A blistered toe or a scraped heel may be a minor annoyance to most people, but to patients with diabetes, these injuries can allow deadly bacteria to enter the body, leading to foot ulcerations. More than 15% of foot ulcers result in amputation. Because these patients often have poor circulation in the lower limbs, they have a harder time fighting off this bacterial invasion, and if the infection spreads, it can lead to gangrene, amputation, or even death.
More than 200 million people in the world have diabetes. Diabetic foot infections are one of the most common causes of hospital admission of the diabetic patient. Of the approximately 120,000 lower extremity amputations performed in the US alone each year, more than half are attributed to diabetes. 85% of all diabetes-related amputations are preceded by an ulceration. It is for this reason that aggressive management of wounds may help save limbs in patients with diabetes.
Associated risk factors
The etiology of pedal ulcerations among patients with diabetes is usually multifactorial. It is important to understand that the risk factors for ulceration rarely occur alone. There are many factors which contribute to diabetic ulcer formation. The most frequent component causes for lower extremity ulcers are peripheral neuropathy, deformity and trauma.
Based on the Rochester Diabetic Neuropathy Study from the Mayo Clinic, 60 to 65% of patients with either type 1 or 2 diabetes had neuropathy. More importantly, in a randomised clinical trial, the diabetic patients who were found to have a vibratory perceptive threshold (VPT) of greater than 25 had an increased chance of developing a foot ulceration.
One study showed that patients who were unable to detect the 5.07 Semmes-Weinstein monofilament, a semi-quantitative measure of light touch, had an increase relative risk (2.03) of developing foot ulcerations.
Once peripheral neuropathy affects a limb, it increases the patient’s susceptibility to abnormal mechanical stresses, which may go unnoticed thereby causing tissue destruction and subsequent ulceration.
Essentially manifestations of peripheral neuropathy include:
- Sensory neuropathy which results in decreased sharp/dull and vibratory sensation as well as decreased proprioception.
- Motor neuropathy which is responsible for intrinsic muscle wasting and imbalance of long and short flexors. This in turn results in dorsal dislocations of the toes and retrograde pressure on the metatarsal heads.
Impairment of blood flow to the foot is often the result of atherosclerosis. As blood flow decreases to the area, the risk of Ischemic ulcers increases and the healing potential of existing ulcers decreases. Peripheral vascular status is often assessed by palpation of the posterior tibial (PT) and dorsalis pedis (DP) arteries. While peripheral arterial occlusive disease rarely leads to foot ulceration directly, once an ulcer develops, arterial insufficiency will lead to prolonged healing, imparting an elevated risk of amputation.
Static as well as dynamic deformities in the feet which often serve to increase peak plantar pressures also contribute to ulcerations. Additional causes include limited joint mobility, and minor trauma caused by inappropriate shoe gear, puncture wounds and various types of foreign bodies found in the shoes.
Assessment and treatment
Prior to initiating management of a diabetic foot ulceration, a complete assessment of the ulcer needs to be performed. Assessment should include:
- staging of the ulcer using a classification system
- systematically recording the characteristics of ulcerations
- monitoring treatment effectiveness
- predicting clinical outcomes
- improving communication among healthcare providers.
- foot radiographs taken to rule out osteomyelitis.
Sheehan and associates concluded that a percent change in the foot ulcer area at four weeks is a strong predictor of healing at 12 weeks. When at least half the size of the wound does not reduce in four weeks clinicians should consider more advanced methods of treatment in order to achieve healing of wounds. For this reason when a patient presents with an ulcer it is crucial to intervene with the treatment as soon as possible.
A key factor in helping wounds heal is wound bed preparation, which includes debridement, reducing the bioburden and exudate management. Aggressive debridement down to healthy bleeding tissue is performed in order to establish the degree of penetration and to remove all of the non-viable tissue. Once the underlying infection has been ruled out, management of the ulcer is initiated.
First and foremost it is important to decrease the peak plantar pressures. The gold standard in offloading is total contact casting, which involves applying a plaster cast from the knee to toes.
Another method of decreasing plantar pressures and immobilising the foot is the removable walking boot. The boots allow for even pressure distribution while allowing them to be removed for ongoing wound treatment.
Other offloading techniques have been tried, such as felt to foam padding, where the area of the ulcer is cut out and the peak plantar pressure is allowed to redistribute around the ulcer. This technique is typically used in conjunction with an offloading boot.
A proper wound healing environment needs to be maintained for all ulcers/wounds. It is now well accepted that maintaining a moist wound environment facilitates the wound healing process. Benefits of moist wound healing include: prevention of tissue dehydration and cell death, accelerated angiogenesis, and increased breakdown of dead tissue and fibrin. Moist wound healing can be achieved using various wound dressings and/or topical agents. Because there are so many types of wound care products on the market it is worth reviewing their relative indications:
Enzymes. Wound closure will not proceed until the wound bed is free of necrosis. Surgical debridement is the most expedient method of accomplishing this goal. However, for those patients that are not candidates for surgical debridement, enzymatic therapy can effectively debride the wound bed. Enzymatic therapy is generally a faster method of debridement than autolytic debridement.
Transparent adhesives. These are semi-permeable dressings, which allow for gaseous exchange between the wound and the environment while protecting against bacterial invasion. While these dressings can protect against friction, they are non-absorptive and should not be used on exudating wounds.
Absorbent dressings. While the goal of topical wound therapy is to maintain a moist wound surface, it is important to absorb excess exudate. Large amounts of exudate can dilute the wound-healing factors and nutrients at the wound surface. Excessive moisture may also promote maceration and decreased tissue tensile strength leading to greater tissue damage. Exudate may also increase matrix metalloproteases (MMPs) which can be deleterious to the healing process. Some commonly used absorbent dressings include polyurethane foams and calcium alginates. These dressings are indicated for heavily exudating ulcers and frequency of dressing change is determined by the amount of drainage.
Hydrogels. Hydrogels vary in composition (from about 94% water to 96% glycerin) and in form. Gel dressings are used to maintain a moist wound surface and are most effective on granular wounds with low exudate. Because they provide moisture to the wound bed they are also effective in autolytically debriding the wound. When using hydrogels, care must be taken to protect the surrounding skin from becoming macerated which occurs when the wound is overfilled. The advantage of a hydrogel dressing over a normal saline dressing is that the gel will stay moist for longer periods of time thereby decreasing dressing change frequency to once per day or in some wounds once every 72 hours.
Topical antibiotics. Topical antibiotic preparations may be indicated for heavily contaminated wounds, which interfere with wound healing.
Negative pressure wound therapy. A non-invasive therapy that uses negative pressure to remove exudate from heavily draining wounds. This therapy removes edema and chronic exudate, reduces bacterial colonisation, enhances neo-vascularisation, increases cellular proliferation, and improves wound oxygenation as a result of applied mechanical force. The apparatus can be used over exposed bone, tendon, and hardware to generate granulation tissue.
Bio-engineered skin repair products (such as Apligraf® and Dermagraft®) take the wound healing process one step further. These products deliver growth factors, and cytokines to the wound that may be lacking these necessary factors which provide an extra boost to the healing process.
They provide living, fast-growing human cells that deliver ingredients such as growth factors, nutrients and proteins directly into the wound. These bio-engineered cells (usually taken from the neo-natal foreskin) can be embedded in a high-tech bioabsorbable mesh which is placed in the wound to activate growth of the patient’s own skin; and that, in turn, promotes epithelialisation.
Shock wave therapy (Sanuwave’s dermaPACE™ device) also works on the principle of marshalling the body’s healing forces. This non-invasive therapy (already in use against kidney stones) aims high-energy pulsed acoustic waves to the wound area. The cellular stress produced by these waves increases circulation in that area and signals the release of specific proteins and growth factors that generate new blood vessels, all of which enhances the body’s self-repair capabilities. This advanced wound healing modailty is currently under investigation, and further data is being accrued.
Tissue expanders. Achieving wound closure after aggressive deep debridement or amputation is important. When residual skin or skin grafts cannot be utilised, the postoperative wound is allowed to close by secondary intention which leaves the patient exposed to infections. Tissue expanders use the skin’s visoelastic properties to achieve primary wound closure. They have been shown to close 40% quicker than traditional secondary intention healing. For example, a new device, DermaClose™ (Figure 1), uses an expander attached to skin anchors and applies a constant 1.3kg of force which approximates the edges of wounds to allow for primary closure.
Oral and systemic antibiotics should be reserved for treating infected ulcers/wounds. Antibiotics should not be used to prevent infections in ulcers/wounds that do not exhibit any clinical signs of infections. When the ulcer/wound is infected, prompt surgical debridement of all infected and necrotic tissue needs to be performed.
While these new treatments represent important breakthroughs in treating diabetic foot wounds, the best approach is to prevent them from developing in the first place. For diabetic patients, that means inspecting their feet daily for blisters and cuts, wearing foot protection at all times, quitting smoking and scheduling regular foot examinations with their healthcare providers.