MS, FRCS, FRCSE, PhD (Hon)
Chairman of the Board of the European Venous Foundation;
Editor-in-Chief of International Angiology; “Special Scientist” at the University of Cyprus;
Chairman of the Cyprus Cardiovascular Disease Educational and Research Trust (CCDERT);
Medical Director of the Vascular Screening and Diagnostic Centres in London and Cyprus;
Professor Emeritus at Imperial College
and an examiner for MS and PhD degrees for London University, UK
Venous signs and symptoms
Symptoms are what the patient feels and complains of in contrast to signs which are elicited by the doctor. Signs are the basis of the CEAP classification which does not take any account of symptoms. It is important for the doctor to consider both symptoms and signs in planning treatment, because if symptoms persist the patient will not be satisfied.
The underlying cause of both symptoms and signs is venous hypertension whose effect is modified by two natural protective mechanisms. The first is the ability of lymphatic drainage to increase up to 5-10 times in some individuals but only two times in others and none in the presence of lymphedema. The second protective mechanism is the fibrinolytic activity (FA) in the blood and tissues that enables the body to remove extravascular proteins and macromolecules. In the presence of high FA skin changes may be minimal or absent despite a high ambulatory venous pressure. In the presence of low or absent FA severe skin changes may occur with only slightly raised or even normal ambulatory venous pressure. Also, duration of venous hypertension in years is an important factor that determines outcome.
The most exciting new finding comes from the study of the microcirculation in the skin using Orthogonal Polarisation Spectral (OPS) Imaging which provides us with quantitative measurements of functional capillary density (FCD capillaries/mm2), diameter of dermal papilla (DDP, μm) to quantify edema, largest diameter of the capillary bulk (DCB, μm) to assess its degree of change, capillary limb diameter (CD, μm) to describe diameter changes and capillary morphology (CM, % of abnormal capillaries per field). These measurements increase progressively with each increasing CEAP clinical class and have been shown to decrease after treatment with venoactive drugs.
Understanding Venous Scores and Quality of Life
In Chronic venous disorders (CVD) there are two classification systems (CEAP and REVAS) and four scoring systems (Venous disability score –VDS; Venous Segmental Disease Score-VSDS; Venous Clinical Severity Score-VCSS and the Villalta Scale .
Assessment of efficacy of therapy is achieved by several methods of evaluation of symptoms and several aspects for assessment of quality of life (QoL).
CEAP was created by the American Venous Forum as a common language for chronic venous disorders to be used in publications to clarify what patients are involved. This explains why in CEAP there is no information on type of symptoms or their severity.
REVAS stands for Recurrent Varicose veins After Surgery and it was developed at International Consensus meeting in Paris in 1998 to be used in combination with CEAP classification. It has been evaluated in terms of intra- and inter-observer reproducibility and a worldwide survey was conducted in 2006.
VDS has a maximum of 3 grades defined as: 0 = asymptomatic, 1 = symptomatic but able to carry out usual activities without compression therapy, 2 = can carry out usual activities only with compression and/or limb elevation, 3 = unable to carry out usual activities even with compression and/or limb elevation.
VSDS combines the anatomic and pathophysiologic components of CEAP. Based on venous imaging (duplex or venography). Major venous segments are graded according to presence of reflux and/or obstruction.
VCSS is based on nine clinical characteristics: pain or other symptoms, varicose veins, edema, skin pigmentation, inflammation, induration, and number, duration, size of active ulcers and need to use of conservative therapy (compression and elevation). Characteristics are graded from 0 to 3 and are added to produce a 30 point-maximum flat scale. Only 3 points can be contributed by symptoms !
Villalta Scale for PTS. It scores symptoms: cramps, pruritus, pain, heaviness, paraesthesiae and signs: pretibial edema, induration, hyperpigmentation, new venous ectasia, redness and pain during calf compression; severity from 0 (not present) to 3 (severe), for a maximum of 33 points.
Evaluation of Symptoms. Patients can give global ratings of improvement in symptoms or individual symptoms. They can use quantitative scales such as a Likert scale or a visual analog scale (VAS) (0-10 severity).
Quality of life for patients with CVD can be assessed by: (a) Generic Questionnaires e.g. The Medical Outcome Study Short Form Health Survey (SF-36) or EQ5D-5L TM or (b) Disease-specific measures e.g. the Chronic Venous Insufficiency Questionnaire (CIVIQ), The Aberdeen Varicose Vein Questionnaire (AVVQ), VVSymQ or CXVUQ
Pathophysiology of Chronic Venous Disease (CVD)
Primary varicose veins (VVs) occur in the absence of previous DVT. Recanalisati on after DVT may give rise to relative obstruction and incompetence of the deep, superficial and perforating veins. VVs are present in 14-35% of the population and their prevalence and severity increase with age. 40% of venous leg ulcers are the result of long-standing VVs in the presence of normal deep veins. 60% of venous ulcers are due to the post thrombotic syndrome as a result of previous DVT. Venous hypertension results from obstruction (failure of recanalization) and recurrent DVT, reflux (damage to valves) or from a combination of reflux and obstruction.
Leukocyte-endothelial interaction is the cause of primary VVs. Environmental and local factors plus genetic predisposition produce white cell adhesion, degranulation and leucocyte migration under the endothelium. A chronic inflammatory process produces vein wall and valve remodelling. Eventually valves become incompetent with tortuous dilated veins with venous hypertension as a consequence. Skin changes occur when reflux exceeds 5 ml/sec and ulceration when reflux exceeds 10 ml/sec.
Leukocyte adhesion occurs also in the microcirculation where it produces local edema, red cell extravasation and skin pigmentation due to haemosiderin deposition. The veno-arteriolar reflex is abolished, total skin flow is increased with reduction in blood flow in the nutrient capillary loops with eventual skin ulceration. The most exciting new finding comes from the study of the microcirculation in the skin using Orthogonal Polarisation Spectral (OPS) Imaging which provides us with quantitative measurements of functional capillary density (FCD capillaries/mm2), diameter of dermal papilla (DDP, μm) to quantify edema, largest diameter of the capillary bulk (DCB, μm) to assess its degree of change, capillary limb diameter (CD, μm) to describe diameter changes and capillary morphology (CM, % of abnormal capillaries per field). These measurements increase progressively with each increasing CEAP clinical class and have been shown to decrease after treatment with venoactive drugs.
Professor Andrew Nicolaides is a graduate of the Pancyprian Gymnasium (Nicosia) and Guy’s Hospital Medical School (London University 1962), and a fellow of the Royal College of Surgeons England, and the Royal College of Surgeons Edinburgh (1967).
His higher surgical training was in Oxford University, Kings College Hospital Medical School and St Mary’s Hospital Medical School, London. He was awarded the Jacksonian prize by the Royal College of Surgeons England in 1972 for his work on the prevention of venous thromboembolism and obtained the degree of M.S. (Master of Surgery) in 1976.
He was the Professor of Vascular Surgery at the Imperial College School of Medicine (St Mary’s Hospital) and Consultant Vascular Surgeon at St Mary’s Hospital from 1983–2000 and Medical Director of the Cyprus Institute of Neurology and Genetics from 2001-2004. His research group is known internationally in several areas which include noninvasive vascular screening and diagnostic investigation, early detection and prevention of cardiovascular and venous disease. His research is now directed towards the genetic risk factors for cardiovascular disease, identification of individuals at risk and the development of effective methods of prevention, especially stroke.
He is Past-President of the International Union of Angiology and Past-President of the Section of Measurement in Medicine of the Royal Society of Medicine.
He has received many awards and honorary memberships from many scientific societies. He is Chairman of the Board of the European Venous Foundation, Editor-in-Chief of International Angiology and is on the Editorial Board of many vascular journals. He is Professor Emeritus at Imperial College and an examiner for MS and PhD degrees for London University. He is now a “Special Scientist” at the University of Cyprus, Chairman of the Cyprus Cardiovascular Disease Educational and Research Trust (CCDERT) and Medical Director of the Vascular Screening and Diagnostic Centres in London and in Cyprus. He has trained over 200 vascular surgeons who are practicing all over the world; twelve of them are holding prestigious Chairs as professors in vascular surgery in UK, USA, Greece, Australia and South Africa.
He was made Archon Megas Referendarios, an Honor bestowed by the Patriarch of Constantinople in 1994.
He is co-author of over 500 original papers and editor of 14 books.