Pathophysiology

Chronically reduced sensation leaves the limb vulnerable to injury that may go undetected, thereby leading to ulceration at pressure areas (heel, ankle, metatarsal heads). There may be associated chronic joint destruction and malformation (e.g. Charcot’s joint).

Aetiology

• Diabetes mellitus (by far the most common!).
  
• Ischaemic neuropathy (e.g. post-acute limb).
  
• Alcoholic neuropathy.
  
• Vitamin B12 deficiency.
  
• Certain medications (amiodarone, isoniazid, cytotoxic agents).
  
• Rare causes include chronic renal failure, hypothyroidism, tabes dorsalis, leprosy, porphyria, amyloidosis, progressive sensory neuropathy, Charcot-Marie-Tooth disease.

Clinical

Decreased or absent sensation in the foot ± decreased vibration sense and joint position sense (if posterior spinal columns affected). If there is no arterial element, perfusion (+pulses) will be normal or even increased because of vasodilatation (associated infection or autonomic neuropathy [both common in diabetes!]).

Pathophysiology

Chronic venous hypertension leads to tissue oedema with venous + capillary congestion and relative tissue hypoxia. The skin is vulnerable to minor trauma or spontaneous breakdown with poor healing ability. Ulceration is large and irregular because the surrounding ischaemic tissue area (penumbra) is large.