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Effects of Diabetes

One group at heightened risk for foot and lower extremity trauma and inpaired skin integrity is the diabetic population. Accelerated atherosclerosis of the diabetic cardio-vascular system, diabetic retinopathy and sensory polyneuropathy all contribute to a higher risk of poor tissue perfusion, trauma, ulceration, gangrene and lower extremity amputation for the diabetic patient. The prevalence of diabetes in the United States was estimated by the National Institutes of Health in 1995 at 16 million individuals. Diabetes mellitus, complications notwithstanding, ranks as the 7th most common principal diagnosis requiring a patient to be seen by their primary care provider (Ostergaard & Schmittling, 1997).

Alarming statistics for lower extremity amputations reveal that 50 - 70% of all non-traumatic lower extremity amputations involve diabetic patients (Ahroni, 1993); the Centers for Disease Control (CDC) reports 54,000 such procedures are performed yearly (1995). Through early detection and treatment, it has been estimated by the CDC that half of these lower extremity amputations are preventable. Recommendations by both The American Diabetes Association (ADA) and the CDC include an examination of the feet of diabetic patients by the primary care provider at every visit (1991).

Disruption of arterial flow from micro and macro angiopathies and atherosclerosis occurs at a heightened rate in the diabetic patient (Jaffe, 1991). Thickening of the capillary walls, restricted blood flow to the site of invading bacteria (typically polymicrobial) and impaired oxygen perfusion at the cellular level combine to evidence as pale, cool extremities with shiny skin and a weak or absent pulse (Garrison & Campbell, 1993). Almost 20% of diabetic patients with palpable pedal pulses do have significant small vessel disease (Kosinski & Ramcharitar, 1994).

Although foot lesions can arise anywhere pressure or repeated friction occurs, common hot-spots are under plantar calluses, in the toe-nail bed or in tandem with neuropathic ulcers (Garrison & Campbell, 1993). The sequela of minor trauma, ulceration and eventual failure of a wound to heal occurred in 72% of lower extremity amputations studied (Pecoraro).

Neuropathic ulcers may present as red, warm, painless, circular lesions, surrounded by callus, and located over bony prominences. Deformity, muscle weakness, dry skin and tight shoes have all been implicated as causative (Dorgan et al, 1995).

Autonomic, sensory and motor neuropathies act together to create foot ulceration (Ahroni, 1993). Diabetic impairment of the autonomic nerves causes a reduction in blood flow and glandular activity, resulting in drier skin that is prone to fissures and infection (Garrison & Campbell, 1993). Motor neuropathy leads to muscle weakness and changes in the shape of the foot. "Weaker intrinsic muscles allow flexors to predominate, lesser toes become hammered or clawed. Toe tips may ulcerate" (Ahroni, 1993).

Sensory neuropathy allows patients to experience a progressive insensitivity to pain, pressure and temperature. To test for sensory loss, "the APN applies a 5.07 (10-g) monofilament perpendicular to the skin until it bends, to the count of 1-second touch, 1-second bend, and 1 second lift. Four areas are screened, including the distal fat pad areas of the great and fifth toes, and the metatarsal head areas below these two toes" (Kelechi & Lukacs, 1996). Eyesight may be impaired by diabetic retinopathy or macular degeneration to the extent that it is not the protective sense of sight, but the foul smell of an infected wound that prompts the patient to seek attention (Garrison & Campbell, 1993).

Posterior tibial pulse

Thus, the APN should check each foot for the presence of dorsalis pedis and posterior tibial pulses, with referral to specialists for absence of pulses. Skin temperature should be checked by feeling both feet simultaneously to compare any "hot-spots" that may indicate problems. The dorsal surfaces of the hands may be used, with detection of any difference greater than 2 degrees Centigrade both determinable and potentially significant (Dorgan et al, 1995). Capillary refill is measured in seconds after blanched pressure to the nail bed. Less than 3 seconds is consistent with a normal finding.

Capillary nail bed pressure

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