Diabetes is now the leading cause of foot ulcers and their complications, with an incidence of 2.0–6.8% per year in Europe and the United States. Other common causes include venous and arterial ulcers. Skin malignancies represent a fair proportion of foot ulcers and suspicious lesions warrant early biopsy. It is clearly important to be able to recognize the different ulcers in clinical practice as their management differs significantly. Diabetic foot ulcer management should focus on prevention as diabetes continues to affect more people worldwide.1,2
2. Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation. Basis for prevention. Diabetes Care 1990;13(5):513–521 One quarter of patients with diabetes will develop a foot ulcer during their lifetime. Half of these will become infected at some stage. Of the infected ulcers, a fifth will ultimately require amputation. More than half of all nontraumatic limb amputations across all health care are performed because of diabetes. Of the foot ulcers occurring, half are on the plantar surface and the consequences of problematic foot ulcers are the leading cause of hospitalization in the UK and Europe. These figures highlight the importance of preventing and treating ulcers early in this population group with patient education, tight control of blood glucose, and practical steps to avoid foot trauma.1,2
The classic triad of risk factors for development of diabetic foot ulcers is peripheral neuropathy, foot deformity, and minor trauma. Neuropathy is the most significant single factor. Other contributing factors include poor selection of footwear (which can contribute to repeated minor trauma), poor self-care, smoking, peripheral arterial disease, obesity, and hypertension.1
classification system. Numerous classification systems have been developed for diabetic foot ulcers, suggesting that no uniformly accepted ideal exists. Three factors are particularly relevant to healing and these are wound depth, infection status, and vascularity as indicated by the presence or absence of peripheral arterial disease. For this reason, the ideal classification should include these three factors as a minimum. The Meggitt-Wagner system is most commonly used and has six grades as follows: 0: Preulcerative/high-risk foot 1: Superficial ulcer 2: Deep to tendon, bone, or joint 3: Deep with abscess/osteomyelitis 4: Forefoot gangrene 5: Whole foot gangrene Weaknesses of this system are that the presence or absence of wound infection is not considered in grades 0 to 2, and peripheral arterial disease is considered only in grades 4 and 5.1 The University of Texas Wound Classification System uses a 4 × 4 matrix and considers wound depth, infection, and peripheral arterial disease, so it contains the three key criteria described above. It is therefore a useful system, but does not take into account wound size or chronicity, which are two additional factors that will influence healing.2 The International Working Group on the Diabetic Foot (IWGDF) developed the PEDIS (perfusion, extent/size, depth/tissue loss, infection, and sensation) system, which does cover the key criteria. The Infectious Disease Society of America (IDSA) system describes the presence of infection in diabetic foot ulcers and has four grades: not infected, mild, moderate, and severe infection.3 It is essentially the same as the infection component of the PEDIS classification. However, it does not assess other key components such as wound size, depth, and sensation.3,4
healing? According to the American Diabetes Society (ADA), the management of neuropathic diabetic foot ulcers requires six essential factors. Of these, off-loading pressure is the most important. The goal is to off-load pressure at the ulcer site while the patient remains ambulatory. The other essential factors are the following: • Debridement early and often • Moist wound healing environment • Treatment of infection • Correction of ischemia (below-the-knee disease) • Prevention of amputation All factors should be addressed in conjunction with optimization of medical therapy to successfully manage diabetic foot ulcers.1
This patient demonstrates Charcot foot, which is a condition of unknown cause that occurs in diabetic patients. It presents as a red, hot, swollen foot and ankle and can be confused with either cellulitis or deep venous thrombosis.1 If it is not diagnosed, the outcome is poor with irreversible destruction of the bony architecture of the foot. Serial radiographs can be useful for monitoring bony changes. If a wound is present, osteomyelitis should be excluded with an MRI. It may be reasonable to begin antibiotic therapy for this patient. However, he is less likely to have infection because he is well and has normal blood results such as white blood cell count.
Common sites for diabetic foot ulcers are those where pressure and shear are most likely to occur, in conjunction with the poorest areas of blood supply. Overall, the most common site is under the hallux. Other areas include the heel (because pressure is transmitted when lying or standing), the tips of the toes (especially with clawing and pressure when weight bearing), and those that are exposed to high repetitive trauma during walking.1
The goal of contact casting is to evenly distribute pressure across the foot, rather than to completely relieve the ulcer site of pressure at the expense of other vulnerable areas. Infection and ischemia should be aggressively treated before casting begins. Casts should be applied by a skilled clinician to prevent iatrogenic ulceration. Patient compliance is very good because it is difficult to remove a full cast. Healing rates are 72–100% over 5–7 weeks.1
aureus (MRSA) and vancomycin-resistant Enterococcus (VRE). Debridement of chronic ulcers is important in order to remove devitalized tissue and biofilm in order to reset the acute healing process. Debridement may be achieved mechanically or chemically. Mechanical debridement includes wet-to-dry dressings, surgical debridement, and maggot therapy. Chemical debridement includes enzymatic debridement with collagenases or other active dressings such as honey. Maggots (Phaenicia sericata) are the larvae of green blowfly and they selectively consume devitalized tissue in wounds, while preserving healthy tissue. A secondary benefit is that they are resistant to both methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococcus (VRE). They are normally left in situ for 3 days (not 1 week) beneath a mesh dressing before being changed. Not only are wet-to-dry dressings nonselective in the tissue removed, they are also painful for patients, can lead to surface cooling, and are labor intensive. Surgical debridement can be with a traditional blade or can be hydrosurgical debridement using systems like the Versajet (Smith & Nephew, Memphis, TN). Such systems are highly effective at debriding wounds accurately using high-velocity streams of saline and a vacuum. This appears to remove necrotic tissue and the biofilm. Wet gangrene should be debrided promptly to minimize systemic illness, but dry gangrene without cellulitis should remain in situ until revascularization is achieved to minimize progressive tissue loss and promote subsequent wound healing.1–6
Lower limb ulcers have some distinct features according to the cause. Factors to be considered when assessing an ulcer include location, appearance, symptoms, and risk factors. The hallmark features of an arterial ulcer are a round or punched-out appearance with a well-demarcated border. There may be a fibrinous yellow base or true eschar. Bone and/or tendon may be evident in the wound base. The typical location is over the distal bony prominences. Other features include a shiny appearance in the adjacent skin, loss of hair, dystrophic toenails, and absence of foot pulses. The hallmark features of a venous lesion are a shallow ulcer with irregular borders located near the medial malleolus. Other features include varicose veins, leg edema, dermatitis, lipodermatosclerosis, and purple pigmentary changes. Diabetic ulcers arise on pressure points on the feet. There is often callus surrounding the wound with undermined edges, blisters, hemorrhage, or necrosis present. Exposure of deeper structures may be observed. The key indicators of a skin malignancy, such as squamous cell carcinoma (SCC) or melanoma, are rapid growth with bleeding and ulceration. There may well be a keratin scabs itch, an SCC, and the lesion may appear de novo or in the setting of a chronic wound. Wound edges may be poorly defined and such lesions require biopsy to exclude or confirm the suspected diagnosis. Other skin malignancies such as basal cell carcinoma (BCC) or melanoma can also present with nonhealing ulcerated appearances. Melanomas are often, but not always, pigmented. Radiotherapy ulcers arise in previous treatment sites and appear as unstable patches of skin. A high suspicion for malignancy should be maintained until biopsies have been performed.1,2
The presence of a new ulcer in a chronic wound or old injury such as a burn should be investigated with a tissue biopsy under local anesthetic in order to exclude a skin malignancy such as a squamous cell carcinoma. The development of skin cancers in chronic wounds is termed a Marjolin’s ulcer.1 Surgical debridement is warranted in chronic wounds that are not healing in order to help remove dead tissue and biofilm and thereby kick-start the healing process. Hyperbaric oxygen has a potential role in management of diabetic foot ulcers and may contribute to reducing subsequent need for amputation.2 Ankle and toe-brachial indices are useful markers of arterial insufficiency. An ankle-brachial index less than 0.9 is suggestive of arterial insufficiency, while a toe-brachial index above 0.6 can be predictive of healing. Vascular intervention can be very useful in the management of leg ulcers. Revascularization with angioplasty and/or bypass can help healing in both diabetic foot and arterial ulcers. In this case once a tissue diagnosis has been confirmed, in the absence of malignancy, a vascular referral should be made. 3,4