Book contents
- Frontmatter
- Contents
- List of Contributors
- Detailed Contents
- Acknowledgements
- Abbreviation List
- 1 Endothelium
- 2 Vascular smooth muscle structure and function
- 3 Atherosclerosis
- 4 Mechanisms of plaque rupture
- 5 Current and emerging therapies in atheroprotection
- 6 Molecular approaches to revascularisation in peripheral vascular disease
- 7 Biology of restenosis and targets for intervention
- 8 Vascular arterial haemodynamics
- 9 Physiological Haemostasis
- 10 Hypercoagulable States
- 11 Platelets in the pathogenesis of vascular disease and their role as a therapeutic target
- 12 Pathogenesis of aortic aneurysms
- 13 Pharmacological treatment of aneurysms
- 14 Pathophysiology of Aortic dissection and connective tissue disorders
- 15 Biomarkers in vascular disease
- 16 Pathophysiology and principles of management of vasculitis and Raynaud's phenomenon
- 17 SIRS, sepsis and multiorgan failure
- 18 Pathophysiology of reperfusion injury
- 19 Compartment syndromes
- 20 Pathophysiology of pain
- 21 Post-amputation pain
- 22 Treatment of neuropathic pain
- 23 Principles of wound healing
- 24 Pathophysiology and principles of varicose veins
- 25 Chronic venous insufficiency and leg ulceration: Principles and vascular biology
- 26 Pathophysiology and principles of management of the diabetic foot
- 27 Lymphoedema – Principles, genetics and pathophysiology
- 28 Graft materials past and future
- 29 Pathophysiology of vascular graft infections
- Index
25 - Chronic venous insufficiency and leg ulceration: Principles and vascular biology
Published online by Cambridge University Press: 05 June 2012
- Frontmatter
- Contents
- List of Contributors
- Detailed Contents
- Acknowledgements
- Abbreviation List
- 1 Endothelium
- 2 Vascular smooth muscle structure and function
- 3 Atherosclerosis
- 4 Mechanisms of plaque rupture
- 5 Current and emerging therapies in atheroprotection
- 6 Molecular approaches to revascularisation in peripheral vascular disease
- 7 Biology of restenosis and targets for intervention
- 8 Vascular arterial haemodynamics
- 9 Physiological Haemostasis
- 10 Hypercoagulable States
- 11 Platelets in the pathogenesis of vascular disease and their role as a therapeutic target
- 12 Pathogenesis of aortic aneurysms
- 13 Pharmacological treatment of aneurysms
- 14 Pathophysiology of Aortic dissection and connective tissue disorders
- 15 Biomarkers in vascular disease
- 16 Pathophysiology and principles of management of vasculitis and Raynaud's phenomenon
- 17 SIRS, sepsis and multiorgan failure
- 18 Pathophysiology of reperfusion injury
- 19 Compartment syndromes
- 20 Pathophysiology of pain
- 21 Post-amputation pain
- 22 Treatment of neuropathic pain
- 23 Principles of wound healing
- 24 Pathophysiology and principles of varicose veins
- 25 Chronic venous insufficiency and leg ulceration: Principles and vascular biology
- 26 Pathophysiology and principles of management of the diabetic foot
- 27 Lymphoedema – Principles, genetics and pathophysiology
- 28 Graft materials past and future
- 29 Pathophysiology of vascular graft infections
- Index
Summary
DEFINITIONS
Chronic Venous Insufficiency
Chronic venous insufficiency (CVI) is a term that is used to describe changes in the leg that include a variety of different clinical problems, which are caused by several types of abnormalities in the veins, and which may occur at a number of different locations in the leg. For these reasons it has been difficult to make accurate comparisons of reports of chronic venous insufficiency from different institutions. As a result attempts have been made to formulate systems of classification that enable accurate comparisons to be made.
The most recent classification, referred to as the CEAP classification, was devised by an international panel and encompasses features of some of the earlier classifications. This classification has four categories which include – Clinical (C), Etiology (E), Anatomy (A) and Pathophysiology (P). Within each category the different levels are each given a number or a letter or both. The clinical classification has seven levels from no visible or palpable signs of venous disease through to skin changes with active ulceration (table 25.1). In addition the Clinical categories are further characterized according to the presence or absence of symptoms. The Etiological classification recognizes the roles of congenital (Ec), primary (Ep) and secondary (Es) causes in venous dysfunction. The Anatomical classification can be represented as a simple or more detailed form. The simple form refers to the site at which the veins are involved as superficial (As), deep (Ad) or perforating (Ap).
- Type
- Chapter
- Information
- Mechanisms of Vascular DiseaseA Reference Book for Vascular Specialists, pp. 459 - 474Publisher: The University of Adelaide PressPrint publication year: 2011
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