reaches bone, and once osteomyelitis is established, healing without prolonged antibiotics or surgery becomes unlikely

Assessing the foot

Neuropathic, ischaemic or both

The annual foot check

• Inspect - both feet, with shoes and socks off, including between the toes and the heels. Look for ulceration, callus, deformity, colour change, dry skin and nail problems.
• Test sensation - 10 g monofilament at standard plantar sites, 128 Hz tuning fork at the hallux, ankle reflexes and pinprick
• Palpate pulses - dorsalis pedis and posterior tibial
• Assess footwear - fit, wear pattern and foreign bodies inside the shoe
• Ask whether the patient can see and reach their own feet, who cuts their nails, and whether they have noticed anything

Risk stratification

Vascular assessment

• Ankle-brachial pressure index (ABPI) - but interpret with caution. Medial arterial calcification in diabetes makes vessels incompressible, producing a falsely normal or elevated ABPI, sometimes above 1.3, in a limb that is severely ischaemic.
• Toe pressures and the toe-brachial index - digital arteries are usually spared calcification, making these far more reliable in diabetes
• Doppler waveform analysis - a monophasic or damped waveform indicates significant disease even with a normal ABPI
• Duplex ultrasound, CT or MR angiography where revascularisation is being considered
• Refer to vascular surgery for critical limb ischaemia, rest pain, or an ulcer failing to heal despite good wound care

Infection

Infection in a diabetic foot spreads faster and further than the surface appearance suggests, and systemic features are frequently absent - a patient may have deep sepsis with a normal temperature and white cell count. Assess severity clinically rather than biochemically.

• Do not take a superficial swab of an ulcer surface - it grows colonising organisms and misleads. Take a deep tissue or bone sample after debridement, or aspirate pus.
• Staphylococcus aureus and streptococci predominate; chronic, previously treated and severe infections are frequently polymicrobial with Gram-negatives and anaerobes
• Consider MRSA in patients with previous colonisation or recent hospital exposure, and Pseudomonas in macerated wounds and after prolonged soaking
• Ulcers are not treated with antibiotics unless infected - a clean, non-infected ulcer needs offloading and debridement, not antimicrobials

Osteomyelitis

• Suspect it where an ulcer probes to bone, is larger than 2 cm squared, has been present for more than 2 weeks, overlies a bony prominence, or where the ESR is markedly raised. A sausage toe - a diffusely swollen, red digit - is a classic sign.
• Plain X-ray first, though changes take 2 to 3 weeks to appear and a normal early film does not exclude it
• MRI is the imaging test of choice, being far more sensitive early and defining the extent of soft tissue involvement
• Bone biopsy gives the definitive microbiological diagnosis and is preferred to guide prolonged therapy
• Treatment - prolonged antibiotics, typically at least 6 weeks, with surgical resection of infected bone where medical treatment fails or the infection is extensive

Managing an ulcer

Care is delivered by a multidisciplinary foot care service - diabetologist, podiatrist, vascular surgeon, orthopaedic surgeon, microbiologist, orthotist and specialist nurse. The evidence that such services reduce amputation rates is strong, and the referral pathway matters as much as the wound care.¹

1. Offloading - the single most important intervention for a plantar neuropathic ulcer. A non-removable total contact cast is the gold standard, precisely because it cannot be taken off; removable devices are less effective for the obvious reason. Alternatives include removable cast walkers, felt padding and bespoke footwear.
2. Debridement - sharp removal of callus and non-viable tissue, repeated as needed, which converts a chronic wound into an acute healing one
3. Infection control - antibiotics only where infected, guided by deep tissue culture
4. Revascularisation - angioplasty or bypass where ischaemia is limiting healing. Ischaemic ulcers will not heal without adequate perfusion, however good the wound care.
5. Dressings - to maintain a moist wound environment and manage exudate. NICE advises using the lowest-cost dressing appropriate to the wound; there is little evidence favouring expensive proprietary products.
6. Optimise the whole patient - glycaemic control, nutrition and albumin, smoking cessation, statin and antiplatelet therapy, oedema control and pressure relief for the heels in bed-bound patients
7. Adjuncts - negative pressure wound therapy, larval debridement and dermal substitutes have a role in selected cases; hyperbaric oxygen has limited and disputed evidence

Charcot neuroarthropathy

Charcot neuroarthropathy is progressive destruction of the bones and joints of an insensate but well-perfused foot. Repetitive unperceived trauma, combined with neuropathy-driven hyperaemia that increases osteoclastic bone resorption, causes fracture, dislocation and eventual collapse of the arch.

It is uncommon but devastating, and it is the most time-critical diagnosis in the diabetic foot - because the destruction happens over weeks, and immobilisation started early prevents deformity that cannot be undone.

Prevention

Almost everything that reduces amputation happens before the ulcer appears.

• Annual foot check for everyone with diabetes, with risk stratification and a documented risk category
• Structured education - daily inspection of both feet including between the toes, using a mirror or asking someone else if they cannot see or reach; never walking barefoot; checking bath water temperature by hand or thermometer rather than by foot; checking inside shoes before putting them on; moisturising dry skin but not between the toes
• Never use over-the-counter corn or callus removers - they contain salicylic acid and cause chemical ulceration in an insensate foot
• Regular podiatry for nail and callus care in moderate and high-risk patients - patients should not cut their own callus
• Appropriate footwear, with bespoke shoes and insoles where there is deformity or previous ulceration
• Report any new lesion, colour change, swelling or discharge immediately - give patients a specific number to ring rather than telling them to see someone
• Smoking cessation, glycaemic and cardiovascular risk management
• Heel protection for inpatients - pressure ulceration on the heels of an immobile diabetic patient is a common and entirely preventable hospital-acquired harm

Red flags

Prognosis

The prognosis of a diabetic foot ulcer is far worse than most clinicians assume, and worth stating plainly because it changes how seriously the problem is treated.

• Around 5-year mortality after a first diabetic foot ulcer approaches 50% - comparable to or worse than many common cancers. The deaths are overwhelmingly cardiovascular; an ulcer is a marker of widespread arterial disease.
• Five-year mortality after a major amputation is around 70%
• Recurrence is the rule - roughly 40% of healed ulcers recur within a year and 65% within 5 years, which is why lifelong surveillance and protective footwear are not optional
• Healing rates - most uncomplicated neuropathic ulcers heal within 12 to 20 weeks with proper offloading; ischaemic and infected ulcers take considerably longer and a proportion never heal

Set against this, outcomes are strikingly modifiable. Multidisciplinary foot care services reduce major amputation rates substantially, and the interventions responsible are simple: finding the at-risk foot, educating the patient, offloading the ulcer, treating infection properly, and revascularising the ischaemic limb. Amputation rates vary several-fold between UK regions, and that variation reflects service organisation rather than biology.

The most useful thing to carry from this topic is the reframing: a foot ulcer is not a dermatological inconvenience but a systemic warning sign with a mortality worse than most cancers, and it should trigger the same urgency of referral and the same attention to cardiovascular risk that a new diagnosis of vascular disease would.