Diabetic Foot



  • Decreased blood supply to the nerves
  • Sorbitol deposition in Schwan cell -> disturbed signal transmission


  • Sensory
  • Motor, how?
    • Usually there’s a balance between flexors and extensors -> when certain muscles get atrophic bc of poor nerve supply -> the effect of the counter group gets more pronounced
    • Loss of the foot arch -> new areas of pressure; head of first metatarsal, tips of the toes, interphalangeal joints (claw deformity)
    • If progresses -> rocker bottom \ Charcot deformity
  • Autonomic, how?
    • Increased shunting -> decreased time for tissue perfusion
    • Loss of innervation to sweat glands -> dry\cracked skin -> entry of bacteria
    • Blunting of C fibers, which are responsible for neuroinflammatory response



  • Atherosclerosis
    • How is it different from non-diabetic athero? Distribution (but same histopathology)
    • If the pt is hypertensive, dyslipidemic, diabetic -> total risk of comorbidities is not cumulative, but synergistic\multiplied\augments the other
  • Thickening of the basement membrane



  • Prevention by controlling risk factors
  • Fluid\electrolyte
  • Abx
    • Commonest organism in diabetic foot? multi microbial
  • Strict glycaemia control
  • Soft tissue debridement\amputation


Download the PDF version: here


  • Dr Alabeidi’s lecture

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