April, 2003 - Sixty percent of hospital admissions of patients with diabetes are caused by complications of foot ulcers. More than 70 percent of these admissions require surgical intervention with 40 percent resulting in amputations. Of those with below knee amputations, 40 percent will require an amputation on the contralateral limb within three years.
It is estimated that at least half of the amputations are preventable through improved foot care programs. Unfortunately, significant portions of patients continue to develop plantar (sole of the foot) ulcers even with prescriptive footwear compliance. Consequently, efforts to understand the skin vasculature response to plantar pressures may provide insight into re-ulceration issues, since cutaneous perfusion is suspected to be influenced by arterial circulation but and the mechanical effects of repetitive pressure.
Background
Type II diabetes is related to poor glycemic control and if uncontrolled, leads to microvascular and neuropathic complications that can result in foot ulceration and amputation. Paramount to diabetes control is glycemic control due to the strong relationship between hyperglycemia, microvascular complications and neuropathic symptoms. Much work is being done to evaluate treatments for improved glycemic control. Research is ongoing, but the strong causal relationship between poor glycemic control, poor microcirculation and peripheral neuropathy continues to cause insensate feet, poor skin circulation, high plantar pressures, ulceration, and eventually amputation.
Fifty percent of diabetic patients have some degree of peripheral sensory neuropathy, with nerve damage increasing in incidence with the duration of disease. The most common type of peripheral neuropathy affecting diabetic patients is symmetric polyneuropathy involving distal sensory and motor fibers. This causes sensory loss and motor abnormalities in the distal parts of the extremities, found most often with increased age, longer duration of diabetes, and male gender.
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The location of increased plantar pressures correlates well with the presence of foot ulcers. The absence of muscle and nerve stimuli results in changes in walking behavior which positions the center of mass directly over the center of the stance foot; thus increasing body sway and increasing plantar pressure on the lateral aspect of the foot. Additionally, repetitively high dynamic plantar pressures contribute to callus formation, which is the most likely location of foot ulcers in neuropathic patients and is where highest maximum load and peak plantar pressures occur.
Preventing the occurrence of these ulcers is explored in "Pressure and Perfusion Imaging As Predictors of Diabetic Plantar Ulceration Risk," authored by Karen L. Perell PhD, RKT, of California State University at Fullerton's Division of Kinesiology and Health Promotion and the VA Greater Los Angeles Healthcare System; Oscar U. Scremin, MD, PhD, of the VA Greater Los Angeles Healthcare System; and Dante Chialvo, MD, of the VA Greater Los Angeles Healthcare System. The researchers will present their findings in detail during the American Physiological Society's (APS) annual meeting, part of the "Experimental Biology 2003" conference. More than 8,000 attendees will attend the conference being held in San Diego from April 11-14, 2003.
Methodology
The research team used a laser technique in concert with plantar pressure distribution to map areas of greatest/lowest plantar pressure and skin perfusion distribution of the plantar surface of the foot. Five subjects (>50 years old) with diabetic peripheral neuropathy participated in the plantar pressure measurements and laser Doppler imaging. Subjects walked with specially designed insoles embedded in their shoes to record a two-dimensional graphic display of the plantar pressures during walking.
The peak plantar pressure value, which occurred during any point in the gait cycle, was obtained for specific points on the foot (first phalange, first metatarsal head, second metatarsal head, third and fourth metatarsal head, fifth metatarsal head, three consecutive areas on the medial and lateral borders of the foot, and heel). Each of the five trials required an average of three to five steps per foot.
A similar display of skin perfusion distribution over the plantar surface of the foot was recorded using a laser beam to scan the subjects they were lying prone. Scores measured highest skin perfusion to the lowest; plantar pressures scaled from highest to no pressure.
Results
In the absence of compression (subjects lying prone on a bed) images showed maximal estimated skin perfusion at the heel and metatarsal heads, with intermediate levels on the lateral edge of the sole and minimal values in the rest of the plantar surface. The patterns of plantar pressures during walking generally reproduced the same distributions as the LDI images, with the striking exception at the first and second metatarsal heads where flow pattern is substantially less than that observed for pressures. The first and second metatarsal heads are locations of high incidence of ulceration.
In review of an initial 30 charts randomly selected from over 500 potential charts representing patients since in the VA Greater Los Angeles Healthcare System Podiatry clinics during calendar year 2001, 45 ulcerations were recorded via podiatric review.
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Of the 45 ulcerations, 64 percent occurred across the metatarsal heads (13 percent under each of metatarsal heads one through four; four percent under metatarsal head number four; and 20 percent under metatarsal head number five). Only two percent (one ulcer) was observed on the plantar surface of the heel. The single largest percentage of ulcerations occurred on the plantar surface of the first toe.
Conclusions
A widely held belief is that the plantar surface of the heel rarely ulcerates in ambulatory diabetic peripheral neuropathy patients. The skin perfusion and plantar pressure relationships at each of these locations suggest an explanation for high incidence of ulceration across the metatarsal heads in diabetic patients. These areas (metatarsal heads) have high plantar pressures but lack high skin perfusion. On the other hand, the heel, which also experiences high plantar pressures, has high skin perfusion potentially serving as a protective mechanism against ulceration. Further work to evaluate this relationship in non-diabetic older adults and diabetic non-peripheral neuropathy patients is necessary to understand the phenomena more clearly.
This work provides the basis for the use of the reactive hyperemia response as a predictor of future ulceration. Ultimately, this research will lead to treatments, which propose to alter the repetitive pressures experienced by the plantar surface of the foot to improve skin vascular compensatory mechanisms.
Source: American Physiological Society
