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What are the signs and symptoms of ulceration?
How does ulceration progress to infection and gangrene?
How is foot ulceration managed?

Foot deformities are common in diabetic patients, due to motor nerve damage, and lead to focal areas of high pressure. Coupled with the lack of sensation resulting from peripheral neuropathy, a foot ulcer may develop (Figure 1). This is often exacerbated by ill-fitting shoes.

Figure 1. Neuropathic ulceration of the foot in a diabetic patient.

What are the signs and symptoms?
Most diabetic ulcers form over prominent bony areas, such as beneath the first metatarsal head or between the toes (Figure 2).

Figure 2. Typical locations of ulcers in the diabetic foot. Enlarge

If the ulcer is infected, erythema, pain and tenderness may be present. However, especially in neuropathic ulcers, these signs may be absent or minimal. Powerful indicators of infection are a purulent discharge, crepitation or deep penetrating sinuses [Boulton, 1997].

Diabetic patients with a history of previous ulceration or amputation are at increased risk of further ulceration, infection and amputation. Altered foot dynamics arising from ulceration, joint deformity or amputation can cause abnormal distribution of plantar pressures and result in the formation of new ulcers.
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How does ulceration progress to infection and gangrene?
Autonomic neuropathy leads to decreased sweating as a result of denervation of dermal structures. This causes fissures to form in the dry skin, providing a portal of entry for infection. The hyperglycaemic tissue environment may enable the infection to go unchecked and, together with oedema and peripheral vascular disease (both of which will impair arterial inflow), may ultimately lead to diabetic gangrene [Boulton, 1997].
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How is foot ulceration managed?
Ulcers may be prevented by meticulous attention to foot care and proper management of minor foot injuries. Daily foot inspections (by a carer if necessary) are fundamental to effective foot care.

If ulceration does occur, the treatment strategy should be focused on treating the current ulcer and preventing future ulceration. The key fact that often goes unnoticed is that patients without pain sensation will invariably walk on a plantar ulcer.

An ulcer will always heal if three factors are attended to:

1. the circulation is adequate.
2. infection is treated.
3. pressure is removed from the ulcer.

It is the failure of healthcare professionals to attend to the last of these that most frequently results in failure of ulcer healing. For this reason, the total contact cast, which does not permit the patient to put pressure on the ulcer, is the gold standard in the management of the plantar neuropathic ulcer.

High plantar foot pressures in diabetic patients are strongly predictive of subsequent plantar ulceration, especially in the presence of neuropathy [Veves et al, 1992]. Therefore, the key goal of successful ulcer treatment and relapse prevention is the effective reduction of pressure on the foot [Armstrong and Lavery, 1998b]. A variety of custom-made footwear, orthotic insoles, walkers and casts are effective in off-loading diabetic foot wounds, and reduce the likelihood of ulcer relapse [Colagiuri et al, 1995; Mueller et al, 1989; Myerson et al, 1992; Uccioli et al, 1995]. However, total-contact casts appear to heal a higher proportion of wounds in a shorter amount of time than either the removable cast walker or the half-shoe [Armstrong et al, 2001].

Studies have shown that ulcers heal slowly in the presence of oedema [Apelqvist et al, 1992] and so diuretics or ACE inhibitors should be instituted [Boulton, 1997].

Ulcers are frequently covered in callus or fibrotic tissue. Trimming or debridement of hyperkeratotic tissue is therefore important for comprehensive wound evaluation. Debridement should remove all necrotic tissue and surrounding tissue until a healthy bleeding edge is reached.

If on evaluation the ulcer is infected, it should be initially treated with a broad-spectrum antibiotic, such as co-amoxiclav, in conjunction with effective debridement. Subsequent antibiotic therapy is dependent upon the results of the bacterial culture. The route of administration and length of therapy will depend on the severity of the infection. Superficial infections are treated orally for several weeks while deep infections require initial intravenous therapy followed by up to 12 weeks of oral therapy [Boulton, 1997].

If the patient has peripheral vascular disease, an aggressive approach, such as angioplasty or proximal or distal bypass surgery, will reduce the risk of amputation [LoGerfo et al, 1992; Pomposelli et al, 1991].
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