An 82-year-old man with peripheral artery disease (PAD) was evaluated for a painful right foot. Over the past 3 weeks the patient began to have constant dull aching in his foot that improved when standing or walking. His pain was particularly intense at night, and he found that sleeping in a chair helped the disomfort. Three weeks prior to this presentation, small sores on the dorsal surface of the foot evolved and subsequently coalesced with dry gangrene in the small toe (Figure 92-1). The right foot was found to be tender, pulseless, cool, and ruborous with mild edema and elevation pallor.

Debridement of the wounds was subsequently performed (Figure 92-2) and aspirin and cilostazol were started. The ankle pressure on the right was 48 mm Hg with an ankle-brachial index (ABI) of 0.29. Infrainguinal arterial duplex ultrasound revealed diffusely monophasic waveforms with an occlusion of the distal superficial femoral artery. An angiogram further delineated an occlusion of the right external iliac artery that was treated with percutaneous atherectomy, angioplasty, and stent placement. The patient required a small-digit amputation that healed within 6 weeks after revascularization (Figure 92-3).

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  Lower extremity ulcers caused by ischemia from arterial disease are becoming more frequent in aging populations in Western countries.

  
  
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  In addition to age, risk factors include smoking, diabetes, hypertension, and dyslipidemia.

  
  
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  Chronic critical limb ischemia (CLI) is defined as ulcers and tissue loss or rest pain for more than 2 weeks without open lesions due to a lack of nutritive blood flow.

  
  
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  The 2007 TransAtlantic Inter-Society Consensus (TASC II) further defined CLI as an absolute ankle pressure of less than 50 mm Hg or a toe pressure of less than 30 mm Hg.

  
  
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  The incidence and prevalence of CLI has been difficult to calculate, but based on the assumption that 25% of patients with CLI will require amputation and that roughly 5% of claudicants will progress to CLI, one can estimate anywhere from 300 to 1000 affected patients per million per year.¹

  
  
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  Arteriosclerosis occurs at a much younger age in diabetics with its hallmark involvement of the tibioperoneal arteries and relative sparing of the pedal vessels. Amputation is 10 times more frequent in diabetics with PAD and 45% of major amputees are diabetic.¹

  
  
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  Purely ischemic ulcers without a neuropathic component only account for around 15% of ulcers in diabetics.²

Etiology

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  A lack of nutritive perfusion to the periphery leads to decreased tissue resilience and tissue death.

  
  
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  At ankle pressures less than 50 mm Hg and digital perfusion of less than 30 mm Hg, dermal ischemia impairs normal repair mechanisms of cell regeneration, especially over areas of mechanical pressure that lack sufficient cushioning.

  
  
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  The amount of oxygen-rich blood supply needed for healing of damaged and ulcerated dermis and subdermal tissue is much higher than that to maintain tissue integrity.

  
  
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  Chronic ischemic wounds are not able to adequately enter the initial inflammatory phase of healing where vasodilation and increased vascular permeability occur along with platelet and neutrophil infiltration, fibrin deposition, and mucopolysaccharide production to produce a natural protective barrier.

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  A chronically ischemic leg will usually exhibit thin, dry, shiny skin that is hairless and hypohidrotic.

  
  
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  Ischemic ulcers are extremely painful and typically involve the dorsum of the foot, the toes, or the lateral aspects of the foot (first and first metatarsal heads) and ankle where friction and pressure will lead to devitalization of skin.

  
  
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  Purely ischemic ulcers are rarely on the plantar surface of the foot, although areas of the heel may become involved with prolonged bed rest (Table 92-1). Other examples of ischemic ulcerations are shown in Figures 92-4 and 92-5.