The Diabetic Foot

Foot ulcers are relatively common in patients with diabetes occurring in up to 15% of all diabetic patients.

The associated health-care costs are enormous. It has been estimated that the attributable cost for a patient's foot ulcer care is nearly $28 000 during the 2 years after diagnosis. Observational studies suggest that 6-43% of patients with a diabetic foot ulcer will ultimately progress to amputation. The costs associated with this are even more formidable. The tragedy is that such morbidity and costs result from lesions that may be prevented by the institution of, and compliance with, diabetic foot care policies.

The main causes of foot ulceration are neuropathy, medium and small vessel peripheral vascular disease and abnormal foot biomechanics. These factors are frequently compounded by bacterial infection with organisms such as Staphylococcus aureus and Streptococcus pyogenes, often accompanied by anaerobes such as Bacteroides species. Neuropathy is thought to be the main factor in over one-half of ulcers with trauma occurring as a result of loss of pain sensation. Minimal trauma, such as a foreign body in the shoes, ill-fitting shoes or walking barefoot on a hot surface may lead to devastating effects (see Figures 108 and 109). Excessive pressure loading on the sole, especially over the metatarsal heads and heels, predisposes to the formation of callus which can break down and lead to ulceration. Indeed callus is an important predictor of ulceration. Such excess pressure is generated by motor-nerve damage altering the posture of the foot, limited joint mobility and local deformities including Charcot arthropathy. Autonomic nerve damage leads to reduced sweating and a dry skin which may crack or split more easily allowing the ingress of infection. Atherosclerotic disease of the peripheral vessels, especially the small vessels, is common in diabetic patients and is a predisposing factor in most cases of diabetic foot ulceration. Ulcers attributable purely to ischemia are relatively rare and, as neuropathy usually co-exists, are described as neuro-ischemic as opposed to the more common neuropathic ulcers where neuropathy is the critical antecedent factor. When ulcers are infected they exhibit local signs of inflammation such as erythema, warmth and tenderness, although such signs might be unimpressive despite definite infection. Deep-seated infection and osteomyelitis are important to diagnose. If bone can be felt when probing an ulcer, osteomyelitis can be assumed. Deep infection is suggested by the presence of deep sinuses, a foul discharge and crepitus on palpating the foot.

It follows from the above discussion that risk factors for the development of diabetic foot ulcers include presence of neuropathy (and other microvascular complications), peripheral vascular disease, previous amputation and foot deformity together with previous foot ulceration, poor footcare advice and advanced age.

Management of diabetic foot ulceration is complicated and requires great expertise and experience, particularly because most, if not all, approaches to treatment are not evidence based. A multidisciplinary approach is warranted involving, as necessary, dia-betologists, podiatrists, orthopedic surgeons, vascular surgeons, microbiologists, primary-care physicians, nurses and orthotists. Debridement and removal of slough and necrotic eschar is vital to promote healing. Surgical debridement may occasionally be necessary for an extensive lesion. Relief of pressure is a basic principle of management of all neuropathic ulcers using such methods as an insole encased in either a temporary shoe or plaster cast (total contact cast or Scotchcast boot). Dressings should be absorbent enough to deal with wound exudation. A moist wound environment may be preferable to encourage granulation tissue. Infection must be treated when present but may be difficult to determine as may be the causative organism. There is no consensus as to which antibiotic regimens to use. In the absence of deep infection, monotherapy with a broad-spectrum antibiotic, such as co-amoxiclav, is appropriate. Deep ulcers necessitate initial intravenous administration of a combination of antibiotics, such as ampicillin, flucloxacillin and metronidazole, changing to oral administration when the infection seems to be responding. Clindamycin is useful when there is a suspicion or proven osteomyelitis as it has good penetration into bone. Routine radiography may be helpful in showing the presence of gas or evidence of osteomyelitis. It often reveals calcification of the small vessels of the foot. Osteomyelitis can be confirmed by alternative imaging techniques such as magnetic resonance imaging (MRI) or white-cell scanning. In all cases a vascular assessment should be made and amputation may be necessary if there is extensive gangrene or spreading necrosis in a toxic patient. Revascularization may be possible for neuroischemic ulcers.

Many new and experimental treatments for diabetic foot ulcers have emerged in recent years. Dermagraft®, Smith and Nephew (cultured human dermis) and Apligraf®, Novartis (Graftskin) (bi-lay-ered bioengineered skin substitute) have been shown to shorten healing time and to produce a significantly greater proportion of healed ulcers. Platelet-derived growth factor (becaplermin) has been used to heal small low-grade ulcers. Hyperbaric oxygen has been shown to accelerate the rate of healing and increase the number of wounds completely healed. Debride-ment with maggots is simple and effective for cleaning chronic wounds and initiating granulation. None of these techniques has become an accepted standard therapy for the treatment of diabetic foot ulcers and further assessments of efficacy and cost-effectiveness are required.

The assessment of foot ulcer risk, the dissemination of good foot care advice and early and urgent treatment of established ulceration are the mainstays of the prevention of amputation secondary to diabetic foot ulcers. Comprehensive screening programs and treatment programs have been shown to reduce the risk of amputation. Preventative podiatric care should be given to all patients at risk. Simple measures, such as the debridement of callus and the fitting of appropriate shoes, often with the help of an orthotist, may be all that is necessary to prevent one of the most devastating and feared complications of diabetes, amputation.

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