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Pathophysiology of Critical Leg Ischaemia

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Critical Leg Ischaemia

Abstract

Critical leg ischaemia has been defined previously in this volume as foot ischaemia which is of sufficient severity to cause either pain at rest or skin necrosis (ulceration or gangrene). It is likely that rest pain arises from nerve endings in ischaemic skin, stimulated by the end-products of hypoxic metabolism. However it has been suggested that ischaemic neuropathy may also cause foot pain. In contrast, skin necrosis is commonly painless in diabetics, due to anaesthesia from diabetic neuropathy (see Chapter 10). A low ankle pressure (less than 50 mm Hg), or absent ankle pulses in diabetics, is also included in the definition. This criterion confines the syndrome to the common problem of ischaemia produced primarily by occlusive disease of the large proximal arteries supplying the lower limb, and excludes ischaemia produced by primary microvascular occlusion (e.g. microthromboembolism).

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Authors
  1. Gordon Lowe
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Editors and Affiliations

  1. Department of Vascular Surgery, St. George’s Hospital and Medical School, Blackshaw Road, SW17 OQT, London, England, UK

    John A. Dormandy

  2. Research Laboratories, Schering AG, D-1000, Berlin 65, Federal Republic of Germany

    Günter Stock

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© 1990 Springer-Verlag Berlin Heidelberg

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Lowe, G. (1990). Pathophysiology of Critical Leg Ischaemia. In: Dormandy, J.A., Stock, G. (eds) Critical Leg Ischaemia. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-75625-2_4

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  • DOI: https://doi.org/10.1007/978-3-642-75625-2_4

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-75627-6

  • Online ISBN: 978-3-642-75625-2

  • eBook Packages: Springer Book Archive

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