Body Mass Is a Poor Predictor of Peak Plantar ... - Diabetes Care

Peter R. Cavanagh, PhD David S. Sims, jr., PT, MS Lee J. Sanders, DPM

Body Mass Is a Poor Predictor of Peak Plantar Pressure in Diabetic Men

Objective: To examine the relationship between peak plantar pressure during walking and body mass in diabetic patients and age-matched control subjects. Research Design and Methods: A volunteer sample of 56 male diabetic veterans (12 insulin dependent, 44 non-insulin dependent) with a mean age of 58.9 yr, mean duration of diabetes of 16.9 yr, and mean vibration perception threshold of 30.8 and 27 agematched noindiabetic control subjects comprised the study. Result: Peak plantar pressure was measured with a 1000-element piezoelectric platform during the first step of gait. The correlation between body mass and peak pressure was found to be only 0.37 in the patients with diabetes and 0.36 in the control subjects, indicating that body mass accounts for 20 V (>4 |xm displacement), as determined with a hand-held Biothesiometer. Monofilament perception thresholds (MPTs) were also measured and graded as follows: 1, ability to feel 4.17 filament; 2, ability to feel 5.07 filament; 3, ability to feel 6.10 filament; 4, inability to feel 6.10 filament. (Filament units are log10 [10 x buckling force in mg].) The average duration of disease in the diabetic group was 16.9 ± 9.2 yr. Groups differed significantly when compared on body mass, VPT, and MPT but were similar in age, height, foot contact area, and arch index. Plantar pressures were obtained at a rate of 50 Hz during the first step of walking. Details of the data collection and analysis methods have been described elsewhere (9). A 1000-element piezoelectric pressuresensitive mat with an element size of 5 x 5 mm was used for data collection. The pressures from all active elements were scanned by a computer to identify the maximum pressure that occurred in any region of the foot at any time during ground contact. All results presented herein are averages of five such peak values from successive trials. Although a detailed analysis of pressures in different anatomical regions was conducted, these data are not reported herein. In 48 of 56 diabetic patients (and in 90% of all subjects), the peak pressure was under the metatarsal heads or hallux. Pressure is

DIABETES CARE, VOL. 14, NO. 8, AUGUST 1991

expressed in pascals (100 kPa = 14.2 Ib/in 2 = 1.02 kg/cm2). The term body mass (expressed in kg) is used in preference to body weight because the SI unit of weight is the newton, a unit that is somewhat unfamiliar to most people. Footprints were taken during a separate first-step trial with forensic ink and resin-coated paper. The footprints were digitized with a graphics tablet to allow footprint area and arch index to be calculated (10). The arch index represents the percentage of the total foot area that is in the midfoot; thus, an index of 30% represents a planus foot, whereas an index of 5% might result from a cavus foot type. Body mass was measured with the subjects wearing light clothes but no shoes.

RESULTS The relationship between peak plantar pressure and body mass for the 56 diabetic patients is shown in Fig. 1. The Pearson product moment correlation coefficient 2000

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FIG. 1. Relationship between peak plantar pressure and body mass for 56 diabetic patients. Correlation coefficient between two variables is 0.37, indicating that only 13.8% of variance in peak pressure is accounted for by body mass (r = 0.37, R2 = 0.14).

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P.R. CAVANAGH, D.S. SIMS, JR., AND L). SANDERS

for this data set was r = 0.37, which, although significantly different from zero, indicates that body mass accounted for only 14% of the variance in peak plantar pressure. Correlations were also calculated between peak pressure and footprint area (r = 0.10) and peak pressure and arch index (r = 0.17). Similar correlation coefficients for the control group were 0.36, 0.31, and 0.16 between peak pressure and body mass, peak pressure and footprint area, and peak pressure and arch index, respectively. Sample pressure distributions from four of the subjects are shown in Fig. 2.

CONCLUSIONS The lack of a strong relationship between body mass and peak plantar pressure is somewhat of a counterintuitive finding, because it apparently contradicts the definition of pressure as force divided by area. To explain our finding, it is necessary to critically examine what the quantities force and area represent in the current context. The peak ground reaction force during walking has certainly been shown to be related to body mass and also to the speed of walking (11). In this experiment, the effects of speed were controlled by studying the first step in walking, which has been shown to generate pressures that are related to those found in midgait at constant speed (12). Thus, because total force on the foot during walking increases with body mass, attention must be directed toward the denominator in the (force/area) quotient. In a large sample, footprint area will tend to increase nonlinearly with foot size, because area increases as the square of a linear dimension (13). Because foot length is generally well correlated with body height and body mass, heavier individuals would tend to have a disproportionately larger area over which to distribute their increased force. This relationship might, at first, seem to suggest a mechanism that would tend to prevent plantar pressure from increasing with increases in body mass. However, such an argument would not hold for increases in mass that are not accompanied by increases in height, e.g., in load carriage or obesity. We believe the implied assumption, that the ground reaction force is evenly distributed over the entire contact area of the footprint, to be the principal fallacy that has led to the assumption that body mass and plantar pressure are related. Certainly, a value that could be

called theoretical average pressure could be calculated with the total vertical force at any instant and the total footprint area, but this quantity would have little practical relevance. The availability of devices to measure plantar pressure distribution now allow the actual force to be calculated over small regions of the foot (in our case, 0.25 cm2), and thus, the calculation (force/area) yields a result that can be applied to individual anatomical structures. A useful analogy is offered by pressures underneath an automobile tire, the contact area of which is coincidentally called a footprint. Although pressure is typically smoothly (although not uniformly) distributed under the contact area, a foreign body, such as a stone trapped between the tread elements, can cause a focal concentration of high pressure (14). Both the deformity in the foot and the stone in the tire cause the effective contact area of force distribution to decrease to a small fraction of the apparent contact area while the force itself remains constant. The effect is to cause increased pressures that are not directly related to the quotient of force and apparent contact area. In a similar manner, altered structure or function of the foot during walking can reduce the effective foot contact area at a given stage in the gait cycle. Examples of peak plantar pressure distributions taken during the first step of walking are shown in Fig. 2. These diagrams represent the largest pressures applied to each region of the foot regardless of the time during the contact phase when the pressure was applied. The patterns in Fig. 2 show that there is, in general, a very uneven distribution of load over the surface of the foot, often with one or more focal areas of pressure that are considerably greater than the pressure in surrounding areas. For example, in subject A, there are four focal areas of pressure under the hallux, the first and fourth metatarsal heads, and the heel with no significant pressures under the midfoot, lateral forefoot, or toes. Three separate foci of elevated pressure are apparent under the forefoot of subject B, whereas, in contrast, subject C shows a relatively even distribution of low pressures underneath the entire forefoot and rearfoot with no major focal areas. The diverse variation appears to be the result of structural deformity and to a lesser extent functional differences in gait (Fig. 2). The extreme example shown in Fig. ID best illustrates the proposed explanation. This patient has a plantar prominence, described as a rocker-

FIG. 2. Peak plantar pressure diagrams from 4 patients summarizing largest pressure at each point on foot during 1st step walking regardless of time of occurrence. Contour interval is 50 kPa. A: 3 focal areas of pressure in medial forefoot foot of a 44-yr-old man (body mass 62.9 kg, peak pressure 1273 kPa, duration of insulin-dependent diabetes 13 yr). B: focal areas of plantar pressure under 1st, 3rd, and 5th metatarsal heads with no involvement of the toes in a 63-yr-old man (73 kg, peak pressure 948 kPa, duration of non-insulin-dependent diabetes 9 yr). C: broad, even distribution of low pressure under entire footprint with no focal areas in 62-yr-old man (body mass 65.6 kg, peak pressure 373 kPa, duration of non-insulin-dependent diabetes 17 yr). D: an extremely high concentration of pressure underneath midfoot prominence in patient with diabetic neuropathic osteoarthropathy (Charcot foot). Patient was 65 yr old (body mass 96.2 kg, peak pressure 1138 kPa, duration of non-insulin-dependent diabetes 20 yr).


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bottom deformity, as a result of diabetic neuropathic osteoarthropathy (15). The entire ground reaction force during much of the gait cycle is concentrated over the extremely small area of the prominence, resulting in dramatically elevated pressures that are out of proportion to the subject's body mass. The same mechanism probably operates in less severe foot deformities such as forefoot varus or valgus, prominent metatarsal heads, plantar flexed rays, rigid metatarsophalangeal joints, or at the tips of claw toes. Altered foot function during walking may also be partially responsible for the observed plantar pressure patterns. For example, crossing the midline of the body during foot placement will tend to create higher pressures under the lateral border of the foot. It is likely that, in the diabetic population, structural deformity of the foot is of greater importance than abnormal function in reducing the effective contact area. Many authors believe that one of the consequences of peripheral neuropathy is changes in foot structure, in particular clawing of the toes (8). Although this still remains unproven by prospective study, it could be a factor, unrelated to mass, contributing to the increased plantar pressure that has been reported in diabetic patients compared with control subjects. Anterior displacement or atrophy of the submetatarsal fat pads that have been observed in patients with diabetes could also have a similar effect (16). The most important clinical implication of these findings is that concern regarding foot injury should not just be reserved for those neuropathic patients who have high body mass. Elevated plantar pressure is as likely to occur in patients with low body mass as in those who have high body mass. The absence of an important body mass-peak pressure relationship in both diabetic patients and nondiabetic control subjects indicates that this lack of relationship may hold for feet in general and is not just a function of diabetes. However, our results should not be interpreted to mean that weight gain will have no effect on plantar pressure in individual patients. Weight gain in an individual without alteration in foot structure will increase pressure, because the force term in the (force/area) quotient will increase, although the functional area remains the same. When the role of deformity in the pathogenesis of plantar ulceration is considered, it is important to note that Masson et al. (17) have suggested peripheral neuropathy to be a major permissive factor for ulceration. They compared patients with rheumatoid arthritis and diabetes who had a similar incidence of high plantar pressures and similar foot deformity and found a 32% incidence of plantar ulceration in the diabetic group compared with none in the rheumatoid group. However, peroneal nerve conduction velocity and VPTs were markedly impaired in the diabetic group compared with the rheumatoid group. This observation, and the independence of ulceration and body mass, are confirmed in the subset of 14 diabetic patients in our sample who experienced plantar ulceration. Peak plantar pres-

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sure and body mass were not significantly different in this subset from patients who did not ulcerate (pressure 837.8 vs. 804.7 kPa, P = 0.75 and mass 90.3 vs. 89.0 kg, P = 0.8 for ulcer and nonulcer patients, respectively). However, VPTs and MPTs were significantly worse in the patients who ulcerated (VPT 39.3 vs. 28.0, P = .0014 and MPT 2.89 vs. 1.98, P = 0.0003 for ulcer and nonulcer patients, respectively). We believe that foot structure is probably an overriding determinant of elevated plantar pressure. Previous studies relating high pressure in the presence of neuropathy to plantar ulceration may, if methods had been available, also have shown a relationship between deformity and plantar ulceration. Limited joint mobility is one such factor that is now receiving attention as possibly causative of elevated plantar pressures and plantar ulcers (18). Future research should attempt to quantify other foot deformities more precisely so that the hypothesis associating deformity in its broadest sense with elevated plantar pressure can be formally tested. An important corollary of this theory is that foot deformity, in the presence of other permissive factors, may be a more potent risk factor for plantar ulceration in diabetic patients than has been previously realized.

ACKNOWLEDGMENTS This work was supported through Veterans Administration Rehabilitation Research and Development Grant V595P-382.

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14. Browne A, Ludema KC, Clark SK: Contact between the tire and roadway. In Mechanics of Pneumatic Tires. Clark SK, Ed. Washington, DC, U.S. Dept. of Transportation, National Highway Traffic Safety Administration, 1981 15. Sanders LJ, Frykberg RG: Diabetic osteoarthropathy: the Charcot foot. In The High Risk Foot in Diabetes Mellitus. Frykberg RG, Ed. New York, Churchill Livingstone, 1991, p. 297-338 16. Gooding GAW, Stess RM, Graf PM: Sonography of the sole of the foot: evidence for loss of foot pad thickness in diabetes and its relationship to ulceration of the foot. Invest Radiol 21:45-48, 1986 17. Masson EA, Hay EM, Stockley I, Veves A, Betts RP, Boulton AJM: Abnormal foot pressures alone may not cause ulceration. Diabetic Med 6:426-28, 1989 18. Delbridge L, Perry P, Marr S, Arnold N, Yue DK, Turtle JR, Reeve TS: Limited joint mobility in the diabetic foot: relationship to ulceration. Diabetic Med 5:333-37, 1988

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