Guia Esvs Manejo Evc 2015

Management of Chronic Venous DiseaseClinical Practice Guidelines of the European Society for Vascular Surgery (ESVS)

Writing Committee a C. Wittens, A. Davies, N. Bkgaard, R. Broholm, A. Cavezzi, S. Chastanet, M. de Wolf,C. Eggen, A. Giannoukas, M. Gohel, S. Kakkos, J. Lawson, T. Noppeney, S. Onida, P. Pittaluga, S. Thomis,I. Toonder, M. Vuylsteke,ESVS Guidelines Committee b P. Kolh, G.J. de Borst, N. Chakf, S. Debus, R. Hinchliffe, I. Koncar, J. Lindholt,M.V. de Ceniga, F. Vermassen, F. Verzini,Document Reviewers c M. De Maeseneer, L. Blomgren, O. Hartung, E. Kalodiki, E. Korten, M. Lugli,R. Naylor, P. Nicolini, A. Rosales

Keywords: Chronic venous disease, Venous disease, Varicose veins, CEAP, VCSS, Villalta, AVVQ, Vein Qol Sym,

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Eur J Vasc Endovasc Surg (2015) -, 1e60a Writing Committee: Cees Wittens (Netherlands), Chair; Alun Davies (United Kingdom), Co-Chair; Niels Bkgaard (Denmark); Rikke Broholm (Denmark);Attilio Cavezzi (Italy); Sylvain Chastanet (France); Mark de Wolf (Netherlands); Cline Eggen (Netherlands); Athanasios Giannoukas (Greece); Manjit Gohel(United Kingdom); Stavros Kakkos (Greece/United Kingdom); James Lawson (Netherlands); Thomas Noppeney (Germany); Sarah Onida (United Kingdom); PaulPittaluga (France); Sarah Thomis (Belgium); Irwin Toonder (Netherlands); Marc Vuylsteke (Belgium).

b ESVS Guidelines Committee: Philippe Kolh (Chair) (Belgium), Gert Jan de Borst (Co-Chair) (Netherlands), Nabil Chakf (France), Sebastian Debus (Ger-many), Rob Hinchliffe (United Kingdom), Igor Koncar (Serbia), Jes Lindholt (Denmark), Melina Vega de Ceniga (Spain), Frank Vermassen (Belgium), FabioVerzini (Italy).

c Document Reviewers: Marianne De Maeseneer (Review Coordinator) (Belgium), Lena Blomgren (Sweden), Olivier Hartung (France), Evi Kalodiki (UnitedKingdom), Eunice Korten (Netherlands), Marzia Lugli (Italy), Ross Naylor (United Kingdom), Philippe Nicolini (France), Antonio Rosales (Norway).DOI of originalarticle: http://dx.doi.org/10.1016/j.ejvs.2015.02.0141078-5884/ 2015 European Society for Vascular Surgery. Published by Elsevier Ltd. All rights reserved.

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Pleas(20151.4.2. The hydrostatic and dynamic pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

1.4.3. The vein valves . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

1.4.4. The calf muscle and the foot pump . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

1.4.5. Venous tone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

1.4.6. The venous pump: main transport system in the non-supine position . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1.3.2. The deep veins of the lower extremity . . . . . . . . . . . .

1.4. Physiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

1.4.1. The relationship of capacitance/volume to pressure .Duplex ultrasound, Plethysmography, Phlebography, MRV, CTV, Wound dressings, Compression,Ambulatory compression, Sclerotherapy, Thermal ablation, Non-thermal ablation, Laser,Radiofrequency ablation, Stripping, High ligation, Phlebectomy, Stenting, Endophlebectomy, AVstula, Recurrent varicose veins, Venous malformation

TABLE OF CONTENTS

Abbreviations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4

Chapter 1: General Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .5

1.1. History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

1.1.1. Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

1.1.2. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

1.1.3. Development in the last 50 years . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

1.2. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

1.2.1. Risk factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

1.2.1.1. Age . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

1.2.1.2. Gender . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

1.2.1.3. Obesity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

1.2.1.4. Family history . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

1.2.1.5. Ethnicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

1.2.2. Prevalence of reflux . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

1.2.3. Progression of varicose veins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

1.3. Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

1.3.1. The superficial veins of the lower extremity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7://dx.doi.org/10.1016/j.ejvs.2015.02.007

e cite this article in press as: Wittens C, et al., Management of Chronic Venous Disease, European Journal of Vascular and Endovascular Surgery), http://dx.doi.org/10.1016/j.ejvs.2015.02.007

2 C. Wittens et al.1.5. Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8

1.5.1. Venous reflux and obstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

Chapter 2: Clinical Presentation of CVD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .9

2.1. Clinical presentations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

2.2. Classification of chronic venous disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

2.2.1. Clinical Etiological Anatomical Pathophysiological (CEAP) classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

2.2.1.1. Clinical classification: C0eC6 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

2.2.1.2. Etiological classification: Ec, Ep, Es, En . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

2.2.1.3. Anatomical classification: As, Ap, Ad, An . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

2.2.1.4. Pathophysiological classification: Pr, Po, Pr/o, Pn . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

2.2.1.5. Level of investigation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

2.2.1.6. Applying the CEAP . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

2.2.2. Venous Clinical Severity Score, Venous Segmental Disease Score, and Venous Disability Score . . . . . . . . . . . . . . . . . . . . . . . . . 11

2.2.2.1. Venous Clinical Severity Score: measure of severity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

2.2.2.2. Venous Segmental Disease Score: pathophysiology and anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

2.2.2.3. Venous Disability Score: functional impact . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

2.2.3. Villalta-Prandoni Scale . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

2.3. Quality of life measures in venous disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

2.3.1. Health related generic tools . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

2.3.1.1. SF-36, Medical Outcomes Study 36 Item Short Form . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

2.3.1.2. EuroQoL, 5D . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

2.3.2. Disease specific tools . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

2.3.2.1. Aberdeen Varicose Veins Questionnaire . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

2.3.2.2. Chronic Venous Insufficiency Questionnaire . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

2.3.2.3. Venous Insufficiency Epidemiological and Economic study . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

Chapter 3: Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

3.1. Clinical examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

3.1.1. History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

3.1.2. Physical examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

3.2. Diagnostic tools . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

3.2.1. Definition of reflux . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

3.2.2. Handheld continuous wave Doppler . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16

3.2.3. Duplex ultrasound examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16

3.2.3.1. Efficacy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16

3.2.3.2. Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

3.2.3.3. Imaging recurrent disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

3.2.4. Plethysmography and venous pressure measurements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

3.2.4.1. Strain-gauge plethysmography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

3.2.4.2. Photoplethysmography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

3.2.4.3. Air-plethysmography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

3.2.4.4. Foot volumetry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

3.2.5. Phlebography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

3.2.6. Other imaging methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

3.2.6.1. Scientific evidence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

Chapter 4: Treatment Options in Chronic Venous Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

4.1. Dressings for venous ulcers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

4.2. Compression therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

4.2.1. Chronic venous disease without ulceration (C0eC4) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

4.2.2. Venous ulceration (C5eC6) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

4.2.2.1. Venous ulcer healing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

4.2.2.2. Venous ulcer recurrence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

4.2.3. Intermittent pneumatic compression for venous ulceration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

4.2.4. Compression after venous intervention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

4.3. Physiotherapy, leg elevation, and leg massage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

4.3.1. Physiotherapy for leg ulceration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

4.3.2. Leg elevation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

4.3.3. Leg massage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24

4.4. Medical treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24

4.4.1. Chronic venous disease without ulceration (C0eC4) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24

4.4.2. Venous ulceration (C5eC6) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

4.5. Sclerotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

4.6. Transcutaneous laser . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26

4.7. Endovenous treatments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27

4.7.1. Endovenous thermal ablation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27

4.7.1.1. Great saphenous vein . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27

4.7.1.2. Small saphenous vein . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29

4.7.2. Mechanochemical endovenous ablation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29

4.8. Surgery of the superficial veins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29

4.8.1. High ligation with/without stripping . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 294.8.2. Phlebectomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

4.8.3. Ambulatory Selective Varices Ablation under Local anaesthesia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

Please cite this article in press as: Wittens C, et al., Management of Chronic Venous Disease, European Journal of Vascular and Endovascular Surgery(2015), http://dx.doi.org/10.1016/j.ejvs.2015.02.007

4.8.4. Cure conservatrice et Hemodynamique de lInsuffisance Veineuse en Ambulatoire (CHIVA) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

4.8.5. Powered phlebectomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

4.9. Treatment of deep vein pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

4.9.1. Treatment of chronic deep venous obstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33

4.9.1.1. Percutaneous transluminal angioplasty and stenting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33

4.9.1.2. Open bypass procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34

4.9.2. Treatment of deep venous incompetence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34

Chapter 5: Recurrent Varicose Veins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35

5.1. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

5.2. Risk factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37

5.3. Diagnosis of recurrent varicose veins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37

5.4. Treatment of recurrent varicose veins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37

Chapter 6: Congenital Venous Malformations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

6.1. Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

6.2. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

6.2.1. International Society for the Study of Vascular Anomalies classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

6.2.2. Hamburg classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

6.2.3. Puig classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

6.3. Venous malformations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

6.4. Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

6.4.1. Klippel-Trenaunay syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

6.4.1.1. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

6.4.1.2. Clinical characteristics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

6.4.1.3. Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

6.4.1.4. Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

6.4.2. Parkes-Weber syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

6.4.2.1. Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

6.4.2.2. Clinical characteristics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

6.4.2.3. Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

6.4.2.4. Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44

ABBREVIATIONS

AASV Anterior Accessory Saphenous VeinAC AntiCoagulationAP Ambulatory Phlebectomy

HL High LigationHL/S High Ligation/StrippingIPC Intermittent Pneumatic CompressionISSVA International Society for the Study of Vascular

3APG Air-PlethysmoGraphyASVAL Ambulatory Selective Varices Ablation under

Local anaesthesiaAVMs ArterioVenous MalformationsAVP Ambulatory Venous PressureAVVQ Aberdeen Varicose Veins QuestionnaireBMI Body Mass IndexCEAP Clinical Etiologic Anatomic PathophysiologicalCHIVA Conservatrice et Hmodynamique de lInsufs-

ance Veineuse en AmbulatoireCIVIQ ChronIc Venous Insufciency QuestionnaireCT Computed TomographyCTV Computed Tomography VenographyCVD Chronic Venous DiseaseCVI Chronic Venous InsufciencyCVMs Congenital Vascular MalformationsCW Continuous WaveDUS Duplex UltraSoundDVT Deep Venous ThrombosisEBM Evidence Based MedicineESVS European Society for Vascular SurgeryEVLA EndoVenous Laser AblationEVTA EndoVenous Thermal AblationGSV Great Saphenous VeinGWC Guideline Writing Committee

AnomaliesIVC Inferior Vena CavaIVUS IntraVascular UltraSoundKTS Klippel-Trenaunay SyndromeLMWH Low Molecular Weight HeparinMOCA Mechanochemical ablationMPFF Micronized Puried Flavonoid FractionMR Magnetic ResonanceMRV Magnetic Resonance VenographyNIVL Non-thrombotic Iliac Vein LesionsOR Odds RatioPASV Posterior Accessory Saphenous VeinPTA Percutaneous Transluminal AngioplastyPTS Post Thrombotic SyndromePWS Parkes-Weber SyndromeQALYs Quality-Adjusted Life YearsQoL Quality of LifeRCT(s) Randomized Controlled Trial(s)REVAS REcurrent Varices After SurgeryRFA RadioFrequency AblationSEPS Subfascial Endoscopic Perforator SurgerySFJ SaphenoFemoral JunctionSPJ SaphenoPopliteal JunctionSSV Small Saphenous VeinSTS Sodium Tetradecyl SulphateHCSE Horse CheStnut Extract TCL TransCutaneous Laser

Please cite this article in press as: Wittens C, et al., Management of Chronic Venous Disease, European Journal of Vascular and Endovascular Surgery(2015), http://dx.doi.org/10.1016/j.ejvs.2015.02.007

Strategy

members. The nal version of the guideline was submittedon December 22, 2014.

Literature search and selection

A clinical librarian performed the literature search for thisguideline systematically in PubMed, Embase, Cinahl, andthe Cochrane Library up to January 1, 2013. Referencechecking and handsearch by the guideline committeemembers added other relevant literature.

The members of the GWC performed the literature se-lection based on information provided in the title and ab-stract of the retrieved studies.

Criteria for search and selection were:

GWC reviewed and summarized the selected literature.

Language: English, German, and French

4 C. Wittens et al.and other factors.The recommendations are valid only at the time ofTo dene the current guidelines, members of theINTRODUCTION

Members of this Guideline Writing Committee (GWC) wereselected by the European Society for Vascular Surgery(ESVS) to represent physicians involved in management ofpatients with chronic venous disease (CVD). The membersof the GWC have provided disclosure statements of allrelationships that might be perceived as real or potentialsources of conicts of interest. These disclosure forms arekept on le at the headquarters of the ESVS. The GWCreport received neither nancial support nor support fromthe ESVS or any pharmaceutical, device, or surgicalindustry.

The ESVS guideline committee was responsible for theendorsement process of this guideline. All expertsinvolved in the GWC have approved the nal document.The guideline document was reviewed and approvedby the EJVES editorial board and ESVS guidelinecommittee.

THE PURPOSE OF THESE GUIDELINES

The ESVS has developed clinical practice guidelines for thecare of patients with CVD in the lower extremities.

The aim of this document is to assist physiciansin selecting the best management strategy for patientswith CVD. This guideline, established by members of theGWC, who are members of the ESVS or non-members with specic expertise in the eld, is basedon scientic evidence completed with expert opinion onthe matter. By summarizing and evaluating all availableevidence in the eld, recommendations for the evaluationand treatment of patients with CVD have beenformulated.

Guidelines have the purpose of promoting a standard ofcare according to specialists in the eld, in this case repre-sented by members of the ESVS. However, under nocircumstance should this guideline be seen as the legalstandard of care in all patients. As the word guideline statesin itself, the document is a guiding principle, but the caregiven to a single patient is always dependent on the indi-vidual patient (symptom variability, comorbidities, age, levelof activity, etc.), treatment setting (techniques available),

TIPP TransIlluminated Powered PhlebectomyUGFS Ultrasound Guided Foam SclerotherapyVCSS Venous Clinical Severity ScoreVDS Venous Disability Scorepublication, as technology and disease knowledge in thiseld changes rapidly and expanding recommendations canbecome outdated. It is an aim of the ESVS to revise theguidelines when important new insights in the evaluationand management of CVD become available.

Please cite this article in press as: Wittens C, et al., Management of Chronic(2015), http://dx.doi.org/10.1016/j.ejvs.2015.02.007Several relevant articles published after the searchdate or in another foreign language were included, but onlyif they were of paramount importance to this guideline.

Weighing the evidence

Level ofevidence:

Selection of the literature was performedfollowing the pyramid of evidence, withaggregated evidence in the top of the pyramid(systematic reviews, meta-analysis), thenrandomized controlled trials, then observationalstudies. Single case reports, animal studies, and invitro studies in the bottom of the pyramid wereexcluded, leaving expert opinions at the bottomofthe pyramid. The level of evidence per section inthe guideline is dependent on the level ofevidence available on the specic subject.

Sample size: If there were large studies available, with aminimum of 15 subjects per research group, onlythese were included. If not available, smallerstudies were also included.The GWC was convened in 2011 at the annual ESVS meetingin Athens. At that meeting the tasks in creating the guide-line were evaluated and distributed among the committeeMETHODOLOGY

VEINES Venous Insufciency Epidemiological and Eco-nomic Study

VMs Venous MalformationsVSDS Venous Segmental Disease ScoreConclusions were drawn based on the scienticevidence.

The guidelines in this document are based on the Euro-pean Society of Cardiology grading system. For eachrecommendation, the letter A, B, or C marks the level of

Venous Disease, European Journal of Vascular and Endovascular Surgery

5Table 1. Levels of evidence.

Table 2. Classes of recommendations.

Management of Chronic Venous Diseasecurrent evidence (Table 1). Weighing the level of evidenceand expert opinion, every recommendation is subsequentlymarked as either class I, IIa, IIb, or III (Table 2). The lowerthe class number, the more proven is the efcacy and safetyof a certain procedure.

CHAPTER 1: GENERAL CONSIDERATIONS

The term CVD has been used to describe both visual andfunctional manifestations of abnormalities in the peripheralvenous system. It can be dened as (any) morphologicaland functional abnormalities of the venous system of longduration manifest either by symptoms and/or signs indi-cating the need for investigation and/or care.1

The prevalence of CVD in the adult population has beenreported to be as high as 60%, particularly affecting pop-ulations in the developed world.2,3 It has become clear thatCVD is an important cause of patient distress and signi-cantly impacts on healthcare resources.4,5

Although a complete understandingof thepathophysiologyof CVD remains elusive, chronic venous hypertension iswidelyaccepted as the predominant cause of advanced venous skinchanges and ulceration. A sound understanding of the diseaseprocess and its clinical presentations is paramount in assess-ment and management of the patient with CVD.

Please cite this article in press as: Wittens C, et al., Management of Chronic(2015), http://dx.doi.org/10.1016/j.ejvs.2015.02.0071.1. History

1.1.1. PathophysiologyIn ancient times, venous problems were described occasion-ally. Hippocrates (460e377 before Christ) stated that an up-right position was inappropriate for a leg with ulceration,assumingly not knowing the real background at that time. In1544, a Spanish anatomist, Vassaseus, gave a description ofvenous valves and their function.6 At the beginning of theseventeenth century, Harvey published his contribution to theunderstandingof thephysiologyof the venous circulation, andMalpighi demonstrated the existence of capillaries andthereby claried the nal connection in the circulatory sys-tem.7 At the same time, Brodie described symptoms and signsof chronic venous insufciency (CVI).8 In 1670, Lowerdescribed venous return as a result of the arterial propagatingpulsation (vis a tergo), and also described the musclepump.7 The pressure changes caused by thoracoabdominalrespiration, enhancing the venous returne vis a frontee tothe heart, were described in 1710 by Valsalva.7

In 1891, the classical test was invented to differentiate be-tween supercial and deep reux/retrograde ow by Tren-delenburg, and5 years later a test to verify patencyof the deepveins was proposed by Perthes, both tests using compressionof the limb.7 Homans pointed out that ulcerationwas differentin behaviour dependent on whether it was a result of super-cial or deep disease.9 Linton introduced the concept ofambulatory venous hypertension as the fundamental patho-physiologic theory for terminal and distinct CVD.10

1.1.2. TreatmentHippocrates recommended puncture of varicose veins fol-lowed by compression.8 Four-hundred years later, Celsusperformed an avulsion technique with hooks of varicoseveins.The French surgeon Pravaz has been given credit for thedesign of the syringe and needle technique for vascular in-jection in 1831, and later Ptrequin introduced the method ofsclerotherapy for varicose veins. After unsatisfactory resultsby Smith in 1939, the technique was discredited for manyyears.11 In 1944, Orbach introduced the so called air-blocktechnique to avoid dilution of the injected sclerosant and, atthe same time, create close contact with the endothelium,which indeedwas a step forward and also a precursor towardsfoam sclerotherapy.12 Trendelenburg proposed great saphe-nous vein (GSV) ligature atmid-thigh in 1891 as being a step tocontrol distal varicosities.13 The most used methods havebeen the external stripping byMayo and the Babcock methodwith the intraluminal technique, both at the beginning of thetwentieth century, and later pin-stripping by Oesch in 1963.14

Muller revisited the accompanying hook phlebectomy in 1956through minimal incisions.15

Elastic stockings were invented in 1930 as a result of thepersonal experience of Jobst, an engineer, who himselfsuffered from a venous ulceration. While bathing in hispool, he noticed that his symptoms were less pronounced,coming to the conclusion that the increasing depth of thewater was the secret of the healing component. Thus,

graduated compression stockings were invented.16


1.1.3. Development in the last 50 yearsBypass procedures were popularized as the May-Husnioperation at the femoral level,17 and the Palma operationfor iliac occlusion.18 Gloviczki presented experimental workon abdominal bypass surgery with prosthetic grafts andarteriovenous stulae some years later.19 Eklf suggested thebenet of using an arteriovenous stula after iliac throm-bectomy.20 At the same time, the pioneers Kistner and Rajuperformed valve reconstructions and valve transfer.21,22

Hauer introduced subfascial endoscopic perforator surgery(SEPS) in 1985.23 Balloon dilatation and implantation of stentsin the venous system was published for the rst time in 1991by Okrent using ballooning and in 1994 by Semba, who usedthe more durable stenting technique. Both procedures wereused as additional treatments to catheter directed throm-bolysis at the ilio-femoral level.24,25 Stenting of iliac obstruc-tion in patients with CVI was popularized by Nglen in 2000 ina large scale study.26

The endovenous procedures for varicose veins weredeveloped in the 1990s as thermal, chemical, and mecha-nochemical vein ablation for truncal varicose disease butwere based on the initial work of electro puncture andcauterizations of varicose veins dating back to the 1960s.

1.2. Epidemiology

Clinical reporting, usually indicated as the C of the CEAPclassication (from C0 to C6, see further 2.2.1) makes itpossible to report prevalence numbers for each clinical class aswell as progression rates through the clinical classes over timeand relationship to gender, age, obesity, and other risk factors.The prevalences of CVD differ according to these risk factors.The newest and most comprehensive epidemiologic studiesfrom this century will be presented here. Telangiectasiae (alsoknown as spider veins) (C1) have been reported to affect up to80% of the population.2 Varicose veins (C2) are also extremelycommon,with a variable reported incidence ranging from 20%to 64%.2,27e29 The more advanced stages of venous disease,CVI (C3eC6), appear to affect about 5% of the population,with the prevalence of the end stages of CVI (active and healedvenous ulcers, C5C6) estimated at 1e2%.30

1.2.1. Risk factors1.2.1.1. Age. Several studies have revealed older age as themost important risk factor for varicose veins and CVI. In theSan Diego study, older age showed a signicant odds ratio(OR) up to 2.42 for varicose veins and up to 4.85 for CVI.31

In the Bonn Vein study, the most important risk factor forvaricose veins and CVI was older age (OR in the age 70e79years were 15.9 for varicose veins and 23.3 for CVI).32

1.2.1.2. Gender. C2 disease is more common in femaleadults than male adults: 13.9e46.3% females and 11.4e29.3% males based on 50,974 persons with most between16 and 90 years in the ve classical studies from Europe andthe USA.31e35 In the same studies, C3 varied from 4.5% to13.6% and the prevalence of C4eC6 varied from 3.6% to12%.31e33,35 A similar prevalence of C2 was found in women

6who had never been pregnant, and in men.36 In the samestudies, the inuence of gender on C0eC1 is inconclusive.

Please cite this article in press as: Wittens C, et al., Management of Chronic(2015), http://dx.doi.org/10.1016/j.ejvs.2015.02.007However, it has to be mentioned that in the Edinburgh Veinstudy, varicose veins (C2) were more common among malesubjects in the general population.29

The incidence of varicose veins per year is 2.6% in womenand 1.9% in men.37 The gender inuence diminishes withage.38 No obvious gender difference is shown concerningCVI.32,34,35

Oral hormone replacement and contraceptives do not in-crease the risk of varicose veins.32,39 The number of preg-nancies increased the OR from 1.3 to 2.2 for development ofvaricose veins.32 Another recent large scale study could notdemonstrate change in GSV reux following pregnancies.40

Half of the general population in the Bonn Vein studyreported venous symptoms, 49.1% of the males and 62.1%of the females, and the prevalence increased with age.41

Symptoms were more frequently reported in limbs withdeep venous involvement compared with supercial, andwere also more frequent in women.31

In a recent global collection of prospective epidemiologicdata on chronic venous disorder in 91,545 subjects includingareas outside Europe and the USA, almost the same obser-vations weremade, but on a larger scale. Symptomatic C0wasmore frequent in men and C2eC3 more frequent in women,but C4eC6 did not differ between men and women.27

1.2.1.3. Obesity. A body mass index (BMI) greater than 30increases the risk for CVI signicantly, with ORs for men andwomen of 6.5 and 3.1, respectively.41 Another study founda positive correlation between a BMI of more than 30 andvaricose veins (OR 5.8) in postmenopausal women.42 Otherauthors found an association between severe obesity (BMI40 or more) and increasing limb symptoms withoutanatomic evidence of venous disease, suggesting that theobesity itself contributed to the venous insufciency.43

Similar ndings were published in a larger scale investiga-tion with a threshold of BMI of 25.44

1.2.1.4. Family history. Many studies have shown a corre-lation between a positive family history for varicose veins orvenous disease and the risk of varicose veins.32 A cohortstudy revealed that a family history of hospital treatment forvaricose veins was associatedwith an increased risk of similartreatment among relatives.45 Responsible genetic distur-bances have not been found to explain the obvious heredity.Genome-wide association studies should be considered tofurther unravel the genetic basis of venous disease.46

1.2.1.5. Ethnicity. For many years, prevalence studies havebeen based on gures and numbers from the western world.Data from Europe, Latin America, theMiddle East, and the FarEast are now available in the large scale Vein Consult Programwith 91,545 subjects over 18 years of age. C1eC6 involved63.9% of the subjects. The incidence of C2 was signicantlylower in theMiddle East, whereas C1 was signicantly higher.C5 and C6 were unequally distributed in the regions.27

1.2.2. Prevalence of reuxIn the Edinburgh Vein study with 1,566 subjects, the aimwas to correlate venous reux with clinical features. Reux

C. Wittens et al.was dened as reversed ow longer than 0.5 seconds. Noreux was found in 36.5% of the patients. One third of the


rarely (in 1% of patients) the GSV is duplicated, whichmeans two veins are situated in the same saphenous

compartment.53

A few millimetres distal to the saphenofemoral junction(SFJ), the GSV has a terminal valve, and a few centimetresdistal to that valve there is often another valve, called thepre-terminal valve.54,55 Important tributaries (i.e. supercialcircumex iliac, supercial epigastric, and supercialexternal pudendal veins) join the GSV between thesevalves. The anterior accessory saphenous vein (AASV) andthe posterior accessory saphenous vein (PASV) arefrequently present and run parallel to the GSV in the thighin their own saphenous compartment.

The SSV ascends upwards on the posterior aspect of thecalf between the two heads of the gastrocnemius muscle. Inthe popliteal fossa, the main trunk of the SSV frequentlydrains into the popliteal vein. Often, a cranial extension ofthe SSV, called the thigh extension, continues upwardsand uncommonly the SSV does not drain into the poplitealfossa but instead continues cranially and eventually emptiesinto the femoral vein or the GSV. Veins connecting the GSVand SSV are called intersaphenous veins. A particularintersaphenous vein is the Giacomini vein running from theSSV in the popliteal fossa to the GSV.55 The SSV lies in itssubjects had incompetence limited to the supercial sys-tem. The frequency of reux in both supercial and deepsegments increased with the clinical severity of disease. CVIincreased with age. Symptoms were strongly related to theseverity of CVI.47 Pattern of reux has also been examinedin the Bonn Vein study with 3,072 subjects.48 Pathologicalreux was dened as longer than 0.5 seconds. The preva-lence of supercial reux was signicantly higher in women,whereas deep venous reux was signicantly higher in men.Both types correlated with progression in C stages, but onlysupercial reux showed a marked increase with age.48

1.2.3. Progression of varicose veinsThe prevalence of C6 disease varies from 0.1 to 0.5%.32,33

However, this does not reveal the rate of progression fromlower to higher C classes. A study including 116 limbs withvaricose veins used a second duplex scan a median 19monthsafter the initial examination in the period waiting for surgery.Approximately one-third of the patients had progression, andin 95% of the patients the changes were noted after 6 monthsor more.49 In the large scale Bonn Vein study, the progressionrate from varicose veins to CVI was 4% per year.50

1.3. Anatomy

1.3.1. The supercial veins of the lower extremityThe full length of the GSV is covered by a connective tissuelamina called the saphenous fascia, and typically lies inthe saphenous compartment.51 On B-mode ultrasound itresembles an Egyptian eye in transverse scan with thesaphenous fascia easily being identied.52 In the GSVcompartment there is usually only one truncal vein. Very

Management of Chronic Venous Diseaseown saphenous compartment, delineated by the supercialfascia and the muscular fascia.56,57

Please cite this article in press as: Wittens C, et al., Management of Chronic(2015), http://dx.doi.org/10.1016/j.ejvs.2015.02.007Perforating veins are variable in arrangement and distri-bution, and are numerous (more than 100 in each limb). Themedial perforating veins are most signicant but their rolein CVI and venous ulcers is not well dened.58e61

1.3.2. The deep veins of the lower extremityVenous blood from the foot drains through the deep plantarvenous arch, which at the medial malleolus becomes theposterior tibial veins.62 On the dorsum of the foot the deepdorsal digital veins drain into the dorsal metatarsal veins. Thedorsalis pedis vein located on the dorsumof the foot becomesthe anterior tibial veins at the ankle. The tibioperoneal trunkand the anterior tibial veins join and form the popliteal vein inthe popliteal fossa.

The main tributaries of the popliteal vein are the gastroc-nemius veins, the tibial veins, and the SSV, although thegastrocnemius veins may join the SSV before joining thepopliteal vein. The saphenopopliteal junction (SPJ) is oftenlocated within 5 cm of the popliteal skin crease, but this levelvaries.

The popliteal vein continues in a cephalad direction, andascends in the adductor canal becoming the femoral vein(the previously used term supercial femoral vein hasbeen abandoned).63 Approximately 10 cm below theinguinal ligament, the femoral vein joins with the deepfemoral vein to form the common femoral vein. The com-mon femoral vein is situated medially to the correspondingartery and it ends at the inguinal ligament. The vein receivesthe GSV at the SFJ. Both the popliteal and the femoral veinmay be duplicated in segments of various lengths.64,65

Above the inguinal ligament the common femoral veincontinues as the external iliac vein, and at the junction ofthe internal and external iliac veins anterior to the sacroiliacjoint they form the common iliac vein.

As well as the supercial veins, the deep veins containvalves. The frequency of valves increases from the moreproximal veins to the more distal. The calf veins containnumerous valves, whereas the femoral and popliteal veinshave only one or two valves.66,67 Additional valves are seen,however, in the femoral vein near the junction with the deepfemoral vein. The common femoral vein usually contains onlyone valve. Cranial to the SFJ, there is only one or no valve. Inthe common iliac vein, valves are practically absent or rudi-mentary, andvalves are absent in the inferior venacava (IVC).66

1.4. Physiology

The venous circulation is a low pressure, low velocity, largevolume, low resistance vascular system. The primary func-tion of the venous system is to return blood to the heart.Venous return is inuenced by the interaction between acentral pump (the heart), pressure gradients, the peripheralvenous pump, and competent valves in patent veins. In anupright position these factors work together to overcomethe hydrostatic pressure induced by gravity, which is quitedifferent in the supine position. Furthermore, the system ischaracterized by its capacitance, which allows pronounced

7uid variations. Finally, the system has an impact on theregulation of body temperature.


supercial veins, thus creating a pressure gradient craniallyIn steady state, the venous return equals the cardiacoutput. The venous system contains at least 60% of totalresting blood volume, with half of this being in the post-capillary venules in the lower extremity. About 25% re-sides in the splanchnic circulation.68,69

1.4.1. The relationship of capacitance/volume to pressureVariations in venous blood volume of up to 10e20% aretolerated.68,70 A simple shift from a supine to an uprightposition can be responsible for a 10% volume change in thelower extremity.69 An increase in capacitance is normal late inthe day after standing or sitting, and almost 20% of normalvolunteers will demonstrate valvular dysfunction.71

The system has a unique function based on the veincompliance.Tomaintain anacceptable lowpositivepressure of5 mmHg, the veins become accid, and the pressure can evenbe negative with minimal volume. In contrast, a considerableincrease in volume will result in only a relatively modestchange in pressure. A change in vein shape from elliptic tocircular indicates high volume and high pressure. In otherwords: over a normal pressure range of 5e25 mmHg, volumecan change remarkably without affecting either ow orpressure.70

1.4.2. The hydrostatic and dynamic pressureIn the non-supine situation, gravity exercises a hydrostaticinuence on the venous system.The hydrostatic pressure at agiven anatomical point is determined by measuring the ver-tical distance between the heart and the point of interest.72 Inthe upright position, the hydrostatic pressure, measured in adorsal foot vein, is determined by the blood column betweenthe right atrium and the foot. For example in a person 175 cmtall, the venous pressure at the foot may reach approximately95mmHg, with the pressure at the groin being 30e35mmHg,dependent on the anthropometric shape of the body.

The dynamic pressure is basically caused by propagation ofarterial pulsation from the pumping heart. Through pre-capillary arterial vasoconstriction - among other factors -most of the dynamic pressure is decreased, resulting in apressure of 12e18 mmHg in the venous side of the capillary.The atrial pressure of 4e7mmHg causes the resulting dynamicpressure gradient to facilitate return of blood to the heart inthe supine position. The respiratory inuence is positive forvenous return. Inspiration creates a negative pressure in thethoracic cavity, creating a kind of suction of blood, whileincreased abdominal pressure during inspiration reduces owin the abdomen. During expiration the opposite owpattern isseen. This mechanism is mostly seen in the supine position.73

1.4.3. The vein valvesThe valves divide the column of blood into segments andprevent retrograde ow.74 The greater number of valves in theinfrapopliteal segment suggests their greater functionalimportance at this level.75 A normal valve can resist a pressureabove 300 mmHg, but reux will occur at a higher pressure. Inpatients with supercial or deep vein valvular imcompetencereux develops at a much lower pressure because of valve

8disease and/or vein dilatation.73 In the presence of normalvalve function the blood is conducted from the supercial

Please cite this article in press as: Wittens C, et al., Management of Chronic(2015), http://dx.doi.org/10.1016/j.ejvs.2015.02.007and from the calf.78 During relaxation the blood is directedfrom the supercial veins to the deep veins, with the lowestpressure at this stage. The foot pump is quite different infunction with elongation of the plantar veins during walking,thus squeezing the blood antegradely.79 The compression ofthe plantar venous plexus during walking is a primer of the calfpump.62Half of the blood can be ejected upwards in one singlecontraction.80,81 The contribution of thigh muscle contractionis minimal compared with the above mentioned pumps.81

1.4.5. Venous toneVenous tone is managed by the muscle layer in the veinwall. Several mechanisms, such as sympathetic-adrenergicnerve activity, circulating vasoactive substances, and localmetabolites will stimulate it.73

1.4.6. The venous pump: main transport system in thenon-supine positionIn an upright position venous return is still inuenced by thedynamic effect from the heart. The increase in hydrostaticpressure is the same in both the arteries and veins. Fortu-nately the potent veno-arterial reex, activated by the venousdilatation, involves an arteriolar constriction restricting thearterial blood ow by 50%.73,82 Even in a so called relaxedstanding position therewill bemuscle contractions, whichwilldiminish the capillary pressure distally in the extremity. Withuse of the muscle pumps and the valves, together called thevenous pump, the pressure distally will be decreased toapproximately 30mmHg during walking or tiptoe/heel raisingmanoeuvres. This pressure is called the ambulatory venouspressure (AVP), which can bemonitored through a needle in afoot vein. Measuring AVP is potentially meaningful. It hasbeen shown that no ulceration was observed in limbs withAVP less than 30 mmHg, but there was 100% incidence withAVP above 90 mmHg.83

1.5. Pathophysiology

The pathophysiology of CVD is characterized by reux,obstruction, or a combination of both. This results in reducedability to empty the leg veins efciently during exercise, whichmeans theAVP remains high and this eventually leads to all theclinical features of venous hypertension. Apart from reux andobstruction, other underlying factors may compromiseadequate venous emptying, such as failure of the calf and footmuscle pump (decreased mobility of the ankle joint and otherveins to the deep veins through the perforating system. Anexception is the perforating veins in the foot, where bidirec-tional ow is normal.75 One study has described the valvescreating jet streams in the venous system.76 Thisowpattern islater described as helical, especially at venous junctions.77

1.4.4. The calf muscle and the foot pumpThese pumps act together during walking. Intramuscularpressure can increase up to 200e300 mmHg, creating apressure three times higher in the muscle veins than in the

C. Wittens et al.neuromuscular problems).80,83,84 Whereas most patients withuncomplicated varicose veins (C2) still have normal venous


pressures during ambulation, all those with more advancedstages of CVD progressively develop venous hypertension,characterized by symptoms and signs of CVI (C3eC6). Theclinical manifestations of CVI are oedema and skin changes,from hyperpigmentation, eczema, atrophie blanche and lip-odermatosclerosis to venous ulcers.

Deep vein valve incompetence will result in minor or noreduction in AVP, and venous obstruction will even elevatethe pressure during calf contractions, both representingambulatory venous hypertension.85,86 Outow obstructionat ilio-femoral level with or without valvular incompetencein the femoral and/or popliteal vein can lead to venousclaudication described as a bursting pain while walking,only relieved by rest or even better by elevation. In multi-level post-thrombotic obstruction, the iliac vein lesions arethe key pathology as infrainguinal obstructions are bettertolerated because of adequate collateralization.87 Thepathophysiological combination of reux and obstruction issignicantly more common in patients with venous ulcera-tion than in those with less advanced stages of CVD.88

1.5.1. Venous reux and obstructionIn incompetent supercial veins, reux is primarily caused byvein wall abnormalities.89,90 Varicose veins contain anincreased amount of collagen and decreased number ofsmooth muscle cells and elastin leading to disorganization ofmuscle components, disruption of elastic bres, andbrosis.91e93 The weakness of the vein wall results in dilata-tion and enlargement of the valve ring, making the valveunable to work sufciently, with reux as the consequence.94

The reux can be axial or segmental. For many years, it hasbeen accepted that this process starts cranially, mainly at thelevel of the SFJ or SPJ, and from there extends to the maintrunks and further to the supercial tributaries. This is the socalled descending pathophysiological theory. More recentresearch has proposed a rather multifocal origin of varicoseveins, which states that, rst, tributaries become dilated andincompetent, and only thereafter the main trunks, andeventually the junctions. This corresponds with theascending theory of varicose vein development.95

The pathology in the deep veins is more complex. Acuteobstruction occurs in the case of deep vein thrombosis.This isnot discussed further in the present guideline. Chronicobstruction, resulting in increase of resistance to blood ow, ismainly caused by post-thrombotic changes consisting of ste-nosis, occlusion, intraluminal synechia, and increased rigidityof the vein wall, or any combination of these abnormalities.96

Valves may be damaged and collaterals will develop at anyplace parallel to a deep obstruction, and even these can beincompetent. Chronic deep venous incompetence occurs in80% of cases because of post-thrombotic valvular changes,and in 20% because of primary valvular incompetence.75

Ilio-femoral venous occlusion is less likely to recanalizecomparedwith other venous segments. Almost two thirds willremain more or less obstructed with variable collateraliza-tion.97 Obstruction in combinationwith reuxoccurs in 55% of

97,98

Management of Chronic Venous Diseasesymptomatic patients. In patients with ulceration, thecause is distributed almost equally between supercial and

Please cite this article in press as: Wittens C, et al., Management of Chronic(2015), http://dx.doi.org/10.1016/j.ejvs.2015.02.007deep venous incompetence.99 Perforator incompetence hasproven to be a signicant factor in the determination of CVDseverity.100

CHAPTER 2: CLINICAL PRESENTATION OF CVD

2.1. Clinical presentation

The symptoms of CVD are extremely variable and causesignicant morbidity to patients, negatively impacting onquality of life (QoL).101,102 Self reported symptoms areworse in women.5,35 Patients present with heaviness,tiredness, itching of the skin, nocturnal cramps, andthrobbing and aching of the legs, which is exacerbated byprolonged standing.16 These symptoms can interfere withday to day activities and work, particularly in patients whoneed to stand for prolonged periods of time. Symptoms areworse at the end of the day, and symptomatic relief may beachieved by leg elevation, mobilization, and exercise.

In patients with chronic outow obstruction, venous clau-dication may typically occur during walking or climbing stairs.

Supercial veins can thrombose, resulting in painfulthrombophlebitis and localized cellulitis. Deep venousthrombosis, particularly if found in the ilio-femoral segment,may lead to the development of venous claudication, abursting pain affecting the buttocks, thighs, or legs whenwalking, requiring rest and leg elevation to achieve symp-tomatic relief.

Uncommonly, bleeding can be a presentation of CVD. Thisis commonly associated with a traumatized supercial var-icosity, but signicant bleeding can also arise from an areaof ulceration. The resulting blood loss may be profound andeven life threatening.103

Studies have demonstrated that clinical signs correlatewith patterns of venous reux as identied by duplex ul-trasound (DUS) examination. This is true for the supercialvenous system (including both great and small saphe-nous)104 and the deep venous system.47 There is evidencesuggesting that clinical signs of disease also correlate withGSV vein diameter, with increasing diameter being associ-ated with greater disease severity.105

QoL scores also correlatewith disease severity. Patientswithmore severe signs and symptoms report worse QoL scores.106

Clinical recurrence of varicose veinsmay present in a similarfashion to primary supercial venous disease. A multicentrestudy was performed to assess the presence of recurrence inpatients who had undergone previous varicose vein sur-gery.107 Following the CEAP classication,123 the vast majorityhad recurrence associated with oedema (C3) (70.9%), while29.1% had skin changes (C4). Varicose veins were present in24.6% (C2), in 43% two clinical classes were present, and in24% four classes were present. There was a mixture of C0eC6classes, from reticular veins and telangiectasiae, to varicoseveins, oedema, hyperpigmentation, and ulceration.

2.2. Classication of chronic venous disease

The diverse nature of presenting signs and symptoms of

9patients with CVD means that objective classication ofdisease severity presents a signicant challenge.


Classication of CVD may be performed using clinical,anatomical, haemodynamic, or patient reported criteria. Acomprehensive classication system would ideally take intoconsideration all of these factors.

Dramatic variations and inconsistencies in the assess-ment of disease severity have made it difcult to interpretand compare published reports in the literature. The chal-lenge of inconsistent reporting and the recognition thatthere was a need for a uniform, applicable and standardizedclassication system for venous disease, was the mainmotivation for the development of classications, particu-larly the CEAP classication.

2.2.1. Clinical Etiological Anatomical Pathophysiological(CEAP) classicationThe CEAP classication was published in 1994 by an inter-national ad hoc committee of the American Venous Forumand endorsed by the Society for Vascular Surgery.108

Following the meeting, it was published in 26 journalsand books and in nine languages, making it a truly universaldocument in the eld of CVD. It was revised in 2004 and is awidely endorsed classication system for clinical papersreporting on CVD (Table 3).109

The CEAP classication system was developed to take

10into account not only clinical (C) aspects of venous disease,but also etiological (E), anatomical (A), and pathophysio-logical (P) components, enabling a more comprehensiveassessment of the severity of venous disease. The CEAPclassication system has largely replaced the previousseverity tools, allowing a standardized approach to the signsand symptoms of CVD and enabling correlation betweendifferent studies and reports. Nonetheless, CEAP has been

Table 3. CEAP Classication.C: Clinical ClassicationC0: no visible or palpable signs of venous diseaseC1: telangectasia or reticular veinsC2: varicose veinsC3: oedemaC4a: hyperpigmentation or eczemaC4b: lipodermatosclerosis or atrophie blancheC5: healed venous ulcerC6: active venous ulcers: symptomatic, including ache, pain, tightness, skin irritation,heaviness, muscle crampsa: asymptomaticE: Etiological ClassicationEc: congenitalEp: primary (undeterminate cause)Es: secondary (e.g. post thrombotic)En: no venous cause identiedA: Anatomical ClassicationAs: supercial veinsAp: perforator veinsAd: deep veinsAn: no venous location identiedP: Pathophysiological ClassicationPr: reuxPo: obstruction

Pr,o: reux and obstructionPn: no venous pathophysiology identiable

Please cite this article in press as: Wittens C, et al., Management of Chronic(2015), http://dx.doi.org/10.1016/j.ejvs.2015.02.007reported as having moderate inter-observer reproducibilitywhen deciding medical indication for treatment.110

2.2.1.1. Clinical classication: C0eC6. Clinical signs formthe basis of the clinical component of CEAP, which is scoredfrom 0 (no evidence of venous disease) to 6 (active ulcer-ation). Although increasing C classication is generallyconsidered to represent increasing disease severity, thisshould not be considered a linear progression or severityscore. Unlike the Widmer and Porter classications, theCEAP classication allows more detail to be recorded.Symptoms of CVD, including aching, pain, tightness, skinirritation, heaviness, and muscle cramps are denoted by theletter S in subscript, for example C2S (symptomatic) or C2A(asymptomatic). Even if skin changes have occurred, a pa-tient may be asymptomatic, for example C5A.2.2.1.2. Etiological classication: Ec, Ep, Es, En. Assessmentand management of CVD varies depending on the under-lying etiological process. The CEAP classication recognizesand records three different causative factors: congenital(Ec), primary (Ep), and secondary or post-thrombotic (Es). Incases where no etiology is found, (En) is used.

Congenital factors are present from birth, and are relatedto disorders in the development of the venous system.Klippel-Trenaunay syndrome (KTS), Parkes-Weber syndrome(PWS), and vascular malformations are examples ofcongenital anomalies.

Primary venous disease commonly results in supercialvenous incompetence, particularly located at the connect-ing points between deep and supercial veins, SFJ, SPJ, orperforating veins. Incompetence (or reux) of the super-cial venous system may result in venous hypertension andthe development of signs and symptoms of CVD.

Secondary venous disease usually occurs as a result ofprevious deep venous thrombosis, although trauma andintra-abdominal masses may also result in impaired venousdrainage and the development of CVD.2.2.1.3. Anatomical classication: As, Ap, Ad, An. Theanatomical classication allows accurate description of thelocation of venous disease. The classication recognizessupercial (As), perforating (Ap), and deep (Ad) venoussystems as the site of venous incompetence.

This can be inferred with the aid of clinical tests and thehandheld Doppler probe, but determined much more reli-ably with DUS examination. Where examination cannotidentify the location of venous incompetence, the patient isclassied as (An). Supercial disease may affect either thegreat or small saphenous systems. Clinical examination andDUS imaging can provide detailed information to enabletargeted assessment and management planning.2.2.1.4. Pathophysiological classication: Pr, Po, Pr/o, Pn.The pathophysiological mechanism for CVD has been denedas reux (Pr), obstruction (Po), both (Pr/o), or not identied(Pn). In the advanced CEAP classication, the venous systemhas been described as 18 named (and numbered) venoussegments, which could be included in the classication toprovide a detailed description of CVD in each leg, in an indi-

C. Wittens et al.vidual patient. Although the detailed elaboration in theadvanced CEAP may seem unnecessarily complex or


intimidating, it is the only classication to provide a widelyaccepted and understandable description of all aspects ofCVD.2.2.1.5. Level of investigation. The diagnostic evaluation ofvenous disease can be classied as111:

Level 1: history and examination, with or withouthandheld Doppler assessment

Level 2: non-invasive imaging with colour venous duplexand plethysmography, if available

Level 3: invasive or complex imaging, including veno-graphy, computerized tomography, or MR imaging.

2.2.1.6. Applying the CEAP. The CEAP classication is widelyaccepted as the best available (and most widely used)classication system, and should be used by investigatorsreporting on CVD.112 It is important to realize that this is ameasure that can be repeated to classify changes in pa-tients clinical presentation. It should be initialized at the

tools have been described to address some of thesecriticisms.2.2.2.1. Venous Clinical Severity Score: measure of severity.The Venous Clinical Severity Score (VCSS) was developed tosupplement (rather than replace) the CEAP classication.VCSSoffers a broad quantication of the severity of venous diseaseand is not a detailed descriptive tool for CVD in an individualpatient. It takes into account the disease severity, and thedegree to which patients are affected by it (Table 4). A total of10 clinical characteristics are evaluated by a healthcare workerand graded from absent (score 0) to severe (score 3), with atotal of 30 points attributable. It was developed to assess theprogression of CVD and also to give additional weight to moresevere clinical disease (C4eC6).115,116

The VCSS provides a more accurate measure of theseverity of disease and the effect on the patients day today activities. Although it is used as a severity score, it hasalso been found to be a useful screening tool because of itscorrelation with severity on imaging.117,118 It has been usedand evaluated in different studies, and appears to be

r ar

r ar

r ar

Management of Chronic Venous Disease 11rst patient encounter and revised on follow up. Many ofthe limitations of CEAP have been addressed during re-visions, resulting in updated terminology and amendeddenitions.109 However, there are aspects that are not takeninto account by this classication system, including mixedarterial/venous disease, venous neuropathy, venous clau-dication, corona phlebectatica, and obesity.16 Furthermore,it has been acknowledged that CEAP cannot be used as areliable technique to rationalize patient treatment.113,114

Nevertheless, the CEAP classication is currently the mostcommonly used assessment tool for venous disease.105,106

2.2.2. Venous Clinical Severity Score, Venous SegmentalDisease Score, and Venous Disability ScoreAlthough the CEAP classication provides a descriptiveclassication tool for patients with CVD, there have beencriticisms that it lacks responsiveness in the long term andwith repeated evaluation of patients. Three other clinical

Table 4. Venous Clinical Severity Score (VCSS).

Attribute Absent (0) Mild (1)Pain or other discomfort(ie aching, heaviness, fatigue,soreness, burning Presumesvenous origin

None Occasional

Varicose Veins None Few, scatteredAlso includes coronaphlebectatica

Venous oedema(presumes venous origin)

None Limited to foot or ankle

Skin Pigmentation None orfocal

Limited to perimalleola

Inammation None Limited to perimalleola

Induration None Limited to perimalleola

Number of active ulcers None 1Active ulcer duration None 3 months but 1yearDiameter 2e6 cm Diameter >6 cmgs Uses stockings most days Full compliance withstockings


venous segments can be described accurately using theadvanced CEAP classication, VSDS attributes differentscores to different venous segments to indicate the level ofoverall impact on venous function.

Reux describes all valves in a specic segment as incom-petent. Obstruction describes a total occlusion at a point in the

measure of change following venous surgery.119 As withVCSS, VDS is designed to complement the CEAP classica-tion by providing greater detail on the level of disabilityexperienced by the patient.

2.2.3. Villalta-Prandoni ScaleThe Villalta-Prandoni Scale was described in the 1990s to

Table 5. Venous Segmental Disease Score (VSDS).

Reux Small saphenous1 Great saphenous

Thigh perforators1 Calf perforators2 Calf veins, multiple (Posterior Tibial only 1)2 Popliteal vein 2 Popliteal vein1 Femoral vein 1 Femoral vein1 Profunda femoris vein 1 Profunda femoris vein1 Common femoral vein and above 2 Common femoral vein

1 Iliac vein1 Inferior Vena Cava

10 Maximum reux score 10 Maximum obstruction score

12investigated segment or a >50% stenosis in at least half thesegment. Importantly, traumatic obstruction, ligation, orexcision of deep venous segments count as thrombosis.However, the same is not true for supercial veins. Perforatorinterruption and saphenous ligation/ablation count as areduction of the reux score, not as an obstruction score.

VSDS was found to correlate with clinical scores, with themagnitude of reux correlating with symptom severity.119

2.2.2.3. Venous Disability Score: functional impact. TheVenous Disability Score (VDS) provides a simple measure ofthe functional impact of CVD, using a 4 point scale (0e3;Table 6).115 This evaluates the effect of CVD on daily ac-tivities. VDS has been validated against the CEAP as ameasure of disease severity, and has been used as aTable 6. Venous Disability Score (VDS).0 e Asymptomatic1 e Symptomatic but able to carry out usual activities withoutcompressive therapy2 e Able to carry out usual activities only with compressionand/or limb elevation3 e Unable to carry out usual activities even with compressionand/or limb elevationUsual activities: dened as patient activities before the onsetof disability from venous disease

Please cite this article in press as: Wittens C, et al., Management of Chronic(2015), http://dx.doi.org/10.1016/j.ejvs.2015.02.007classify the severity of post-thrombotic syndrome (PTS), acomplication of deep venous thrombosis.122 Essentially, thescale consists of ve symptoms (patient rated) and six physicalsigns (clinician rated), with each of the 11 factors scored out of3 (total score out of 33; Table 7). A score of >14, or thepresence of venous ulceration, indicates severe PTS.

TheVillalta-Prandoni Scale is specic to the post-thromboticlimb and is a reliable, valid measure of PTS in patients withconrmed deep venous thrombosis (DVT).123 It also correlateswell with patient perceived health burden and QoL scores. Adrawback of this scale is that it does not take into accountvenous claudication or venous ulcer severity, as the presenceof a venous ulcer is given a xed score irrespective of severity.Obstruction

1 Great saphenous (if thrombosed from groin tobelow knee)

1 Calf veins, multiple

C. Wittens et al.2.3. Quality of life measures in venous disease

The burden of CVD lies with the patients, with up to 30%displaying symptoms suggestive of a depressive illness.124

Assessment of QoL in patients with CVD is integral to a com-plete and thoroughevaluationof their disease status. Evidenceshows that increasing clinical severity correlates strongly withdeterioration in QoL measures, both general and diseasespecic.113 Similarly, clinical improvement correlates withprogression in QoL measures.125 Clinical classication systems


2.3.1.2. EuroQoL, 5D. The EuroQoL group is a multinational,multicentre, and multidisciplinary network of researchersdedicated to the measurement of health status. The Euro-Qol questionnaire was devised in the 1990s with the aim ofdeveloping a standardized, simple, and generic measure ofhealth for clinical and economic appraisal.129 It consists of adescriptive part, evaluating ve dimensions (EuroQol e 5D),and a vertical, visual analogue scale (VAS), recording therespondents self-rated health (EuroQol e VAS).

Together, the EuroQol, 5D and EuroQoL-VAS, provide acomprehensive measure of health state. This tool is

Table 8. SF-36.

- Physical function- Role physical- Bodily pain- General health

Physical component

- Mental health- Role emotional- Social function- Vitality

Mental component

13are in place to assess the severity of CVD. QoL tools areavailable to assess patient reported outcomes. The ideal QoLtool should be generally applicable to any disease process,

Table 7. Villalta-Prandoni Scale.[severity scoring: none (0), mild (1), moderate (2), severe (3)]. Eachsign/symptom is scored 0e3; scores are added to obtain the nalresult (maximum of 33).5 Venous symptoms - Pain

- Cramping- Heaviness- Pruritus- Paraesthesia

6 Clinical signs - Oedema- Induration- Hyperpigmentation- Venous ectasia- Redness- Calf tenderness

Severity of post thromboticsyndrome (PTS)

- No PTS 14 orvenousulceration

- Total pointsrange 0e33

Management of Chronic Venous Diseaseirrespective of severity, outcome measures, or geographiclocation.16 The tool should be valid (i.e. measure what isintended), reliable (i.e. provide the same measurements for asingle individual despite different conditions), and responsive(i.e. sensitive to assess change e.g. after treatment). Ideally, itshould also assess all aspects ofQoL, including physical,mentaland social wellbeing. A number of global QoL instrumentsexist; however, they lack sensitivity to changing clinical con-ditions. Health related measures are used instead. A largenumber of tools have been developed and are in widespreaduse. There have been greater efforts to standardize the use ofQoL assessments in recent years.

Generic and disease specic instruments measuring healthrelated QoL in patients with CVD are discussed below.

2.3.1. Health related generic tools2.3.1.1. SF-36, Medical Outcomes Study 36 Item ShortForm. The SF-36 form is a widely used, generic QoLassessment tool with both physical and mental domains,providing a global assessment of patient wellbeing(Table 8).126 The physical component of this patientcompleted questionnaire has been shown to correlate withvenous disease severity. Studies have shown that all sub-domains of the physical component (physical role, pain,physical functioning, and general health perception) corre-late signicantly with disease severity as measured by theCEAP classication. This is not true for the mental compo-nent, as correlations with vitality127 and mental health128

are weak and inconsistent.

Please cite this article in press as: Wittens C, et al., Management of Chronic(2015), http://dx.doi.org/10.1016/j.ejvs.2015.02.007particularly useful for measuring utility or quality-adjustedlife years (QALYs; a measure of disease burden), and hasbeen used as a QoL measure in the assessment of patientswith symptomatic varicose veins (Table 9).124

2.3.2. Disease specic tools2.3.2.1. Aberdeen Varicose Veins Questionnaire. TheAberdeen Varicose Veins Questionnaire (AVVQ), is a patientcompleted QoL assessment tool comprising 13 questionswith domains including physical symptoms, social effect,and cosmesis (Table 10).130 Each question is graded in

Table 9. EuroQoL e 5D.

1. Mobility - No problems- Some problems- Bed bound

2. Self care - No problems- Some problems washingor dressing

- Unable to wash or dress

3. Usual activities - No problems

- Some problems- Unable to perform

4. Pain/discomfort - None- Moderate- Extreme

5. Anxiety/depression - None- Moderately- Extremely

Euro e QoL VASPerceived health Visual analogue scale

0 (worst state)e100 (best state)


terms of severity/presence or absence, and the results arecollated into the Aberdeen Varicose Veins SymptomSeverity Score from 0 to 100, where the higher the score,the worse the QoL.

The AVVQ has been validated as a measure of healthoutcome in patients with varicose veins against the SF-36questionnaire.131 It was found to be reliable, with signi-cant association with patient symptoms. Many consider theresponsiveness and sensitivity of the AVVQ to be greaterthan generic QoL questionnaires. However, generic QoL toolsallow simpler calculation of health utility (QALYs), which is anecessity for meaningful health economy comparisons.2.3.2.2. Chronic Venous Insufciency Questionnaire.

14dated in its French version, as well as in a number of otherlanguages.134,135

In 2010 psychometric validation was carried out, revali-dating the questionnaire and providing evidence for its

Table 10. AVVQ.1. Distribution of veins2. Duration of pain3. Duration of analgesia4. Degree of ankle swelling5. Use of support stockings6. Extent of itching7. Presence of discolouration8. Presence of rash or eczema9. Presence of skin ulcer10. Degree of concern at appearance11. Inuence on choice of clothes12. Interference with work/household jobsDeveloped in 1996 in France, the Chronic Venous Insuf-ciency Questionnaire (CIVIQ) is a 20-item self reporting QoLtool covering four dimensions: physical, psychological, socialfunctioning, and pain (Table 11).132 The items are graded ona 5 point Likert scale.133 The questionnaire has been vali-13. Interference with leisure

(score 0e100; 0 best, 100 worst)

Please cite this article in press as: Wittens C, et al., Management of Chronic(2015), http://dx.doi.org/10.1016/j.ejvs.2015.02.007CHAPTER 3: DIAGNOSTICS

Introduction

This chapter describes the value of available diagnostic toolsused in patients with CVD. It describes the physical exami-nation and additional tests including continuous wave [CW]Doppler, duplex ultrasound [DUS], phlebography, plethys-mography, venous pressure measurement, and modern im-aging techniques such as magnetic resonance venography[MRV] and computed tomography venography [CTV], as wellas describing clinical and radiological diagnostic criteria ofrecurrent disease.

In the diagnostic work up the nature of the problem andthe severity of the disease should be determined.

3.1. Clinical examination

3.1.1. Historyconsistency, reliability, and value in assessing changes inQoL after treatment.136

2.3.2.3. Venous Insufciency Epidemiological and Economicstudy. The Venous Insufciency Epidemiological and Eco-nomic study (VEINES) was an international, prospectivecohort study evaluating the epidemiology and outcomes ofCVD.137 As part of this project, a validated venous diseasespecic QoL and symptom measure was developed (VEINESQoL/Sym; Table 12).138 The aim of this tool was to provide anassessment of QoL and symptoms across the range of con-ditions in CVD (including telangiectasia, varicose veins,oedema, skin changes, and leg ulcers). Psychometric testingrevealed the questionnaire to be acceptable, reliable, andvalid in four different language versions, as well as demon-strating correlation with both SF-36 and C class. The VEINESQoL/Symwas also found to be reliable and valid as a measureof QoL and symptoms in patients with acute DVT.139

C. Wittens et al.Scientic evidence. Patients with varicose veins and/orsigns of CVD should be asked, prior to any clinical or


diagnostic investigation, about symptoms suggestive ofvenous pathology.140 This applies also to patients withrecurrent varicose veins following intervention, who maypresent with characteristic symptoms of CVD. Possiblethromboembolic antecedents should be investigated,together with any allergy, medication (oral contraceptivesprimarily), and concomitant relevant diseases including

orthopaedic, rheumatological, or neurological pathology(muscle pump function). The main circumferences of bothlegs should be measured when indicated (e.g. phlebolym-phedema, suspicion of vascular malformations).

Traditional clinical tests such as Trendelenburg, Perthes, andothers have proven unreliable and have no place in the map-ping of venous incompetence in general, and of varicose veinsin particular.144,145

examined.146 Distinctions were made between the iliacveins, the femoro-popliteal axis, deep veins in the calf, andsupercial and perforating veins. Both normal subjects andpatients with known CVD were studied and compared,including the differences between supine and upright ex-amination by DUS.

When the duration of retrograde ow in patients withCVD was compared with healthy subjects, there was a sig-

thigh or lower leg perforators, mostly on the medialaspect of the limb, should be examined with diametersmeasured at fascia level. Perforators should also be testedfor their inward and/or outward ow during distal calfcompression (systole) and release (diastole).147 Saphenousdiameter should be measured at specic locations: theGSV 3 cm below the saphenofemoral junction, at mid-thigh, at the knee, and lower leg; the AASV 3 cm below

Management of Chronic Venous Disease 153.2. Diagnostic tools

3.2.1. Denition of reuxScientic evidence. In a study using DUS, reux times in thevarious venous segments of the lower extremity wereheart and renal failure, which may inuence CVD.140 Finally,the number and timing of pregnancies should be noted.141

A differential diagnosis is very important. Even in thepresence of trunk varices, many lower limb symptoms couldh

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