Current Concepts In Treating Diabetic Foot Wounds
- Volume 16 - Issue 3 - March 2003
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Managing foot wounds in diabetes patients forms much of the core practice of wound care and podiatry. In the United States, the annual cost for the care of diabetic foot wounds exceeds $5 billion.1 It’s been estimated that anywhere from 2.5 to 10.7 percent of patients with diabetes develop a foot wound each year. Even for wounds that heal, the recurrence rate is approximately 55 percent over the next five years.
According to one study, the prevalence of neuropathy in the diabetic population is 33.5 percent, the prevalence of vascular disease is 12.7 percent and the prevalence of foot ulcer is 4.75 percent.2 Given these statistics, let’s take a closer look at how the current literature supports (or doesn’t support) our fundamental perceptions about treatment, and examine how the risk of developing foot wounds corrrelates with the patients’ age, height, fasting blood sugar and duration of diabetes.
A Few Thoughts About Ulcer Etiology
Aside from a previous foot ulcer, the most significant predictor of ulcer occurrence is altered sensation in the foot. Other key etiologic factors include the duration of diabetes, poor control of blood sugars, microvascular problems and structural abnormalities.
Microangiopathy tends to occur at a younger age in diabetic patients than in the general population and can lead to neuropathy, nephropathy and retinopathy. Although atherosclerosis is typically diffuse, atherosclerotic disease involving the tibioperoneal vessels (rather than the aortoiliac segment) characterizes the diabetic population. A thickened basement membrane in arterioles and capillaries impairs white cell migration.
Microangiopathy leads to neuropathy. Autonomic neuropathy impairs capillary vasodilation in response to injury. Actual occlusion of arterioles is not the problem, a fact attested to by the success of bypass surgery.
Neuropathy in the diabetic patient results from abnormalities in the polyol pathway, deficiencies in nerve regeneration and defects of sodium and calcium channels.5 Neuropathy allows repeat episodes of minor trauma to go unnoticed. This results in deformity such as clawing of the toes and collapse of the distal metatarsals and arch, which causes Charcot foot (rocker-bottom deformity).
Diabetic patients with a history of foot ulcers have a significantly greater incidence of extension deformity of the first, second and third metatarsophalangeal joints and of arthropathy of the second, third and fourth metatarsophalangeal joints. Interestingly, there is no significant difference in the soft tissue thickness beneath the metatarsal heads or in bone density.6
Many structural abnormalities predispose to diabetic first toe ulcers.7 These include gastrocnemius/soleus equinus, structural hallux limitus, hallux interphalangeal abductus, first ray elevatus or dorsiflexion deformity, functional hallux limitus, interphalangeal joint sesamoid bone, hyperextended interphalangeal joint, prominent plantar-medial condyle of the proximal aspect of the distal phalanx, hallux malleus and metatarsus primus adductus.
A Review Of Key Clinical Findings
Diabetic ulcers usually occur on the plantar aspect of foot, especially the metatarsal head areas and the tips of the toes. Clinical findings suggesting associated arterial insufficiency include thickened nails, skin atrophy (shiny cool skin), intermittent claudication or pain at rest, pallor on elevation, rubor on dependency, cyanosis, absent pedal pulses and gangrene.
Findings characteristic of neuropathy are comprised of abnormalities in response to pinprick, light touch (Semmes-Weinstein monofilaments), vibration, pressure and ankle reflexes. Sensory neuropathy may cause painless ulceration. Motor neuropathy causes muscle atrophy leading to hammertoes, callus formation and ulceration. Autonomic neuropathy, given the absence of sweating, leads to dry skin (xerosis), fissures, bacterial colonization and frank infection.