You are in: eMedicine Specialties > Orthopedic Surgery > FOOT AND ANKLE Diabetic FootArticle Last Updated: Sep 12, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 11
  Author: Michael S Pinzur, MD, Professor, Department of Orthopedic Surgery and Rehabilitation, Loyola University Stritch School of Medicine Editors: John S Early, MD, Clinical Professor of Orthopedic Surgery, Department of Orthopedics, University of Texas Southwestern Medical School; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Shepard R Hurwitz, MD, Director of Clinical Services, Department of Orthopedic Surgery, University of Virginia School of Medicine; Director, Division of Foot and Ankle Surgery, Department of Orthopedic Surgery, University of Virginia Health System; Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital; Jason H Calhoun, MD, FAAOS, Chairman, J Vernon Luck Distinguished Professor, Department of Orthopedic Surgery, University of Missouri Author and Editor Disclosure Synonyms and related keywords: Charcot foot, diabetic foot ulcer, DFU, DFUs, peripheral neuropathy, ischemic peripheral vascular disease, foot infection, Charcot osteoarthropathy, Charcot arthropathy, hypertrophic osteoarthropathy, lower extremity amputation, LEA, LEAs, foot amputation INTRODUCTIONSection 2 of 11
  Diabetic foot ulcers (DFUs) precede 85% of nontraumatic lower extremity amputations (LEAs). Approximately 3-4% of individuals with diabetes currently have foot ulcers or deep infections. Among persons with diabetes, 15% develop foot ulcers during their lifetime. Their risk of LEA increases by a factor of 8 once an ulcer develops. At 2 years following transtibial amputation, 36% of these patients are known to have died. ProblemIndividuals who develop foot ulcers have a decided health-related decrease in their quality of life and consume a great deal of health care resources. FrequencyAmong persons with diabetes, 15% develop DFUs during their lifetime. Currently, 3-4% of individuals with diabetes have deep infections or DFUs. EtiologyPeripheral neuropathy Optimal control of blood glucose levels decreases the incidence of most diabetes-associated organ system morbidity. The primary risk factor for the development of DFUs is loss of protective sensation, best measured by insensitivity to the Semmes-Weinstein 5.07 (10 g) monofilament (see Image 1). Abnormal white blood cell (WBC) function and the presence of peripheral vascular disease allow wounds to become contaminated and infected by organisms that normally are nonpathogenic. This explains the identification of unusual bacteria from the wounds of patients with diabetes. Autonomic neuropathy produces chronic venous swelling. Motor peripheral neuropathy or Charcot arthropathy can produce bony deformity, which, combined with the loss of protective sensation, can result in skin ulceration from pressure or from shear forces. Associated factors are a history of foot infection or ulceration and previous partial or whole-foot amputation. Motor neuropathy leads to muscle weakness and intrinsic muscle atrophy in the hands and feet. Patients with motor neuropathy can develop bunion, claw toe, and hammertoe deformities as a result of muscle imbalance. They lose normal vascular tone and thermal regulation, often developing severe venous swelling that can be managed only with compression hose. Severe tissue swelling can lead to ulceration and infection. The patients develop dry, cracked skin as a result of autonomic dysfunction, with the cracks allowing the entry of bacteria. Nail deformity or pathologic proliferation may make the areas adjacent to the nails foci for skin breaks or for infection. Vascular disease Immune deficiency Each of these potential abnormalities make the diabetic foot susceptible to abnormal mechanical stresses that can lead to a break in the normal soft-tissue envelope. This can initiate a foot infection that cannot be resolved easily. PathophysiologyPressure over a bony prominence has often been cited as the cause for skin breakdown in patients with diabetes. Skin breakdown occurs at far lesser loads when the pressure is applied by shear forces. The accompanying loss of protective sensation prevents the patient from being warned that intolerable loads have been applied. This leads to blister formation and full-thickness skin loss. The process is heightened in the presence of severe venous swelling, which further lowers the injury threshold. Shoes become tight due to swelling, thus increasing the direct pressure and shear forces applied to skin overlying the bony prominence. Thickened, hypertrophic nails increase pressure on the soft tissues surrounding the nails. The common result is tissue failure and ulcer formation. Once the skin barrier is broken, wound healing can be impaired by abnormally functioning WBCs. Moreover, patients often are malnourished. Many have a marginal vascular supply, with less ability to achieve resolution of infection and wound healing. ClinicalClassification of diabetic foot ulcers Most experts use some variant of the classification system developed by Wagner and most currently modified by Brodsky.1, 2 Table 1. Depth-Ischemia Classification of Diabetic Foot Lesions*
*Adapted from Brodsky JW: The diabetic foot. In: Coughlin MJ, Mann RA, eds. Surgery of the Foot and Ankle. St Louis, Mo: Mosby; 1999: 911. INDICATIONSSection 3 of 11
From a practical standpoint, vascular surgery consultation is warranted only when the patient is symptomatic with ischemic pain or a nonhealing ulcer. Ischemic ulcers generally require angioplasty or vascular bypass surgery to achieve wound healing. Neuropathic ulcers require debridement of nonviable or infected tissue, combined with local wound care and offloading. Grade 3 ulcers require debridement of infected or gangrenous tissue. Partial foot amputation, more complex offloading or non—weight bearing, and culture-specific parenteral antibiotic therapy are necessary. Grade 4 ulcers require partial or whole foot amputation. RELEVANT ANATOMYSection 4 of 11
See Medical Therapy. CONTRAINDICATIONSSection 5 of 11
The 1 or 2 elective issues in this topic are clearly indicated within the text. Most of the substance of this chapter is nonsurgical. Failure to follow the guidelines discussed here leads to deep infection and amputation. WORKUPSection 6 of 11
Imaging StudiesImaging can often be useful in determining the treatment of patients with diabetic foot lesions. Soft-tissue pathology, such as abscesses and sinus tracts, can be better defined through ultrasonography, computed tomography (CT) scanning, and magnetic resonance imaging (MRI). The most common use of imaging is for the detection of bone pathology and the confirmation of the development of osteomyelitis. Plain radiographs may at times be useful in confirming bone infection if it reveals changes beneath an ulcer, but it is most likely to be sufficient for diagnosis when the infection is already well established and when the bones of the forefoot or hindfoot are involved. With osteomyelitis, radiographic changes will accurately reflect the destructive process but will lag at least 2 weeks behind the progress of the infection. See also Foot Infections. Diagnostic ProceduresQualitative and quantitative measures are used to assess the level of sensation. Qualitative methods include light touch and pinprick sensation, 2-point discrimination, and proprioception. These are often lowered in patients with sensory neuropathy, usually in a stocking-type pattern below the knee. Quantitative methods offer more objective data. Most commonly, nylon Semmes-Weinstein monofilaments of differing sizes are pressed into the skin perpendicularly until they bend. The threshold of the patient’s sensation is the smallest filament that he/she can feel. Protective sensation is assumed to be present if the patient can feel the 5.07 monofilament; still, approximately 10% of patients with sensation at this level develop neuropathic joints or ulcerations. In addition, although a number of studies have utilized monofilaments for the assessment of neuropathy, there are no substantive data that support any one standard method of application of the monofilament. Generally, testing is recommended at 8-10 anatomic sites, although a test of only 4 plantar sites on the forefoot—the great toe and the base of the first through third metatarsals—can be used to find 90% of patients with an insensate site.3 StagingTREATMENTSection 7 of 11
Medical TherapyPreventive strategies The major focus of current diabetic foot care is prevention. Preventive strategies combine patient education, prophylactic skin and nail care, and protective footwear. Foot-specific, individualized patient education is the most important element of a comprehensive diabetic foot program. Low-risk individuals must wear nonconstrictive shoes. Soft leather or athletic footwear decreases the risk of tissue breakdown from direct pressure (see Image 2). Cushioned stockings are helpful, and white socks make identification of skin breakdown easier, especially in individuals with impaired vision. Nails should be cut transversely to decrease the risk of an ingrown toenail. Once a problem arises, the patient is instructed to seek medical attention immediately. Often, the earliest sign of infection is slowly increasing blood sugars and insulin requirement. When applied to diabetic populations, the above strategies have been shown to markedly decrease the rates of DFU and LEA. Patient education materials are available through the American Orthopaedic Foot and Ankle Society, the American Diabetes Association, the American Podiatric Medical Association, and the National Institutes of Health (NIH) web site Feet Can Last a Lifetime. When individuals progress to a higher degree of risk, they require accommodative footwear and prophylactic skin and nail care. Depth-inlay, soft leather, Oxford-laced shoes with accommodative pressure and custom-made shear-dissipating foot orthoses (insoles) have been shown to appreciably decrease the development of DFUs. The complexity and individualized nature of the shoes and custom-made foot orthoses vary with the magnitude of deformity and loss of protective sensation. Calluses should be pared to decrease the incidence of shear-mediated ulcer formation. Trained professionals should perform skin and nail care in these individuals. Ulcer treatment The first step in the treatment of a patient with diabetes who has a foot ulcer is medical management of the systemic diabetes. Many individuals with diabetes are malnourished due to chronic renal disease or chronic infection. Many are also immunocompromised. Once the systemic condition of the patient is optimized, specific attention can be directed to the foot ulcer. Ulcers can be neuropathic or ischemic. Neuropathic ulcers are caused by pressure or by shear forces. Once the ulcer is unroofed and the necrotic tissue is debrided, the soft-tissue base reveals healthy granulation tissue. If the ulcer is unroofed and the tissue at the base is necrotic, the ulcer is likely to be ischemic. A vascular surgeon should evaluate patients with ischemic ulcers to determine if the limb can be salvaged. A risk-benefit analysis then can then be performed to determine whether treatment should entail limb salvage, amputation, or a combination of both. If the ulcer is neuropathic, noninvasive vascular testing is in order in the absence of palpable pedal pulses. From a practical standpoint, vascular surgery consultation is warranted only when the patient is symptomatic with ischemic pain or a nonhealing ulcer. Ischemic ulcers generally require angioplasty or vascular bypass surgery to achieve wound healing. Neuropathic ulcers require debridement of nonviable or infected tissue, combined with local wound care and offloading. Wet-to-dry wound care does not promote wound healing because dry wounds desiccate. This allows potential wound-healing cells to die and opportunistic infection to propagate. Dry wounds should be kept moist with saline-soaked dressings or hydrocolloid gels. Wounds that produce massive quantities of exudative material should be treated with absorbent materials (calcium alginate) and dressings while the wound is kept moist. Growth factor gels have been shown to promote wound healing in wounds with reasonable wound-healing potential. Offloading distributes weight-bearing pressure over a larger surface area and provides an interface to decrease shear forces. Elimination of weight bearing is generally not required. The optimal offloading device is the total contact cast (TCC). This device acts to dissipate weight-bearing and shearing loads by eliminating foot or ankle motion, using an interface material to distribute pressure and shear forces. Venous swelling is lessened by the compression effect of the cast. When the ulcer shows appreciable improvement, foot care can be simplified with prefabricated walking braces that have a plantar weight-bearing surface lined with Plastazote or other pressure-dissipating materials (see Image 3). When the swelling decreases or when ankle immobilization is not necessary, healing shoes can be used (see Image 4). The grade 0 foot has no ulcers but is at risk. Treatment involves foot-specific patient education and appropriate footwear. Prefabricated, pressure-dissipating insoles are appropriate. Occasionally, a bony prominence or deformity (eg, bunion, hammertoe) cannot be accommodated by therapeutic footwear. In this situation, removal of the bony prominence (exostectomy) or correction of the deformity is advised to prevent ulceration. As ulcers increase in grade, they require additional treatment. Grade 1 ulcers require debridement of nonviable or infected tissue, local wound care, and offloading. Grade 2 ulcers require debridement, culture-specific antibiotics, local wound care, and more extensive offloading techniques. Grade 3 ulcers require debridement of infected or gangrenous tissue. Partial foot amputation, more complex offloading or non–weight-bearing strategies, and culture-specific parenteral antibiotic therapy are necessary. Grade 4 ulcers require partial or whole foot amputation. Surgical therapyAmputation Any discussion of the diabetic foot requires introduction of the concept of function-preserving amputation surgery. Partial and whole foot amputations frequently are necessary as treatment for infection or gangrene. The goal of treatment is the preservation of function, not just the preservation of tissue. Amputation surgery should be the first step in the rehabilitation of the patient. Because most of these individuals are ambulatory, surgical planning should be directed at the creation of a load-bearing terminal end organ that can interface most easily with accommodative footwear, a prosthesis, or a combination of both (ie, prosthosis). The principles that direct construction of a residual limb for weight bearing with a prosthesis should be employed when performing debridement or partial foot amputation. The major value of partial foot amputation is the potential for the retention of plantar load-bearing tissues, which are uniquely capable of tolerating the forces involved in weight bearing. The soft-tissue envelope should be capable of minimizing these forces. Avoid the use of split-thickness skin grafts in load-bearing areas. Deformity should be avoided as much as possible. Tendo-Achilles lengthening should be used to avoid equinus deformity and increased loading of the residual forefoot in partial foot amputations. Retention of a deformed foot with exposed bony prominence leads only to decreased walking ability and recurrent ulceration. COMPLICATIONSSection 8 of 11
Failure to follow the above prevention and treatment guidelines leads to deep infection and amputation. OUTCOME AND PROGNOSISSection 9 of 11
Individuals who develop foot ulcers have a significant health-related decrease in their quality of life and consume a large quantity of health care resources. At 2 years following transtibial amputation, 36% of these patients are known to have died, which means that preventive programs are extremely important. Preventive programs have been shown to markedly decrease the rates of DFU and LEA in diabetic populations. For excellent patient education resources, see eMedicine's Diabetes Center. Also, visit eMedicine's patient education article Diabetic Foot Care. MULTIMEDIASection 10 of 11
REFERENCESSection 11 of 11
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