Part 1: Epidemiology and aetiology
Diabetic foot problems can occur in type-1 and type-2 diabetes, with men and the elderly being at most risk.1 The annual population-based incidence for diabetic foot ulcers is estimated to be 1-4 per cent, and prevalence is believed to be 4-10 per cent, suggesting a lifetime risk of 25 per cent.2
The most feared and costly complication of diabetic foot disease is amputation. Diabetes accounts for up to 80 per cent of non-traumatic amputations, with 85 per cent of these being preceded by a foot ulcer. 3
Amputation carries a significantly elevated mortality at follow-up, ranging from 13-40 per cent at one year to 39-80 per cent at five years.2
Diabetic foot complications are usually the result of an interplay of causative factors (see box), of which neuropathy is considered the most important. Diabetic neuropathy is present to some degree in more than half of diabetic patients over the age of 60 and increases the risk of foot ulceration seven-fold.4
Sensory neuropathy renders the foot impervious to stimuli, predisposing it to repetitive trauma, which is likely to go unnoticed until it eventually ulcerates. The motor neuropathy leads to muscle atrophy, foot deformity, altered foot biomechanics and redistribution of foot pressures. Autonomic neuropathy results in loss of sweating, with the resultant dry skin being predisposed to fissures.
Diabetes is associated with a two- to three-fold increased risk of accelerated atherosclerosis.
Patients with peripheral vascular disease are predisposed to poor wound healing. This underlines the importance of identifying and managing associated vascular risk factors, such as hyper- tension and smoking.
Poor glycaemic control also contributes to impaired wound healing. It impairs polymorphonuclear leukocyte function and predisposes to onychomycosis and toe-web tinea infections that can lead to skin disruption.5,6
Reassuringly, the daily level of physical activity does not in itself predispose to new or recurrent foot ulceration.7
Factors predisposing patients to diabetic foot complications
- Peripheral vascular disease
- Poor glycaemic control
- Improper footwear
- Others: old age, smoking, low socioeconomic status, psychological factors
Part 2: Assessing the diabetic foot
Assessment of the foot is a key element of the annual diabetic review. Any dry skin, tinea and onychomycosis should be identified and footwear carefully inspected to ensure a proper fit.
Examining the feet for structural abnormalities, such as calluses and flat foot, is important. There are devices that can identify high plantar pressures, but these are not commonly used in routine assessment.
The history should enquire about neuropathic symptoms, such as or nocturnal leg pains.
Pressure sensation is assessed using the 10g nylon Semmes-Weinstein monofilament. This is placed at a right angle to the skin on the plantar surface with pressure being applied until the filament buckles, which indicates that a specified pressure has been applied. Inability to perceive the 10g force is associated with clinically significant large fibre neuropathy.8
Vibration sense is tested with a 128Hz tuning fork applied on the bony prominence of the big toe, moving upwards if any impairment is noted.
A biothesiometer is an electrical device that assesses vibration perception threshold. A vibration threshold of more than 25V has been reported to have a sensitivity of 83 per cent and specificity of 63 per cent for predicting foot ulceration over a period of four years.9
Palpation of pedal pulses (dorsalis pedis and posterior tibial) should be incorporated in the routine diabetic clinic.
Ankle brachial pressure index (ABPI) is the ratio of systolic BP at the ankle to that at the brachial artery and is used to detect peripheral vascular disease. While an ABPI <0.90 suggests the presence of peripheral vascular disease, ABPI >1.1 may represent a falsely elevated pressure caused by medial arterial calcification.2
Doppler arterial waveform is a non-invasive tool used to assess vascular status. The normal arterial waveform is pulsatile with a positive forward flow in systole, followed by a short reverse flow and a further forward flow in diastole. Even with neuropathy, the successful demonstration of this triphasic waveform can exclude arterial disease in more than 90 per cent of limbs.
Identifying Charcot's foot
It is crucial to identify the presence of Charcot's neuroarthropathy because this is likely to go unnoticed by the patient until a grossly deformed insensitive foot results. This foot is at increased risk of ulceration.
During the acute stage, the affected foot may become swollen and painful, and may be misdiagnosed as cellulitis, osteomyelitis, inflammatory arthropathy or DVT. A high index of suspicion is necessary to allow early identification and prompt referral.10
Part 3: Management
Following foot risk stratification, NICE has recommended a management plan (see box).11
Educating patients about foot care and seeking early medical advice is crucial.
Optimal glycaemic control is important. Smoking cessation is likely to be of benefit because of its effects on the vasculature. Addressing other associated cardiovascular risk factors, such as dyslipidaemia and hypertension, is also important.
It is essential that patients are promptly referred to a specialised centre with a multidisciplinary foot care team. The ulcer needs to be monitored, classified, debrided and dressed.12
Neuropathic feet invariably need total contact casting, ambulatory braces, splints or modified shoes with rigid rockered soles. Underlying foot ischaemia needs to be identified and, where appropriate, patients may need to be referred for a specialist vascular opinion. Revascularisation may either be performed as an endovascular procedure, or as open bypass surgery.13
The presence of infection needs to be defined clinically and treated empirically pending wound culture/sensitivity results. Commonly used oral antibiotic regimens include amoxicillin-clavulanic acid, ciprofloxacin, cefalexin and clindamycin. Topical antibiotics are often effective in mildly infected ulcers; severe infections may warrant parenteral antibiotics.
|Risk stratification of the diabetic foot |
|Risk stratification||Clinical features|| Suggested foot review |
|Low risk||Normal sensation, palpable pulses||Annual|
|Increased risk||Neuropathy or absent|
|High risk||Neuropathy or absent|
pulses in addition to
deformity or skin
changes or previous ulcer
|Ulcerated foot||Foot ulcer||Active multi-disciplinary foot |
care team follow-up
Part 4: Treatment of PDN
There is as yet no single ideal intervention for this condition. Treating painful diabetic neuropathy (PDN) is therefore a clinical challenge and it is very important to listen to the patient's concerns, with a view to providing reassurance.
This is likely to complement pharmacological therapy by reducing anxiety, which may also reduce the need for analgesics.
Optimising glycaemic control is important; studies have shown that large fluctuations in blood glucose can exacerbate neuropathic pain.14
Should these measures fail, pharmacological therapy would be indicated (see box).
A systematic meta-analysis concluded that tricyclic antidepressants (TCAs), traditional anticonvulsants and opiates have a better efficacy than newer generation anticonvulsants, SSRIs and serotonin noradrenaline reuptake inhibitors.15
Use of antidepressants
Clinical success was defined as a 50 per cent reduction in pain; TCAs were the most effective in achieving this, followed by traditional anticonvulsants.
Newer generation anticonvulsants were most likely to cause adverse events.
TCAs are equally effective in relieving neuropathic pain in patients with and without depression. This would suggest that their mode of action is not primarily based on their antidepressant effect.
Their use may be limited because of their anticholinergic side-effects.
Patients unresponsive to TCAs, or in whom TCAs are contraindicated or not tolerated, may be commenced on anti- convulsants.
Should anticonvulsants fail, other treatment options such as duloxetine and opioid analgesics may need to be tried.15
Should all of these measures fail, combination therapy may be needed, although there are limited studies on the efficacy of this kind of approach.
One study combined gabapentin with morphine and showed that the combination gave better pain relief, with reduced dosage of both drugs and fewer side-effects.16
We suggest treating PDN according to an algorithm based on the NICE guidance (see box).
This article was originally published in MIMS Dermatology. To register to receive copies see www.hayreg.co.uk/specials/
Therapies for PDN
- Tricyclic antidepressants, such as amitriptyline
- SSRIs, such as citalopram
- Dual serotonin noradrenaline reuptake inhibitors, such as duloxetine
- Traditional anticonvulsants, such as carbamazepine
- Newer anticonvulsants, such as gabapentin and pregabalin
- Analgesics, such as tramadol and oxycodone
- Topical agents, such as capsaicin cream
PDN treatment stages
- Step 1. Simple analgesics, such as paracetamol
- Step 2. Tricyclic antidepressants
- Step 3. Gabapentin
- Step 4. Traditional anticonvulsants, such as carbamazepine
- Step 5. Consider opiate analgesics and referral to local chronic pain management service
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10. Jude E, Boulton A. Update on Charcot neuroarthropathy. Curr Diab Rep 2001; 1: 228-32.
11. NICE. Type 2 diabetes: prevention and management of foot problems. Clinical Guideline 10; January 2004.
12. Young M, Cavanagh P, Thomas G et al. The effect of callus removal on dynamic plantar foot pressures in diabetic patients. Diabet Med 1992; 9: 55-7.
13. Goy J, Urban P. Life and limb: bypass versus angioplasty in the ischaemic limb. Lancet 2005; 366: 1,905-6.
14. Oyibo S, Prasad Y, Jackson N et al. The relationship between blood glucose excursions and painful diabetic peripheral neuropathy. Diabet Med 2002; 19: 870-3.
15. Wong M, Chung J, Wong T. Effects of treatments for symptoms of painful diabetic neuropathy. BMJ 2007; 335: 87.
16. Gilron I, Bailey J, Tu D et al. Morphine, gabapentin, or their combination for neuropathic pain. N Engl J Med 2005; 352: 1,324-34.
Contributed by Dr Manish Khanolkar, specialist registrar, Dr Jeffery Stephens, senior clinical lecturer, Morriston Hospital, Swansea, and Professor Steve Bain, professor of medicine (diabetes) at the University of Wales.