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Related Experiment Videos

Abnormal foot pressures alone may not cause ulceration.

E A Masson1, E M Hay, I Stockley

  • 1Department of Medicine, Manchester Royal Infirmary, Sheffield, UK.

Diabetic Medicine : a Journal of the British Diabetic Association
|July 1, 1989
PubMed
Summary

Diabetic foot ulcers are linked to neuropathy, not just high foot pressure. Loss of sensory awareness is key in developing these ulcers, highlighting the importance of nerve function in diabetes management.

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Area of Science:

  • Podiatry
  • Diabetology
  • Rheumatology

Background:

  • Both diabetes and rheumatoid arthritis can cause high foot pressures and ulceration.
  • Neurological abnormalities are also common in these conditions.
  • The relationship between foot pressure, neuropathy, and ulceration requires further investigation.

Purpose of the Study:

  • To examine the relationship between high foot pressure, neurological abnormalities, and ulceration in diabetic and rheumatoid arthritis patients.
  • To determine the primary drivers of foot ulceration in these patient groups.

Main Methods:

  • Studied two groups: 38 diabetic patients and 37 rheumatoid arthritis patients with similar foot abnormalities.
  • Assessed history of plantar ulceration.
  • Measured peroneal nerve motor conduction velocity and vibration perception threshold to evaluate neuropathy.

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  • Recorded elevated plantar pressures.

    • Main Results:

    • 32% of diabetic patients had a history of plantar ulceration, versus 0% in the rheumatoid arthritis group (p<0.01).
    • Diabetic patients exhibited significantly more severe neuropathy (lower motor conduction velocity, higher vibration threshold; p<0.001).
    • Elevated plantar pressures were similarly frequent in both groups (51% vs 61%, NS).

    Conclusions:

    • Loss of sensory awareness (neuropathy) is crucial in the development of diabetic foot ulceration.
    • High plantar pressure alone is not a direct cause of ulceration.
    • Neuropathy plays a more significant role than pressure in diabetic foot ulcer pathogenesis.