Appropriate foot care, preventive measures, and early intervention reduce the incidence of complications and lower extremity amputation in patients with diabetic foot ulcers. A thorough lower extremity examination includes assessment of the skin, interdigital areas, skin quality and integrity, and ulcerative or pre-ulcerative changes. The key to prevention is patient education and lifelong commitment to self-care.
In a patient with diabetes mellitus, a small, untreated blister can easily develop into a full-thickness ulceration. A diabetic ulcer, whether of neuropathic or ischemic origin (Figure), is potentially limb-threatening, because it can easily progress to sepsis or gangrene and eventuate in amputation. The outcome depends on timely assessment and initiation of optimal treatment.
Hundreds of millions of dollars are spent each year for the direct care of foot-related pathology in diabetic patients.1,2 Approximately 15% to 20% of the estimated 18.2 million Americans with diabetes are hospitalized because of a foot complication.2 In many cases, these complications-whether the result of infection, ischemia, neuropathy or a combination of these factors-lead to lower extremity amputations. Approximately 82,000 amputations unrelated to trauma are performed on patients with diabetes each year.2
Prevention of diabetic foot wounds is the ultimate goal. The key components of multidisciplinary foot disorder and amputation programs are early detection of foot ulcers and appropriate management of risk factors associated with foot wounds (Table 1). The main risk factors associated with ulceration and eventual amputation are neuropathy, vascular disease, impaired immune response, and structural deformities.3-5 Once a manageable lesion is detected, prompt and aggressive treatment is essential to prevent an exacerbation, thus reducing the risk of amputation. Identification of the cause is crucial to prevent recurrence.
In this article, we discuss the components of a diabetic foot examination, the principles of wound care, and strategies for prevention.
ASSESSMENT OF THE DIABETIC FOOT
A thorough, systematic lower extremity examination is crucial to the initial treatment of a diabetic foot ulcer4,5 and may provide valuable clues about whether the cause of the wound is mechanical, thermal, or chemical. A stepwise approach that addresses key areas-skin, blood flow, sensation, muscle strength, and pedal deformities-is vital (Table 2). Equally important is the inspection of the patient's shoes for appropriate fit, foreign objects, and patterns of wear. The examination findings help determine the risk level for each patient.
Dermatologic assessment. Inspect the skin and interdigital areas of both feet. Pay particular attention to skin quality, integrity, atrophy, and callus formation, as well as ulcerative or pre-ulcerative changes. Skin color changes that are associated with petechial rashes, small eschars, or heel fissures may indicate a critical level of ischemia or autonomic neuropathy. Toenail changes and subungual drainage or paronychias may be sources of more proximal infection. Thickened or dystrophic onychomycotic toenails may cause subungual pressure ulceration. Close inspection of such nail pathology, especially when the nails are loosened from the nail bed, often reveals lesions that might otherwise be missed.6
Wound assessment. Clinical evaluation includes description and measurement of the wound.7 A tracing of the ulcer on a transparent film or plastic sheet can facilitate this process. Record the tracing and remeasure at subsequent visits to evaluate treatment progress. Digital close-up photography is another option; the photographs can be easily incorporated into the patient's chart or electronic medical record.
Explore the depth and extent of the wound with a small, sterile blunt probe. Check for hidden sinus tracts and deep abscesses, as well as for tendon, muscle, bone, and joint involvement. Palpable bone in the depths of diabetic foot ulcers strongly suggests osteomyelitis.8
Clinical signs of infection-such as purulent drainage, odor, cellulitis, fever, and leukocytosis-must be recorded. Fever and leukocytosis are not always evident, even in the presence of osteomyelitis. Aerobic and anaerobic cultures should be obtained from curettage of the ulcer base; such cultures are more reliable than a superficial swab in elucidating the true pathogens.9,10
Order radiographs to detect osteomyelitis; however, bear in mind that radiography has a low sensitivity and should not be the sole determinant of the need for further interventions. Other imaging modalities can aid in the diagnosis of osteomyelitis. Technetium bone scans, indium- and technetium-99m HMPAO-labeled leukocyte scans, monoclonal anti-granulocyte antibody scans, CT, and MRI are all useful; each has its own advantages and limitations. However, it is unclear whether patients for whom these expensive imaging tests are ordered have better outcomes than those who undergo empiric surgical and medical therapy.11
Vascular assessment. This evaluation includes palpation of bilateral lower extremity pulses. When dorsalis pedis or posterior tibial pulses are absent or diminished, evaluation by Doppler segmental blood pressure measurement of the ankle and toes (ankle-brachial index) or transcutaneous partial pressure of oxygen is indicated and vascular consultation should be sought.5,12-14 Arteriography is frequently necessary and is sometimes recommended in lieu of noninvasive testing in the pulseless foot.
Other important indicators of blood flow include digital hair growth, quality of the skin, cool temperature changes, and capillary fill time to the digits. Determine whether the patient has night cramping, pain at rest, or symptoms of intermittent claudication. Also assess the competency of the venous system. Pitting edema, blisters, or superficial leg ulcerations indicate an impaired venous or lymphatic system. Patients with these signs are at increased risk for stasis ulcerations, infection, and recurrent bouts of cellulitis in the edematous extremities.
Neurologic assessment. Assess the patient's sensory perception and deep-tendon reflexes. Ankle and knee reflexes are easily tested with a neurologic hammer. The key elements in evaluating sensitivity are impaired sensation to pain, light touch, hot/cold, and vibration. Pain perception is easily evaluated with a disposable needle. A cotton ball, lamb's wool, or 10-g monofilament may be used to assess light touch, and a 128-Hz tuning fork is recommended for vibratory evaluation. The inability to perceive a 10-g (5.07) Semmes-Weinstein monofilament indicates peripheral neuropathy. Diminution or loss of protective sensation increases the risk of ulceration.5 Cold perception is easily evaluated by submerging the metal handle of the neurologic hammer in cold water and placing it against the patient's skin.
Musculoskeletal assessment. Structural deformities such as hammer toes, previous partial foot amputation, and Charcot neuroarthropathy frequently create high-pressure areas that ulcerate.5,14 The musculoskeletal evaluation involves not only a visual inspection for such findings but also a test for muscle strength, weakness (footdrop, intrinsic muscle atrophy), and contractures (gastrocnemius equinus). Assessment of ankle and great toe joint range of motion and a gait evaluation help determine the mechanical cause of the increased pressure area. Abnormally high plantar pressure areas-often clinically evident from callus formation, erythema, or warmth-are important risk factors for ulceration.5,7 These areas are frequently caused by a tight Achilles tendon or a rigid great toe.
PRINCIPLES OF WOUND CARE
General management. The primary goal of the treatment of diabetic foot ulcers is to close the wound as expeditiously as possible. Management is largely determined by the severity and vascularity of the ulcer and the presence of infection.15-17 Rest, elevation, and relief of pressure are essential components of treatment and should be initiated at the initial presentation (Table 3).
Ensure that the patient discards ill-fitting footwear and replaces it with a postoperative shoe or other type of pressure-relieving footwear. Crutches or a wheelchair might also be recommended to totally off-load the foot. Although the total-contact cast is considered the optimal method of management for neuropathic ulcers, it must be applied weekly, and considerable experience is required if iatrogenic lesions are to be avoided.18 Acceptable alternatives are removable (or nonremovable) walking braces or the "half shoe."19-21
Preparation of wound base. Debridement of all necrotic, calloused, and fibrous tissue is essential.15 Sharply debride unhealthy tissue back to bleeding tissue to fully visualize the extent of the ulcer as well as to detect any underlying abscesses or sinuses. The patient can then apply daily topical enzymes for maintenance debridement.
Dressings. A warm, moist environment that is protected from external contamination is most conducive to wound healing. This environment can be provided by a number of commercially available special dressings, including semi-permeable films, foams, hydrocolloid gels, calcium alginates, and silver.16,17 Topical platelet-derived growth factor gel (becaplermin) is approved for neuropathic diabetic foot ulcers and can expedite healing.22 Growth factors stimulate chemotaxis and mitogenesis of neutrophils, fibroblasts, monocytes, and other components that form the cellular basis of wound healing.
Bioengineered products. Tissue-engineered skin equivalent (Apligraf) and human dermis (Dermagraft), which are derived from fibroblasts of neonatal foreskins, are new types of biologically active implants for ulcers. 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.
Surgical management. Regardless of which topical therapies are used, treatment of underlying ischemia is critical to a successful outcome. Consultation with a vascular surgeon is recommended for ischemic wounds and for ulcers that show no sign of improvement despite appropriate management. Distal arterial reconstruction to restore pulsatile flow to the foot is a major component of the limb-salvage strategy in affected patients.23-28
When infection is present, initiate treatment with broad-spectrum antibiotics after obtaining reliable aerobic and anaerobic cultures.8-10 Antibiotic coverage is subsequently narrowed based on the clinical response and the results of culture and sensitivity testing. Surgical drainage and deep debridement or partial foot amputations are necessary adjuncts to antibiotic therapy of deep or limb-threatening infections.8,9
Osteomyelitis is frequently present in moderate to severe infections and is treated with aggressive resection of infected bone and joints followed by 4 to 6 weeks of culture-directed antibiotic therapy.7 Complications such as deep infection with abscess, cellulitis, gangrene, or osteomyelitis mandate hospitalization and prompt surgical drainage. Even in the absence of bone infection, foot-sparing reconstructive procedures may be necessary to remove prominences that cause high plantar or shoe pressures.16
A multidisciplinary team approach focused on prevention of new or recurrent diabetic foot lesions and complications is the most successful strategy in high-risk patients.23-27 Such teams, which may consist of a podiatrist, internist, endocrinologist, infectious disease specialist, vascular surgeon, orthopedic surgeon, nurse, and pedorthist, have reported dramatic reductions in rates of lower extremity amputations and improved ulceration healing rates.23-27
A key component of prevention is patient education. Educate patients about the importance of daily foot inspection, proper foot care, early intervention, and recognition of risk factors for foot disorders. Regular podiatric visits provide an opportunity for reinforcement of appropriate self-care behaviors. Depending on the level of risk, periodic debridement of calluses and toenails can also facilitate the early detection of new or incipient foot problems. Therapeutic shoes with pressure-relieving insoles, rocker soles, and a high toe box that protect the high-risk foot are an essential element of the prevention program and have been associated with significant reductions in ulcer development. Foot-care suggestions for patients are listed in the Box.
Many brochures and pamphlets are available for patients with diabetes; however, teaching points are much more effective if they are presented and reinforced by the clinician and tailored to each patient's needs. Impress on the patient that he or she is a member of the management team. A patient who is educated about the disease is more likely to take an active role in preventing problems before they begin.
1. Centers for Disease Control and Prevention. Diabetes: a serious public health problem. At-a-glance 2000. US Dept of Health and Human Services.
2. American Diabetes Association. Diabetes and cardiovascular disease. Available at: http://www. diabetes.org/diabetes-statistics/heart-disease.jsp. Accessed January 12, 2005.
3. Pecoraro RE, Reiber G, Burgess EM. Pathways to diabetic limb amputation; basis for prevention. Diabetes Care. 1990;13:513-521.
4. Frykberg RG. Diabetic foot ulcers: pathogenesis and management. Am Fam Physician. 2002;66:1655-1662.
5. Frykberg RG, Armstrong DG, Giurini J, et al. Diabetic foot disorders: a clinical practice guideline. J Foot Ankle Surg. 2000;39(suppl 1):2-60.
6. Lavery LA, Armstrong DG, Vela SA, et al. Practical criteria for screening patients at high risk for diabetic foot ulceration. Arch Intern Med. 1998;158:157-162.
7. Boulton AJ, Meneses P, Ennis WJ. Diabetic foot ulcers: a framework for prevention and care. Wound Rep Reg. 1999;7:7-17.
8. Grayson ML, Gibbons GW, Balogh K, et al. Probing to bone in infected pedal ulcers: a clinical sign of underlying osteomyelitis in diabetic patients. JAMA. 1995;273:721-723.
9. Grayson ML. Diabetic foot infections: antimicrobial therapy. Infect Dis Clin North Am. 1995;9:143-161.
10. Lipsky BA. Antibiotic therapy of diabetic foot infections. Wounds. 2000;12(suppl):55B-63B.
11. Johnson JE, Kennedy EJ, Shereff MJ, et al. Prospective study of bone, indium-111-labeled white blood cell, and gallium-67 scanning for the evaluation of osteomyelitis in the diabetic foot. Foot Ankle Int. 1996;17:10-16.
12. McNeely MJ, Boyko E, Ahroni JH, et al. The independent contributions of diabetic neuropathy and vasculopathy in foot ulceration: how great are the risks? Diabetes Care. 1995;18:216-219.
13. Kalani M, Brismar K, Fagrell B, et al. Transcutaneous oxygen tension and toe blood pressure as predictors for outcome of diabetic foot ulcers. Diabetes Care. 1999;22:147-151.
14. Caputo GM, Cavanagh PR, Ulbrecht JS, et al. Assessment and management of foot disease in patients with diabetes. N Engl J Med. 1994;331:854-860.
15. Pham HT. Wound care in diabetic foot ulceration. Wounds. 2000;12(suppl B):82B-89B.
16. Hogge J, Krasner D, Nguyen H, et al. The potential benefits of advanced therapeutic modalities in the treatment of diabetic foot wounds. J Am Pod Med Assoc. 2000;90:57-65.
17. Seaman S. Dressing selection in chronic wound management. J Am Pod Med Assoc. 2002;92:24-33.
18. Mueller MJ, Diamond JE, Sinacore DR, et al. Total contact casting in treatment of diabetic plantar ulcers. Diabetes Care. 1989;12:384.
19. Catanzariti AR, Haverstock BD, Grossman JP, Mendocino RW. Off-loading techniques in the treatment of diabetic plantar neuropathic foot ulceration. Adv Wound Care. 1999;12:445-452.
20. Lavery LA, Vela SA, Lavery DC, Quebedeaux TL. Reducing dynamic foot pressures in high-risk diabetic subjects with foot ulcerations. Diabetes Care. 1996;19:818-821.
21. Guzman B, Fisher G, Palladino SJ, Stavosky JW. Pressure-removing strategies in neuropathic ulcer therapy. Clin Pod Med Surg. 1994;11:339-353.
22. Wieman TJ, Smiell JM, Su Y. Efficacy and safety of a topical gel formulation of recombinant human platelet-derived growth factor-BB (becaplermin) in patients with chronic neuropathic diabetic ulcers. A phase III randomized placebo-controlled double-blind study. Diabetes Care. 1998;21:822-827.
23. Van Gils CC, Wheeler LA, Mellstrom M, et al. Amputation prevention by vascular surgery and podiatry collaboration in high-risk diabetic and nondiabetic patients. The Operation Desert Foot experience. Diabetes Care. 1999;22:678-683.
24. Dargis V, Pantelejeva O, Jonushaite A, et al. AJM: benefits of a multidisciplinary approach in the management of recurrent diabetic foot ulceration in Lithuania. Diabetes Care. 1999;22:1428-1431.
25. Holstein PE, Sorensen S. Limb salvage experience in a multidisciplinary diabetic foot unit. Diabetes Care. 1999;22(suppl 2):B97-B103.
26. Larsson J, Apelqvist J, Agardh CD, Stenstrom A. Decreasing incidence of major amputation in diabetic patients: a consequence of a multidisciplinary foot care team approach? Diabet Med. 1995;12:770-776.
27. Frykberg RG. Team approach toward lower extremity amputation prevention in diabetes. J Am Pod Med Assoc. 1997;87:305-312.
28. Akbari CM, LoGerfo FW. Limb salvage strategies for the high risk foot. Wounds. 2000;12(suppl B):77B-81B.
29. Consensus Development Conference on Diabetic Foot Wound Care: 7-8 April 1999, Boston, Massachusetts. American Diabetes Association. Diabetes Care. 1999;22:1354-1360.