This photograph shows the typical ulceration seen on the tips of toes and on pressure bearing areas of the
feet in a patient with diabetes mellitus. Such a 'diabetic foot' is seen at some time in about 5% of insulin
dependent diabetic over the age of 60 years. Lower limb amputation is fifteen times more common in diabetic than
The aetiology of the diabetic foot is multifactorial. Diabetic peripheral neuropathy results in sensory loss
and undetected repeated minor trauma that predisposes to ulceration. Diabetics also have an increased incidence
of peripheral vascular disease. Compared to the non-diabetic population they usually have a more peripheral
distribution of this vascular disease. Microvascular disease and infection also contribute to ulceration. About
45-60% of ulcers are purely neuropathic, 10% purely ischaemic and 25-45% of a mixed neuro-ischaemic nature.
Ischaemic ulcer typically occur on the toes and heel. In the absence of significant neuropathy the feet are
often cold with no palpable pulses. The ankle-brachial pressure index (ABPI) is usually reduced but it should be
noted that this index can be inappropriately elevated in diabetic due to calcification of the arterial media.
Neuropathic ulcers occur at sites of trauma and callus formation. As a result of an autonomic neuropathy the
foot is often warm and peripheral pulses may be present.
The treatment of diabetic ulceration is multi-disciplinary. Prevention is better than cure. Prevention
requires the identification of feet 'at risk' ideally in dedicated foot clinics. Patients can be educated and
advised on appropriate foot care. Such an approach has been shown to reduce amputation rates. Neuropathic ulcers
require pressure relief and debridement of callus. Ischaemic ulcers require vascular assessment often including
angiographic assessment down to the pedal vessels. Revascularisation often involves a distal bypass procedure.
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