Abnormal Foot Pressures Alone May not Cause Ulceration

Masson, E. A.; Hay, Elaine M; Stockley, I; Veves, Aristidis; Betts, R. P.; Boulton, Andrew J.M.

doi:10.1111/j.1464-5491.1989.tb01198.x

Cited by 126 publications

(52 citation statements)

References 11 publications

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“…The observation of a reduced hyperaemic response under high-pressure areas suggested that skin breakdown resulted from repetitive pressure (as in walking) under areas such as the metatarsal heads, with a failure of blood flow recovery between footsteps [53]. In a comparative study in patients with rheumatoid feet [54], high foot pressures were common in both diabetic and rheumatoid groups, confirming that high pressures alone do not result in ulceration. It is the combination of pressure and insensitivity that completes the causal pathway.…”

Section: Foot Pressure Studies In Diabetesmentioning

confidence: 94%

The diabetic foot: from art to science. The 18th Camillo Golgi lecture

2004

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Diabetic foot ulceration represents a major medical, social and economic problem all over the world. While more than 5% of diabetic patients have a history of foot ulceration, the cumulative lifetime incidence may be as high as 15%. Ethnic differences exist in both ulcer and amputation incidences, with both being less common in patients of Indian subcontinent origin living in the UK. Foot ulceration results from the interaction of several contributory factors, the most important of which is neuropathy. With respect to the management of acute Charcot neuroarthropathy in diabetes, recent studies suggest that bisphosphonates reduce disease activity as judged not only by differences in skin temperature, but also by assessing markers of bone turnover. The use of the total-contact cast is demonstrated in the treatment of acute Charcot feet and of plantar neuropathic ulcers. Histological evidence suggests that pressure relief results in chronic foot ulcers changing their morphological appearance by displaying some features of an acute wound. Thus, repetitive stresses on the insensate foot appear to play a major role in maintaining ulcer chronicity. It is hoped that increasing research activity in foot disease will ultimately result in fewer ulcers and less amputation in diabetes.

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Section: Foot Pressure Studies In Diabetesmentioning

confidence: 94%

The diabetic foot: from art to science. The 18th Camillo Golgi lecture

2004

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“…The mechanism behind this relationship would be that hyperextension of the metatarsal-phalangeal (MTP) joint, characteristic of claw/hammertoe deformity, causes the protective and shock-absorbent sub-MTH fat-pad cushions to displace distally in the foot, exposing the MTHs to more focal and increased dynamic plantar pressures (Bojsen-Moller, 1979;Ellenberg, 1968;Masson et al, 1989;Sumpio, 2000). Surprisingly, quantitative evaluations of these associations are scant in the literature.…”

Section: Introductionmentioning

confidence: 94%

Elevated plantar pressures in neuropathic diabetic patients with claw/hammer toe deformity

Bus

Maas

Lange

et al. 2005

Journal of Biomechanics

144

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“…Despite the high prevalence of claw/ hammer toe deformity in diabetic subjects (values of 32 and 46% have been reported) (8,9) and other groups (21), studies on the mechanical implications of this condition are rare. Ours is the first study to quantify plantar fat-pad changes with toe deformity, whereas previously we have shown with MRI that intrinsic muscle atrophy does not necessarily predispose a foot to exhibit claw/hammer toe deformity (22).…”

Section: Figure 2-joint Configuration and Fat-pad Geometry In A Neuromentioning

confidence: 99%

Plantar Fat-Pad Displacement in Neuropathic Diabetic Patients With Toe Deformity

et al. 2004

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OBJECTIVE -The aim of this study was to quantify the association between claw/hammer toe deformity and changes in submetatarsal head (sub-MTH) fat-pad geometry in diabetic neuropathic feet.RESEARCH DESIGN AND METHODS -Thirteen neuropathic diabetic subjects (mean age 56.2 years) with toe deformity, 13 age-and sex-matched neuropathic diabetic control subjects without deformity, and 13 age-and sex-matched healthy control subjects without deformity were examined. From high-resolution sagittal plane magnetic resonance images of the second and third ray of the foot, toe angle (a measure of deformity), sub-MTH fat-pad thickness, and subphalangeal fat-pad thickness were measured. The ratio of these thicknesses was used to indicate fat-pad displacement.RESULTS -Sub-MTH fat pads were significantly thinner (2.5 Ϯ 1.3 vs. 6.0 Ϯ 1.4 mm, P Ͻ 0.001) and subphalangeal fat pads significantly thicker (9.1 Ϯ 1.9 vs. 7.6 Ϯ 1.2 mm, P Ͻ 0.005) in the neuropathic group with deformity compared with neuropathic control subjects. As a result, thickness ratio was substantially smaller in the deformity group: 0.28 Ϯ 0.14 vs. 0.79 Ϯ 0.14 in neuropathic control subjects (P Ͻ 0.001). A significant correlation of 0.85 was present between toe angle and thickness ratio (P Ͻ 0.001). No significant differences were found between neuropathic and healthy control subjects.CONCLUSIONS -This study shows a distal displacement and subsequent thinning of the sub-MTH fat pads in neuropathic diabetic patients with toe deformity and suggests that, as a result, the capacity of the tissue in this region to reduce focal plantar pressure is severely compromised. This condition is likely to increase the risk of plantar ulceration in these patients. Diabetes Care 27:2376 -2381, 2004F at pads under the metatarsal heads (MTHs) in the foot provide the primary source of cushioning to protect the skin from damage during gait. These fat pads are invested in the flexor tendons of the toes and originate from the plantar ligaments, which are firmly attached to the proximal phalanges (1,2). In clawing and hammering of the toes, the sub-MTH fat pads are believed to migrate distally as a result of hyperextension of the metatarsal-phalangeal (MTP) joint, exposing the now prominent and unprotected MTHs to elevated levels of mechanical pressure during gait (1,3-5). Elevated plantar pressure has long been established as a major risk factor for plantar ulceration in diabetic neuropathic feet (6,7).Dissection of nondiabetic cadaver feet with hammered toes has shown a distal pull of the plantar fat pad with substantial thinning or even loss of sub-MTH fat tissue and thickening of fat tissue plantar to the proximal phalanx (1). However, despite numerous theoretical and anecdotal reports, there is no quantitative in vivo evidence of fat-pad displacement and resultant thinning of sub-MTH fat tissue secondary to toe deformity in neuropathic diabetic patients.Clawing/hammering of the toes, which is a common deformity in diabetic patients (8,9), has been shown to be a significant predicto...

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Abnormal Foot Pressures Alone May not Cause Ulceration

Cited by 126 publications

References 11 publications

The diabetic foot: from art to science. The 18th Camillo Golgi lecture

The diabetic foot: from art to science. The 18th Camillo Golgi lecture

Elevated plantar pressures in neuropathic diabetic patients with claw/hammer toe deformity

Plantar Fat-Pad Displacement in Neuropathic Diabetic Patients With Toe Deformity

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