INTRODUCTION

More than two million people with diabetes develop foot ulcers during their lifetime. Foot ulcers often go undetected since other ailments associated with diabetes - such as nerve damage, and visual and circulatory problems - make it difficult for patients to feel or see the ulcer as it develops. These open sores often do not heal and may lead to serious complications including severe infection and amputation.

PATHOGENESIS OF DIABETIC FOOT ULCERS

Contrary to popular belief, infection is not the primary cause of diabetic foot ulcers. It is a secondary phenomenon that follows ulceration of the protective epidermis. Infected foot ulcers progress to gangrene and amputation, with immense personal and economic consequences.

In most patients, diabetic peripheral neuropathy plays a central role. Minor trauma, caused, for example, by ill-fitting shoes, walking barefoot or an acute injury, can precipitate a chronic ulcer. Loss of sensation, foot deformities, and limited joint mobility can result in abnormal biomechanical loading of the foot. As a normal response, callus is formed. Often, there is subcutaneous haemorrhage. Finally the skin breaks down. Whatever the primary cause, the patient continues walking on the insensitive foot, impairing subsequent healing (see figure 1). Further, peripheral vascular disease which leads to decreased blood flow can impair healing and promote infection. Thus, a minor wound progressively worsens to a point where it does not heal.

 

INVESTIGATIONS

A thorough evaluation of any ulcer is critical and the findings should direct management of the condition. The evaluation should determine the aetiology of the ulcer and ascertain whether the lesion is neuropathic, ischemic, or neuro-ischemic. Failure to sense the pressure of a 10-g monofilament is a certain indicator of peripheral sensory neuropathy and loss of protective sensation. Other common modalities that can detect insensitivity are a standard tuning fork (128 cycles per second) and a neurologic reflex hammer.

After ascertaining the dimensions and appearance of the ulcer, the physician should examine the ulcer with a blunt sterile probe. Contact of the probe with the bone in presence of infection is indicative of osteomyelitis. The existence of odour and exudate, and the presence and extent of cellulitis must be noted.

Generally, limb-threatening infections can be defined by cellulitis extending beyond two cm from the ulcer perimeter, deep abscess, osteomyelitis, or critical ischemia. Aerobic and anaerobic cultures should be taken when signs of infection, such as purulence or inflammation, are present. Vascular status must always be assessed because ischemia portends a poor prognosis for healing without vascular intervention. The simple palpation of both pedal pulses and popliteal pulses is the most reliable indication of arterial perfusion to the foot.

Following the examination of the foot, subsequent management should be guided by the risk category to which each patient is assigned (Table 1).

TABLE 1: Wagner Ulcer Classification System
Grade	Lesion
0	No open lesions; may have deformity or cellulitis
1	Superficial diabetic ulcer (partial or full thickness)
2	Ulcer extension to ligament, tendon, joint capsule, or deep fascia without abscess or osteomyelitis
3	Deep ulcer with abscess, osteomyelitis, or joint sepsis
4	Gangrene localized to portion of forefoot or heel
5	Extensive gangrenous involvement of the entire foot

TREATMENT

The primary goal of treating diabetic foot ulcers is to obtain closure of the wound. Management is largely determined by the severity (grade) of the ulcer, vascularity and the presence of infection. Rest, elevation of the affected foot, and relief of pressure are essential components of treatment and should be initiated at first presentation. Ill-fitting footwear should be replaced with a post-operative shoe or another type of pressure-relieving footwear. Normally, doctors treat diabetic foot ulcers by cleaning them, applying temporary dressings and advising patients to keep weight off the foot. But these measures tend to have a limited effect.

The mainstay of ulcer therapy is debridement of all necrotic, callus, and fibrous tissue. Unhealthy tissue must be sharply debrided back to bleeding tissue to reveal the extent of the ulcer and to detect underlying abscesses or sinuses.

The genetically engineered platelet-derived growth factor, becaplermin is approved for use on neuropathic diabetic foot ulcers and can expedite healing. Bioengineered skin and human dermis are new types of biologically active implants for ulcers, and are derived from fibroblasts of neonatal foreskins. These bioengineered products enhance healing by acting as delivery systems for growth factors and extracellular matrix components through the activity of live human fibroblasts contained in their dermal elements.

Treatment of the underlying ischemia is critical in achieving a successful outcome, regardless of topical therapies. Extreme distal arterial reconstruction to restore pulsatile flow to the foot is a major component of the limb salvage strategy in these patients. Vasodilator drugs have not been beneficial in healing ischemic lesions. Though hyperbaric oxygen therapy has also been used, the small number of carefully controlled clinical trials limit support for its use.

When infection is present, antibiotic coverage should be tailored according to the clinical response of the patient, culture results and sensitivity testing. Surgical drainage, deep debridement, or local partial foot amputations are necessary adjuncts to antibiotic therapy of infections that are deep or limb-threatening. Last but not the least, it is essential to maintain good glycaemic control.

PREVENTION

High-risk patients should:

• Wash and inspect their feet daily
  
• Use creams or lotions to prevent dry skin and callus formation
  
• Always have their feet measured when purchasing shoes
  
• Avoid walking barefoot
  
• Avoid thermal injury (e.g. from hot water etc)
  
• Seek medical attention for any injury or discomfort, however trivial it may seem
  
• Avoid the temptation to attempt self-treatment of corns, calluses or other disorders

CONCLUSION

Prompt and aggressive treatment of diabetic foot ulcers can often prevent exacerbation of the problem and eliminate the potential for amputation. The aim of therapy should be early intervention to allow prompt healing of the lesion and prevent recurrence. Multidisciplinary management programmes that focus on prevention, education, regular foot examination, aggressive intervention and optimal use of therapeutic footwear have demonstrated significant reductions in the incidence of lower extremity amputations.