DIABETES IS A CHRONIC condition that's become an epidemic worldwide. Two to three percent of people with diabetes will develop a foot ulcer each year, and their lifetime risk of developing a foot ulcer is as high as 25% due to neuropathy and potential coexisting vascular disease.1 When following people with diabetes and neuropathy for 1 year, researchers estimated that 7.2% would develop their first foot ulcer.2,3 Over 80% of all nontraumatic amputations in patients with diabetes are preceded by foot ulcers, which are one of the prognostic indicators for advanced diabetes.2,3
This article will review proper assessment techniques and treatment options for patients with diabetic foot ulcers to help minimize complications.
Assessing for foot ulcers
Inadequate management of diabetes can put patients at risk for many serious complications, including foot ulceration. Hyperglycemia triggers metabolic and cellular abnormalities that lead to excessive production of advanced glycation end-products, impaired leukocyte function, and generation of oxygen-free radicals that can delay healing of foot ulcers.1 Assessing risk factors for diabetic foot ulcers should always be part of a comprehensive patient history.3,4 (See Recognizing risk factors for diabetic foot ulcers.)
Conduct a thorough foot assessment with each patient visit to individualize the plan of care.5 A comprehensive foot assessment is recommended at diagnosis of diabetes and annually or more frequently, depending on the presenting risk factors.6 (See Keeping an eye on the foot for a list of recommendations.)
Types of neuropathy
Diabetic neuropathy is present in almost 60% of patients with diabetes who have foot ulcers. Nerve dysfunction associated with diabetes may be described as sensory, motor, or autonomic.3,4
Sensory neuropathy makes a patient less aware of trauma to the skin. Blisters, erythema, or subcutaneous hemorrhage indicates local damage from friction or shear caused by excessive movement or poorly fitting footwear. Callus formation is a reaction to increased local pressure and leads to skin breakdown and ulceration. By recognizing early signs of injury related to pressure and friction, nurses can initiate prompt interventions to prevent ulceration.
To screen patients for sensory neuropathy, the 5.07/10 g Semmes-Weinstein monofilament test is recommended. Patients with significant sensory impairment (4 or more out of the 10 points) are five times more likely to develop foot ulcers.3,4,6
Motor neuropathy interferes with the normal signaling to the lumbrical and interosseus muscle, leading to atrophy and wasting of muscles, foot deformity, upper displacement of fat pads, and altered foot biomechanics.7 Common foot deformities, including foot drop, equinus deformity, hammertoes, and prominent plantar metatarsal heads, create areas that sustain high impact and pressure, which are prone to ulcer formation.8,9
Charcot foot, often characterized by an outward bowing of the arch that gives it a rocker-bottom appearance, is a serious complication of neuropathy that leads to fractures and marked deformity. Signs of acute Charcot foot may include joint displacement and/or dislocation, and increased warmth, erythema, and edema of the foot. Charcot foot is likely precipitated by repetitive trauma that triggers the release of pro-inflammatory cytokines and increased bone perfusion, leading to bone resorption and demineralization.10
Autonomic neuropathy is associated with decreased production of sweat and components of the natural moisturizing factor, leading to disruption of the epidermal barrier.7 Inspect the skin for dryness, especially the presence of fissures or cracks that may become a portal of entry for bacteria. Fungal infection is common in people with diabetes, so check between the toes for maceration. This warning sign of fungal infection usually starts at the fourth and fifth toe space, where the greatest occlusion occurs. Many antifungal agents such as imidazole, allylamines, and thiazoles are available for local or systemic management of a fungal infection.
Diabetes is associated with a two- to threefold increased risk of accelerated atherosclerosis.11 The severity may depend on the duration and severity of diabetes, severity of dyslipidemia, obesity, hypertension, smoking, a family history of atherosclerosis, and anatomical location of vascular damage (proximal versus distal). Over time, chronic hemodynamic and metabolic alterations damage the endothelium, resulting in functional and structural changes that may involve thickening of the basement membrane and sclerosis of capillary walls.
Peformed with a handheld Doppler, the ankle-brachial index (ABI) is a noninvasive vascular screening test used to identify peripheral arterial disease (PAD) by comparing systolic blood pressures in the ankle to brachial systolic blood pressures. Measuring ABI and assessing the pedal pulses is considered the most convenient noninvasive diagnostic method for detecting PAD. However, false elevation of the ABI is common in people with diabetes due to noncompressible arteries associated with advanced atherosclerosis and vascular calcification.11 (See Common noninvasive studies for PAD.)
The loss of triphasic waveform, as indicated by pulsed-wave Doppler, indicates stiff atherosclerotic vessels and further validates the presence of PAD. Alternatively, the toe-brachial index (TBI) may be superior to ABI because it assesses digital arteries that are less likely to be affected by calcification. A full segmental arterial Doppler exam provides an accurate assessment of lower extremity arterial disease.12
Vascular study results should be considered in conjunction with clinical signs and symptoms of PAD. Physical findings valuable for identifying advanced PAD include absence of pedal pulses, atrophic (thin) skin, decreased skin temperature, blue/purple skin color, absence of lower limb hair, and prolonged capillary refill time.12,13
Treating diabetic foot ulcers
Plantar pressure redistribution should be considered for all patients with diabetic foot ulcers. Most experts advocate walking casts (often made nonremovable with a flexible cohesive bandage or casting material to increase adherence to therapy) or the total contact cast for forefoot ulcers.8,9 The contact cast effectively redistributes pressure, but it's contraindicated in the presence of ischemia or deep infection. Deep-toed shoes and orthotics are more appropriate for maintenance after healing to prevent recurrence. Patients with ulcers in the heel area could benefit from modified shoes rather than pneumatic walkers and contact casts, which actually increase pressure.8,9 Patients should see a foot specialist with appropriate training and be reevaluated at regular intervals (2 to 6 weeks with an active ulcer, 6 to 12 weeks with a deformity or previous ulcer, or 6 to 12 months with neuropathy alone).14 For patients with severe foot deformity and high-risk patients, surgical interventions should be considered to prevent further deterioration and recurrence of foot ulcers.
Nonviable tissue, including eschar or soft slough, promotes bacterial growth and inhibits healing. For wounds with the ability to heal, surgical debridement of calluses and abnormal surface granulation with a curette, scissors, or scalpel blade is the most effective way to destroy the biofilm structure and reduce the number of cells that delay healing.15 Debridement of hyperkeratotic lesions such as calluses can reduce overall peak plantar pressure by as much as 29%.14
Dealing with infection
Patients with diabetes are susceptible to infection related to immunodeficiency, neuropathy, and arteriopathy.16 Phagocytosis and bactericidal capacity is significantly reduced in these patients. Early assessment and prompt treatment may help prevent complications. (For a helpful mnemonic, see Spelling out wound infection). Increased surface bacterial burden may be treated with topical antimicrobials, such as silver, honey, and polyhexamethylene biguinide, while systemic treatment is required for deep tissue involvement.
Diagnosis of wound infection is determined by clinical assessment, not by wound swabs. No one sign or symptom accurately confirms a wound infection diagnosis; clinicians must assess for a combination of two or more indicators.17 Wounds that probe to bone, exist for more than 30 days, recur, and relate to trauma and PAD are independent risk factors for foot infection.18
Osteomyelitis should be suspected if ulcers probe to bone. Although magnetic resonance imaging is more sensitive and specific for the diagnosis of osteomyelitis, changes in radiographic appearance over a 2-week interval are also a reliable indicator of infection.18 Elevation in erythrocyte sedimentation rate and C-reactive protein in the absence of other inflammatory conditions help validate the diagnosis of osteomyelitis.18
Increased bacterial burden on the wound surface results in tissue damage, which is referred to as critical colonization. Recognizing the signs and symptoms of critical colonization and initiating prompt treatment can potentially improve healing and prevent the spread of bacterial invasion into deep tissue. Management of increased bacterial burden in the superficial wound surface may involve an array of antibacterial dressings (such as cadexomer iodine or silver dressings) or topical antimicrobial agents (such as silver sulfadiazine, mupirocin, fusidic acid, or polymyxin B-gramicidin cream).19 When patients exhibit signs and symptoms associated with deep and surrounding wound infection, systemic antimicrobial therapies should be considered.
While most infections are caused by Gram-positive cocci, patients with longstanding and refractory ulcers may need broad-spectrum antibiotic therapy. Systematic reviews of trials to evaluate the effectiveness of antimicrobial treatment for diabetic foot ulcers fail to support the superiority of any I.V. or oral antibiotic regimen over any other.20 When wound healing isn't a realistic goal, use of topical antiseptic agents that are often considered to be cytotoxic such as povidone-iodine may be appropriate because reducing bacteria is more important than the toxic effects on healthy tissues.
Keeping it moist
Moisture balance is critical to the healing process. Although a desiccated wound environment can slow keratinocyte migration, too much moisture can damage the surrounding skin and promote bacterial growth.21
Many dressings have been developed to maintain moisture balance.21,22 Foam dressings wick up and lock in large volumes of exudate. Alginate and hydrofibers can absorb copious amounts of exudate; their gelling effect keeps the wound base moist without maceration.23 Hydrogels and occlusive dressings are usually indicated for dry wounds. Careful monitoring of the wound is required with any dressing regimen.
The optimal care of patients with chronic foot ulcers is complex and time-consuming. Management of these ulcers involves a detailed assessment and discussion with patients to address their concerns and encourage adherence to treatment and lifestyle changes (see The 12 S's of foot care). Patients who adhere to routine foot care, including daily self-exam of the feet and podiatry care, are less likely to develop ulcers than those who don't follow foot care recommendations.19,24 However, many patients fail to maintain self-care measures over time. Studies have documented that less than one-third of patients with diabetes and active foot ulcers regularly wear recommended offloading devices during activities.24
An important step
Patients living with foot ulcers experience poor quality of life due to limited mobility, social isolation, disruption of work and leisure activities, sleep disturbance, depression, and pain.25 Nurses who routinely assess patients with diabetes for foot ulcers can ensure that ulcers are found early and treated properly to minimize complications and improve patients' quality of life.
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