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and associates studied the site of valvular incompetence in 139 limbs with primary
varicose veins and found that in 24% reflux was detected in the main trunk of the long
saphenous or a tributary without junctional incompetence (5).
PATHOLOGY OF VARICOSE VEINS
Studies of the pathology of venous disease have been limited. Ono and colleagues
examined the great saphenous vein (GSV) from 13 patients undergoing varicose vein
surgery in comparison to normal veins removed for coronary artery bypass (6). They found
clear valve leaflet shortening in three of seven specimens examined. In addition, they
demonstrated monocyte/macrophage infiltration at valve sinuses. These findings were
absent in the four specimens of macroscopically normal vein removed from patients
undergoing coronary bypass. In a larger study of proximal great saphenous valves Corcos
et al. demonstrated dilations of the valve annulus and hypoplasia of valve cusps (7).
A variety of other changes in the vein wall have been demonstrated in excised varicose
veins, however, whether any of these findings are primary or secondary is unclear (see
below).
THEORIES REGARDING VARICOSE VEIN ETIOLOGY
The main discussion regarding the etiology of varicose veins is whether the venous
dilatation is secondary to a primary problem in the vein wall or a primary problem in one
or more venous valves.
A Primary Valvular Dysfunction in Varicose Veins
In this theory the primary event is valve dysfunction in the great or small saphenous vein
or possibly a perforator. Resultant increased venous filling leads to secondary vein wall
dilatation.
A Primary Vein Wall Dysfunction in Varicose Veins
In this theory a weakening of the vein wall develops initially as a result of connective tissue
problems within the vessel or perhaps loss of venous tone. The other changes typical of
varicose veins, including valvular incompetence, are secondary changes due to widening of
the valve annulus at the site of vein dilatation.
Arteriovenous Communications as an Etiology for Varicose Veins
Increased inflow to superficial lower limb veins could lead to secondary venous dilatation
and valvular incompetence.
Final Common Pathway
Whatever the initiating factor for the venous dilatation, all theories incorporate a common
final path of prolonged venous filling, further valvular incompetence and transmitted
pressures from the deep to superficial venous systems (Fig. 1).
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VALVE DYSFUNCTION IN VARICOSE VEINS
The original theory regarding varicose veins etiology suggested that valvular failure at the
sapheno-femoral junction was the primary event with secondary failure of more distal
valves as a result of the increased pressure placed on these sites (descending
incompetence) (8). The finding of isolated valvular incompetence at distal sites or
tributaries demonstrates that descending incompetence cannot account for all cases of
varicose veins (5). However, a primary valvular problem could develop at a distal site with
associated increased venous filling and secondary venous dilatation leading to ascending
valvular incompetence (9).
Mechanism of Valve Failure
Congenital Valve Abnormalities
There have been remarkably few studies of valve cusp anatomy. In a recent study Yamaki
and colleagues correlated the findings on pre-operative duplex imaging with those
demonstrated intra-operatively by angioscopy (10). By endoluminal imaging they defined
three groups of valve cusp abnormalities in 75% of patients and absent sapheno-femoral
valves in 25%. While duplex could be used to detect these abnormalities with high
sensitivity, the specificity in defining the type of cusp problem was low (10).
Secondary Valvular Failure
It is likely that most valvular abnormalities which can be detected by the time patients come
to surgery have developed in response to an episode of thrombophlebitis, prolonged venous
stasis or incompetence. An initiating event such as a sub clinical thrombus in the vicinity of
a superficial valve could be the initiating factor for valve inflammation, fibrosis and reflux.
The role of DVT in the etiology of deep venous incompetence is well established (11–13).
Following DVT the incidence of superficial as well as deep reflux appears to be increased.
Meissner andcolleagues carried out repeat duplex imaging on 69 limbs inwhich a DVT had
occurred (14). Thrombus was demonstrated in the GSV initially in 21%. At eight years the
Primary vein wall weakness Primary valvular defect
Segmental venous dilatation
Thrombosis
Secondary valvular defect
Further venous dilatation
Gross varicose veins
AV communications
Figure 1 Theories and mechanisms in varicose vein etiology.
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incidence of GSV reflux was 29% in limbs that had developed a DVT, compared to 15% in
the contralateral limb (14). The reflux incidence was much higher in limbs in which the
initial thrombosis had involved the GSV (77%). Interestingly a recent association has been
demonstrated between polymorphism in the gene for the anticoagulant protein
thrombomodulin and varicose veins (15).
PRIMARY VEIN WALL WEAKNESS AND VARICOSE VEINS
Structural Weakness of the Vein Wall
A primary weakness in the wall of the vein could result in dilatation of the vein with
resultant separation of valve cusps and eventual reflux. Most authors have suggested that
this weakness would be a result of structural problems in the wall of the vein (16–20).
A number of abnormalities in the structural proteins of the vein have been demonstrated.
These include abnormal collagen and elastin content, intimal hyperplasia and changes in
matrix controlling enzymes, although the changes demonstrated have varied from one
study to another (16–20). Andreotti and colleagues demonstrated a reduction in both
collagen and elastin content in varicose compared to macroscopically normal veins (16).
They also found alterations in the collagen content of skin taken from patients with
varicose veins and suggested a systemic collagen disorder in varicose veins (17).
In contrast, most investigators have found an increase in the collagen content of segments
of varicose compared to normal veins (18,19). For example, Gandhi et al. demonstrated an
increase in the collagen content and a decrease in the elastin concentration, without change
in the activity of proteolytic enzymes in the wall of varicose veins (18). Sansilvestri-Morel
et al. found an imbalance in the sub types of collagen synthesized by smooth muscle cells
derived from varicose veins (19). Collagen type I was increased, while type III was
decreased. Badier-Commander and colleagues recently investigated the concentration of
enzymes regulating the extracellular matrix in specimens from patients with varicose
veins (20). They discovered a relatively high concentration of the tissue inhibitor of
metalloproteinase, TIMP-1, and a relatively low concentration of the proteolytic enzyme,
metalloproteinase 2 (20). This balance of matrix controlling enzymes would favor the
accumulation of matrix within the venous wall and is not reflective of a matrix degrading
environment, which might be expected if wall destruction was an important mechanism in
varicose vein development. Thus, to date, the matrix changes demonstrated in the wall of
varicose veins have not been consistent in different studies. This may relate to the fact that
many of the pathological findings are the result rather than the cause of the development of
varicose veins.
Impaired Venous Tone
Another possibility is that venous dilatation and secondary reflux results from inability
of the vein to contract adequately due to smooth muscle cell or endothelial dysfunction.
In support of this theory a number of abnormalities in the contraction and relaxation of
varicose vein have been demonstrated compared to normal vein (21–25). Duplex studies
suggest reduction in vein wall elasticity in patients with varicose veins (21). Brunner et al.
assessed the contraction of a grossly varicosed vein in comparison with a mildly varicosed
vein and a competent vein from the same patient (22). They discovered that phenylephrine
induced contraction was absent in the overtly varicosed segments. However, of note,
the incompetent but macroscopically normal vein contracted normally, suggesting that
a primary contractile abnormality, in response to phenylepherine at least, was not an early
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event in the etiology of valvular incompetence. Mildly varicosed segments had normal
endothelial-dependent relaxation but reduced endothelial-independent relaxation to
nitroprusside, suggesting a global dysfunction of the smooth muscle in varicose veins.
In support of this, in a culture model of varicose veins smooth muscle cells appear to be
heparin resistant compared to cells from normal vein (23). Other investigators have
demonstrated reduction of endothelin B receptors in varicose veins (24). Other functional
abnormalities have also been detected and include reduction in nitric oxide and vascular
endothelial growth factor release under conditions of venous hypertension (25).
Endothelial Activation
The endothelium is fundamental in control of vasomotor tone, inflammation and
thrombosis. All these processes may play a role in varicose vein development. Loss of
venous tone may contribute to venous dilatation and secondary valvular reflux. Sub clinical
thrombosis and inflammation could be responsible for valve cusp fibrosis and resultant
reflux. There is good evidence of endothelial activation in venous disease. For example,
increased expression ofthe endothelialadhesion molecules ICAM-1 has been demonstrated
in varicose veins (26). A study by Biagi and colleagues suggested that varicose veins
produced less prostacyclin but more thromboxane A2 and prostaglandin E2 (27). These
changes would favor platelet activation and thrombosis. However, Nemcova et al. were
unable to confirm these findings in a more recent study (28). In a detailed study by
Badier-Commander and associates the concentration of fibroblast growth factor and
transforming growth factor beta were found to be increased in atrophic varicose veins
segments (29). Thus alteration in endothelial function could play an important role in
varicose vein development, however, the changes demonstrated to date could also be
explained as secondary phenomenon.
ARTERIOVENOUS COMMUNICATIONS AND VARICOSE VEINS
Arteriovenous communications in patients with varicose veins have been reported in
angiographic studies and microsurgical dissections (30,31). Further support for the
presence of arteriovenous shunt in varicose veins comes from studies reporting increased
oxygen partial pressures in the saphenous vein of varicosed compared to normal veins
(32,33). The inability to demonstrate such fistulae during sapheno-femoral ligation to treat
varicose veins has led to little promotion of this theory and limited investigation has been
carried out to prove or refute the mechanism.
CONCLUSION
The pathogenesis of varicose veins has been relatively underinvestigated. Epidemiological
studies have failed to show strong associations between environmental factors and
varicose veins. Pathological studies demonstrate abnormalities within the venous wall in
endothelial cells, smooth muscle cells and extracellular matrix in patients with varicose
veins. However, whether the demonstrated abnormalities are primary or develop
secondary to valvular reflux is unclear. Longitudinal studies employing new imaging
techniques are likely to provide important new information.
Etiology and Pathophysiology of Varicose Veins 241
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KEY POINTS
† Three principal theories for varicose vein development have been suggested:
a primary valvular defect, a primary vein wall defect, and primary arterio-
venous communications.
† Irrespective of the initiating stimulus, secondary phenomenon in varicose veins
are superficial venous dilatation and valvular incompetence.
† Progressive valve dysfunction can be descending or ascending.
† Numerous vein wall abnormalities have been identified in the connective tissue,
smooth muscle cells and endothelium. Whether these changes are primary or
secondary is unknown.
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8. Moore HD. Deep venous valves in the etiology of varicose veins. Lancet 1951; 2:7–10.
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10. Yamaki T, Sasaki K, Nozaki M. Preoperative duplex-derived parameters and angioscopic
evidence of valvular incompetence associated with superficial venous insufficiency.
J Endovasc Ther 2002; 9:229–233.
11. Masuda EM, Kessler DM, Kistner RL, Eklof B, Sato DT. The natural history of calf vein
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evaluation of the late sequelae of deep venous thrombosis. J Vasc Surg 1998; 27:472–478.
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valvular incompetence after deep vein thrombosis: a follow-up study with duplex scanning.
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15. Le Flem L, Mennen L, Aubry ML, et al. Thrombomodulin promoter mutations, venous
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16. Andreotti L, Cammelli D. Connective tissue in varicose veins. Angiology 1979;
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17. Andreotti L, Cammelli D, Sampognaro S, et al. Biochemical analysis of dermal connective
tissue in subjects affected by primary uncomplicated varicose veins. Angiology 1985;
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18. Gandhi RH, Irizarry E, Nackman GB, Halpern VJ, Mulcare RJ, Tilson MD. Analysis of the
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18:814–820.
19. Sansilvestri-Morel P, Rupin A, Badier-Commander C, et al. Imbalance in the synthesis of
collagen type I and collagen type III in smooth muscle cells derived from human varicose
veins. J Vasc Res 2001; 38:560–568.
20. Badier-Commander C, Verbeuren T, Lebard C, Michel JB, Jacob MP. Increased TIMP/MMP
ratio in varicose veins: Possible explanation for extracellular matrix accumulation. J Pathol
2000; 192:105–112.
21. Clarke GH, Vasdekis SN, Hobbs JT, Nicolaides AN. Venous wall function in the pathogenesis
of varicose veins. Surgery 1992; 111:402–408.
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to vasoactive agents. Br J Clin Pharmacol 2001; 51:219–224.
23. Hollingsworth SJ, Tang CB, Baker SGE. The effects of heparin on cultured explants of varicose
long saphenous vein. Phlebology 2001; 16:60–67.
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26. Takase S, Bergan JJ, Schmid-Schonbein G. Expression of adhesion molecules and cytokines on
saphenous veins in chronic venous insufficiency. Ann Vasc Surg 2000; 14:427–435.
27. Biagi G, Lapilli A, Zendron R, Piccinni L, Coccheri S. Prostanoid production in varicose veins:
evidence for decreased prostacyclin with increased thromboxane A2 and prostaglandin E2
formation. Angiology 1988; 39:1036–1042.
28. Nemcova S, Gloviczki P, Rud KS, Miller VM. Cyclic nucleotides and production of
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29. Badier-Commander C, Couvelard A, Henin D, Verbeuren T, Michel JB, Jacob MP. Smooth
muscle cell modulation and cytokine overproduction in varicose veins. An in situ study.
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30. Piulachs P, Vidal-Barraquer F. Pathogenic study of varicose veins. Angiology 1953; 4:59–100.
31. Guis JA. Arteriovenous anastomoses and varicose veins. Observations with the operation
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32. Baron HC, Cassaro S. The role of arteriovenous shunts in the pathogenesis of varicose veins.
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19
Indications for Treatments
of Varicose Veins
Simon Palfreyman and Jonathan Michaels
Department of Vascular Surgery, University of Sheffield, Sheffield, U.K.
INTRODUCTION
This chapter will examine the physical and nonphysical symptoms ascribed to varicose
veins and treatments used to mitigate these. The aim of this chapter is to review the
complex interaction between symptoms, complications, and indications for treatment of
varicose veins. It will also assess the impact of varicose veins on quality of life, the
evidence of effectiveness, and indications for varicose vein treatments.
BACKGROUND
Studies have shownthat varicose veins have a prevalence of between 20%and 60%, with up
to one quarter of the adult population having at least one varicose vein (1). The resultant
impact on health services can be illustrated by the fact that operations for varicose veins are
one of the most commonly undertaken surgical procedures, with around 50,000 patients
admitted for treatment in the National Health Service annually in the United Kingdom (2),
and have a major impact on waiting lists and workload (3). They are also a major reason for
patients to seek redress through legal action against clinicians and healthcare providers (4).
Patients report a wide range of symptoms that they attribute to their varicose veins.
Some of the symptoms patients associate with their varicose veins may not be directly
attributable to the veins themselves (5). A further complication for the clinician is that the
extent of the visible veins does not correlate with the severity or number of symptoms
experienced (6). There appears to be a complex interaction between cosmetic dislike and
perception of symptoms (7).
The reported symptoms for varicose veins include heaviness, aching, itching and
concerns about cosmetic appearance. In addition to these are the complications associated
with varicose veins that can include varicose eczema, pigmentation, bleeding and varicose
ulcers. The patient can experience, to a greater or lesser degree, all of these symptoms and
complications or none at all.
The crux of the dilemma for health service providers is to determine whether
uncomplicated varicose veins should be treated. The current guidance from the National
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Institute for Clinical Excellence (NICE) (8) considers only complications as a clear indi-
cation for surgery. However, patients are presenting at General Practitioner (GP) surgeries
and outpatients clinics with the expectation that their varicose veins should be treated (9).
Symptoms of Varicose Veins
The most comprehensive study to examine leg symptoms in members of the general public
was the Edinburgh Vein Study (5). This study used an age stratified random sample of
1566 people selected from GP practices in Edinburgh, Scotland. Participants were asked to
complete a self-administered questionnaire that asked about the presence of symptoms
attributed to varicose veins. One surprising finding was that the lower limb symptoms
often attributed to varicose veins were present in the general population whether or not
varicose veins were present.
The study found that the prevalence of symptoms increased with age and that there
was a difference between men and women in terms of the prevalence of symptoms. The
most common symptoms for women were aching (53%), cramp (42%), restless legs
(35%), heaviness or tension (28.6%), itching (25%) and swelling (23%). While for men,
the most common symptoms were cramp (34%), aching (32.5%), restless legs (20%),
itching (19%) and swelling (9.2%). But there was no statistical association between
symptoms and the presence of varicose veins, except for itching in men.
Another study (9) used qualitative techniques to examine the reasons patients were
seeking treatment. The sample was drawn from patients referred to vascular surgeons with
varicose veins and so differed from the Edinburgh Vein Study. The patients were therefore
a selected group who had been to their GP with the symptoms associated with varicose
veins and had been referred on to the vascular surgeon. This could have led to some bias in
terms of the patients having an expectation of treatment and the possibility of exaggeration
of symptoms to gain treatment. However, the study found that pain and itching were the
most common symptoms. For some of the patients in the study the severity of the pain was
such that they resorted to taking analgesia—including non steroidal anti-inflammatory
drugs (NSAIDs, e.g., ibuprofen, voltarol and naproxen) and codeine (dihyrocodine).
A study by Michaels et al. (10), was a randomized trial examining the cost-
effectiveness of treatments for varicose veins. The sample were recruited from secondary
care and were patients referred to vascular surgeons. The study compared the self-reported
symptoms at baseline and post-treatment (Tables 1 and 2). The most common complaint
prior to treatment was of aching in the legs (86.3%). After treatment 45.8% complained of
aching and 42.7% stated that the aching was the same as that prior to treatment.
A complicating factor is that there is a subjective element to the perception of the
severity, and extent of, the symptoms experienced (7). Varicose veins can be unsightly,
cause embarrassment and have a significant impact on people’s social activities (9).
Table 1 Symptoms at Initial Assessment of All Patients by Initial Treatment
Conservative Sclerotherapy Surgery Total
N 387 91 531 1009
Aching 306 (79.1%) 85 (93.4%) 480 (90.4%) 871 (86.3%)
Heaviness 191 (49.4%) 53 (58.2%) 339 (63.8%) 583 (57.8%)
Itching 203 (52.5%) 48 (52.7%) 338 (63.7%) 589 (58.4%)
Swelling 157 (40.6%) 45 (49.5%) 277 (52.2%) 479 (47.5%)
Cosmetic concerns 252 (65.1%) 59 (64.8%) 382 (71.9%) 693 (68.7%)
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Underlying problems with the cosmetic appearance may be the motivation for many
patients to complain of symptoms and seek treatment for their varicose veins (5,10), even
though they may deny that this is their primary motivation (9). However, if patients are
approaching clinicians stating that they want relief of symptoms surely it is beholden on
the clinician to try and ease the patients burden.
It is the group of patients who are seeking treatment to relieve the symptoms
they associate with varicose veins who provide the greatest challenge to both the clinician
and health service provider. This is because there is little evidence regarding the cost-
effectiveness of treatments currently available.
Complications of Varicose Veins
The complications of varicose veins are thrombophlebitis; bleeding; skin changes, eczema
and lipodermatosclerosis; and ulceration.
Superficial thrombophlebitis manifests itself with symptoms of swelling, pain and
redness located around a vein. It can occur in the absence of varicose veins and may be
associated with malignancy, autoimmune disease and cancer (11), but varicose veins are
the commonest underlying cause (12). It is often confused with deep vein thrombosis
(DVT) and patients may worry about traveling (particularly flying and the risk of
“economy class syndrome”) (9). There is also a perceived additional risk of developing a
DVT due to having varicose veins, however the evidence for this is equivocal (13).
Bleeding is an uncommon consequence of varicose veins and usually occurs due to
minor trauma but can occur spontaneously (14,15). It almost always occurs through an
area of obviously compromised skin overlying a varicosity in the lower leg. The bleeding
may be minor and internal resulting in a bruise or severe haemorrhage. This can be
alarming and poses a potential threat to life (14–16).
Lipodermatosclerosis and ulceration result from the venous hypertension associated
with varicose veins and is an important cause of damage to the skin and subcutaneous
tissues of the lower leg (17,18). This usually starts with eczema or pigmentation and may
Table 2 Symptoms at One Year in All Patients, by Initial Treatment
None Better Same Worse
Aching Conservative 57 (21.8%) 99 (37.8%) 45 (17.2%) 61 (23.3%)
Sclerotherapy 20 (32.3%) 17 (27.4%) 21 (33.9%) 4 (6.5%)
Surgery 159 (45.8%) 28 (8.1%) 148 (42.7%) 12 (3.5%)
Heaviness Conservative 126 (48.1%) 75 (28.6%) 24 (9.2%) 37 (14.1%)
Sclerotherapy 36 (58.1%) 14 (22.6%) 12 (19.4%) (0.0%)
Surgery 206 (59.4%) 21 (6.1%) 111 (32.0%) 9 (2.6%)
Itching Conservative 133 (50.8%) 62 (23.7%) 23 (8.8%) 44 (16.8%)
Sclerotherapy 38 (61.3%) 8 (12.9%) 14 (22.6%) 2 (3.2%)
Surgery 223 (64.3%) 16 (4.6%) 101 (29.1%) 7 (2.0%)
Swelling Conservative 155 (59.2%) 61 (23.3%) 20 (7.6%) 26 (9.9%)
Sclerotherapy 42 (67.7%) 12 (19.4%) 5 (8.1%) 3 (4.8%)
Surgery 227 (65.4%) 22 (6.3%) 86 (24.8%) 12 (3.5%)
Cosmetic
concerns
Conservative 64 (24.4%) 115 (43.9%) 10 (3.8%) 73 (27.9%)
Sclerotherapy 22 (35.5%) 14 (22.6%) 22 (35.5%) 4 (6.5%)
Surgery 129 (37.2%) 21 (6.1%) 182 (52.4%) 15 (4.3%)
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