Management of Ulcers

Management of Ulcers

The first principle of foot ulcer management is prevention. Regular screen- ing for the presence of risk factors (table 1) requires only very simple skills, and when combined with education (table 2) about footcare for those identified as being at risk, the likelihood of foot ulceration can be significantly reduced.

The management of diabetic foot ulcers relies on relief of pressure, debride- ment of necrotic tissue, aggressive treatment of infection when present and restoration of normal circulation if PVD is present. All people presenting with foot ulcers should have an examination of the peripheral sensation and

Table 2. Principles of footcare education Target the level of information to the needs of the patient. Those not at risk require only

general advice about foot hygiene and footwear Make positive rather than negative recommendations

Do inspect the feet daily Do report any problems immediately – even if painless Do buy shoes with a square toe box and laces Do inspect the inside of shoes for foreign objects every day before putting them on Do attend a fully trained podiatrist regularly Do cut your nails straight across and not rounded Do keep your feet away from heat (fires, radiators, hot water bottles) and check the bath

water with your hand or elbow Do always wear something on your feet to protect them and never walk barefoot

Repeat the advice at regular intervals and check for compliance Disseminate the advice to other family members and other health-care professionals involved

in the care of the patient

circulation to classify the ulcer as neuropathic, neuroischaemic or ischaemic. Most neuropathic ulcers are due to repetitive pressure either from tight-fitting shoes (on the dorsum of the toes) or from walking (over the metatarsal heads). Pressure must be relieved in order to heal the ulcer. Poorly-fitting shoes need to be replaced by shoes with a better fit, while pressure on the plantar surface of the foot usually requires some form of walking cast (such as a total contact cast) to redistribute the load away from the ulcer. If there is any clinical evidence of PVD, Doppler pressures must be measured to determine if angiography is required. If revascularization is possible (by surgery or angioplasty), it should

be performed, both to aid healing and to prevent recurrence. An infected diabetic foot ulcer can lead to limb loss in a matter of days, but by no means are all ulcers infected, although bacterial colonization is almost universal. The distinction between colonization and infection can be difficult and is not usually aided by microbiological investigations. Clinical signs are the most reliable indicators of infection. Evidence of systemic upset (e.g. fever, leukocytosis) is usually absent and signs of local inflammation and the presence of pus usually confirm the diagnosis. Infections are usually polymicrobial, and so broad-spectrum antibiotics (such as clindamycin, or amoxycillin combined with clavulanic acid) are required. Osteomyelitis should

be suspected in any nonhealing ulcer, and in all ulcers in which it is possible to ‘probe to bone’. While it is often apparent on plain X-rays, CT, MRI or isotope scanning may be needed for the diagnosis.

Recent studies have opened up the possibility of manipulating the wound environment in order to accelerate healing. These interventions have sprung from a clearer understanding of the complex processes that underlie normal and delayed wound healing, much of which is orchestrated by growth factors.

A topically applied ‘bioengineered human dermis’ which consists of neonatal dermal fibroblasts cultured on a bioabsorbable mesh is thought to promote healing by the production of growth factors and of matrix elements such as collagen and fibronectin. Evidence suggests that healing rates of neuropathic ulcers can be significantly improved with this material, although this conclusion relied on a post-hoc analysis, which excluded a number of subjects who were judged to have received a product of low metabolic activity. The direct applica- tion of growth factors to foot ulcers is another area of rapid progress. The underlying assumption is that chronic diabetic foot ulcers are slow to heal, at least in part because of a failure to produce adequate amounts of growth factors. Platelet-derived growth factor has now been shown to improve the ulcer healing rate from 35 to 50% at 20 weeks, but a small pilot study of fibroblast growth factor found no benefit.

During the American Civil War, maggot-infested wounds were noted to

be cleaner and to heal better than other wounds. This observation has recently been applied therapeutically to a variety of other wounds, and anecdotal reports suggest a beneficial effect in diabetic foot ulcers. The larvae selectively ingest necrotic slough leaving healthy tissue alone, and possibly also produce substances that directly stimulate wound healing.

Hyperbaric oxygen therapy increases tissue oxygenation, inhibits anae- robic microorganisms and promotes macrophage activity. It is therefore a candidate for treatment of diabetic foot ulcers. In a small trial of limb- threatening (predominantly ischaemic) diabetic foot lesions, a significant reduc- tion in the rate of major amputations was seen in the group randomized to receive hyperbaric oxygen. This finding needs to be reproduced in larger trials before this expensive therapy can be recommended for widespread use.

The surgical management of foot ulcers is usually limited to amputation and the debridement of infected and necrotic tissue, but it may have a role to play in directly facilitating wound closure. A small study has described better 6-month healing and recurrence rates when noninfected ulcers were excised and closed surgically than when treated conventionally.