Diabetic Foot Syndrome

Diabetic foot syndrome is the combination of infection, ulceration or destruction of tissues of the foot associated with neuropathy and/or peripheral artery disease in a person with diabetes.

The majority of the elderly diabetic population is at increased risk of foot ulceration; foot ulcer independently predicts amputation and mortality.

About 70% of lower-limb amputations are precipitated by foot ulceration, and three-year survival after major amputation is only about 50% — worse than many cancers.

Increasing age and a higher level of amputation both increase length of hospitalisation and cost.

Peripheral sensorimotor neuropathy (the primary cause in the vast majority), autonomic neuropathy, peripheral vascular disease, limited joint mobility, abnormal foot pressures and deformity, previous foot problems, visual loss, and alcohol excess.

Limited joint mobility and visual loss are specifically geriatric — they impair the patient’s ability to inspect their own feet.

In India, additional risks are barefoot walking, ill-fitting footwear, delayed presentation, use of traditional remedies, and poor glycaemic control.

Neuropathy causes loss of protective sensation, small-muscle wasting with clawing and high plantar pressures, and callus formation over metatarsal heads.

Autonomic neuropathy produces dry, fissured skin and arteriovenous shunting with a warm, well-perfused but vulnerable foot.

Peripheral artery disease in diabetes is typically infra-popliteal and multi-segmental, with medial calcification producing falsely high ankle pressures.

Neuropathic symptoms include numbness, burning or lancinating pain, “pins and needles” and hyperaesthesia, typically worse at night, with gait disturbance and falls.

Diabetic ulcers form at weight-bearing sites — metatarsal heads and heel — and are typically deep, with undermined edges and surrounding hyperkeratosis, and painless.

Assessment: 10 g Semmes-Weinstein monofilament, 128 Hz tuning fork, ankle reflexes, ankle-brachial index and toe pressures, pedal pulses, footwear inspection, and probe-to-bone test for osteomyelitis.

Charcot neuroarthropathy presents as a hot, swollen, erythematous foot with preserved pulses; misdiagnosis as cellulitis or gout leads to permanent midfoot collapse (rocker-bottom foot).

Management addresses the underlying aetiology plus debridement, control of infection, appropriate dressings and offloading, with optimum glycaemic control as the metabolic foundation.

Offloading is the single most important intervention for a neuropathic plantar ulcer; revascularisation is the key intervention in an ischaemic ulcer.

Infection is graded clinically; mild infections need oral Gram-positive cover, moderate/severe need broad-spectrum cover, urgent surgical drainage and admission.

Multidisciplinary foot care team — diabetologist, podiatrist, vascular surgeon, orthotist, microbiologist and specialist nurse — reduces amputation rates.

Prevention: annual risk stratification, daily foot inspection (with a mirror or by a relative if vision is poor), never walking barefoot, therapeutic footwear, professional nail and callus care, and prompt reporting of any lesion.

Careful caution: corn plasters containing salicylic acid have caused ulceration in diabetic patients with poor skin integrity or neuropathy, and must be avoided.