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24
Varicose Veins, Pregnancy, and
Venous Disorders of the Pelvic Veins
Linda de Cossart
Countess of Chester, NHS Foundation Trust, Chester, U.K.
INTRODUCTION
Myths about varicose veins and pregnancy abound and vascular specialists have done little
to educate doctors and the public about this common condition (1). Classification of
varicose veins has reliedalmost exclusively on their clinical presentation and on the opinion
of a surgeon to guidetreatment. Untilthe developmentof duplexscanning, safeand repeated
imaging of veins was impossible and the characterization of the underlying abnormality of
venous valve reflux which causes them remained a silent contributor to their development.
New imaging technologies are now associating previously unrecognized venous
abnormalities with chronic and common conditions such as chronic pelvic pain (CPP) and
pelvic congestion syndrome (PCS). As a consequence, new classifications of pelvic venous
pathology are being developed and endovascular and surgical procedures pioneered to treat
them (2,3). The association of venous dysfunction with chronic non-vascular clinical
symptoms is gaining prominence and will challenge vascular specialists to provide new
remedies. Women, especially those of child bearing age, form the largest cohort of those
affected (4,5). Pregnancy is the common link.
This chapter therefore sets out to provide details of the current understanding about
varicose veins with respect to pregnancy, and the developing knowledge of PCS and its
association with venous pathology. A scenario is provided at the beginning of each section
to set the context.
Each section concludes with challenges to the profession to establish an informed
and wise way of managing these conditions and ensure that new interventions are
developed, researched and made available to appropriate patients.
VARICOSE VEINS AND PREGNANCY
Typical Scenario
A fit and well 37-year-old woman consults a vascular specialist and says:
I have had three pregnancies, and my varicose veins have gotten worse with each one.
I had phlebitis in the third pregnancy, which was very unpleasant. My GP told me that
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I should wait until I have completed my family before having my veins operated on as
they will only come back if I get pregnant again. What is your advice?
Factors Contributing to the Development of Varicose Veins
Varicose veins are unique to the human species and most commonly occur in the veins of
the lower limbs. Since humans walk in an erect position, blood from the lower limb must
return against gravity, back to the heart. The calf muscle pump and the changing pressures
in the abdominal compartment are the main agents responsible for forcing the blood back
to the heart. The non return valves in the veins of the lower limb facilitate this by closing
in a sequential pattern and moving blood upwards. Each time they close they also
compartmentalize the column of blood thus preventing venous back pressure being
exerted throughout the vascular bed of the leg. They have probably developed this
function as an evolutionary process and the body’s response to the human posture. There is
also emerging knowledge about genetic links and valvular incompetence (6).
Most pathological conditions in the venous system develop in the lower limbs as
a consequence of malfunction of the mechanisms which control venous blood flow. They
present as a variety of clinical manifestations. Varicose veins develop as a consequence of
venous valve malfunction in the superficial veins of the lower limb. This impairs normal
venous flow and creates venous back pressure in the veins distal to the incompetent valve,
leading to clinically obvious varicose veins. It should be noted, however, that in some
cases of reflux in the long saphenous vein there may no visible varicose veins. Pressure
increases induced in the capillary bed by this reflux may lead to chronic venous
hypertension with its complication of ulceration of the skin, classically in the gaiter area of
the leg. The CEAP classification (Clinical manifestations, Etiological factors, Anatomic
involvement, Pathophysiological features) is a useful and now widely used method of
standardizing the clinical presentation of varicose veins (7).
Prevalence of Varicose Veins
The literature suggests that varicose veins are more prevalent in women and their
development is associated with increasing parity, family history and obesity (8–12).
However, the Edinburgh Varicose-vein study (mean age 45 yr) reported an age-adjusted
frequency for the prevalence of varicose veins as 39.7% in men and 32.2% in women,
which challenges the idea of this being a largely female problem (13). The difference in
most published data probably reflects how the data is collected and often contains an
inherent bias as they are usually on presentations to doctors, rather than being population-
based investigations. They have also relied on the clinical manifestation of varicose
veins rather than identifying the underlying problem of refluxing valves. If venous valve
development is related to an adaptive response to erect posture there is no logic to support
a gender difference but genetic associations with varicose veins may turn out to be sex
linked. Clinical presentation however is a different matter and is probably genuinely more
frequent among women than men especially in the younger age group.
Exploring Advice Given to Women About Varicose Veins
Advice offered to women about varicose veins and pregnancy is drawn from a sparsely
populated research base, much of it based on hearsay. Healthcare professionals are
responsible for sustaining these ideas, most of which are unproven by investigation.
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The particular advice that women should defer any definitive treatment of their varicose
veins until their child bearing is over is based on the notion that further pregnancies will
create more varicose veins which themselves will require treatment. Out of expediency the
advice to treat was combined with that of waiting until child bearing was complete. This
takes scant account of the woman’s symptoms or risks that may ensue from her
varicose veins.
Two recent studies have explored this notion. One investigated the understanding of
healthcare practioners about varicose veins and thromboembolic problems in pregnancy;
the other the prevalence of venous reflux in pregnant women and its association with some
of the commonly held beliefs about varicose veins and pregnancy (2,14).
In the first study, a questionnaire was sent to relevant healthcare professionals in one
area in England, and analyzed replies from 849 midwives, 63 obstetricians, 21 vascular
surgeons and 77 general practioners. The replies showed that less than half of those
surveyed knew the incidence of varicose veins in the general population; only 50%
recognized an association between the appearance of varicose veins and multiple
pregnancies, and despite the fact that midwives held the strong belief that deep vein
thrombosis during gestation was associated with the presence of varicose veins, less than
one-third indicted that they would check their mothers for varicose veins. The majority of
midwives, obstetricians and general practioners indicated they would prescribe support
tights for pregnant women with symptomatic varicose veins despite there being no good
evidence for this course of action. The study identified in this community a significant
level of ignorance about venous disease and its association with pregnancy. It would be
interesting to see if this is isolated to Cheshire (I suspect it is not) by questioning
other communities.
The second study, which is the largest reported prospective study of the prevalence
of venous reflux in pregnant women, investigated 331 women who, at their first antenatal
booking at about twelve weeks gestation, consented to take part (14). The opportunity
to scan these women prior to their pregnancy, while desirable, was not feasible. The
investigators were experienced in the use of duplex scanning in pregnancy and
investigated the women using their standard technique for examining the lower limb
venous system, which was to position them on a tilting table at seventy degrees reversed
Trendelenberg tilt for the test and to use Valsalva’s maneuver and calf squeeze to illicit
reflux. Women were examined during their pregnancy and after delivery. Leg symptoms
were calculated in all women with and without demonstrable reflux, using the CEAP
classification (7).
One in four women had demonstrable superficial venous reflux at between twelve
and sixteen weeks gestation. It was assumed that this reflux had been present prior to the
pregnancy. This was a higher prevalence of venous reflux than expected but is close to that
described by the Edinburgh study (13). The refluxers did not have a higher incidence of
a family history of varicose veins when compared with non-refluxers. No reflux developed
during pregnancy in any of the veins of the lower limbs which were normal at booking.
Looking at the relationship between body weight and venous reflux the study
stratifying 289 women, according to the standard BMI classification, into three groups,
non-obese BMI!25, pre-obese BMI 25.1 to 30 and obese BMI O 30.1. No difference in
the incidence of reflux among any of the groups was identified suggesting that obesity is
not strongly associated with the presence of varicose veins in pregnant women. A surprize
finding, however, was that mothers of normal weight who had reflux had significantly
higher CEAP scores than obese women with reflux and they complained more. The
explanation for these findings is unclear, but many symptoms of varicose veins are
“cosmetic” in nature and relate to the appearance of the veins, leg swelling, and skin
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pigmentation. Leg swelling may be masked by obesity. Obese women may have areas
of skin pigmentation due to obesity and may therefore attribute their symptoms to obesity
rather than varicose veins. As might have been predicted, the mothers showing no reflux
had negligible CEAP scores. The prevalence of varicose veins in non pregnant women in
the same age group would be useful to know, as well as in different ethnic groups, but this
suggests that obesity does not predispose to varicose veins.
Multiparous women with reflux were found to have significantly worse venous
symptoms than primiparous women (mean CEAP scores for each group 2.14 and
1.5, respectively). Their vein diameters were also greater. By comparison there was no
difference in symptoms between multiparous and primiparous women without reflux
(CEAP scores 0.37 and 0.29, respectively). This provides a clear link between venous
valve reflux and the degree of dilation of the veins and the symptoms experienced by
pregnant women.
Venous Changes in Pregnancy
Venous dynamics are altered during pregnancy. This occurs as a response to both the
physiological effects induced by pregnancy and the physical effects on venous outflow
from the lower limb veins of an enlarging uterus. These physiological changes are
essential to allow the mother to develop a circulation which will safely sustain her and
the growing fetus throughout gestation. They return to normal following delivery. The
mother’s circulating blood volume progressively increases by about a third during
pregnancy, reaching fifty percent of this increase at thirty-four weeks. This blood volume
increase is accommodated by peripheral vasodilatation which is mediated through
endothelial-dependent substances such as nitric oxide synthesis upregulated by oestradiol
and possibly prostaglandins PGI-2 (15). The presence of oestrogen and progesterone
receptors in the vein wall facilitates the changes in tone of the vein wall (16). The role of
mast cells and their relationship to vein wall remodeling may also play a part in this
process (17).
The dilatation of the vein wall progresses as gestation proceeds appearing to reach
a maximum in the superficial and the deep venous systems of the lower limb, at about
34 week (18–20). Most veins return to their pre-pregnancy size after delivery but some
varicose veins do not (18). There has for some time been an assumption that along with
increased relaxation of the vein wall, the venous valves become temporarily incompetent
in order to accommodate these profound, but normal, haemodynamic changes. The
persistence after delivery of this newly developed valve incompetence in superficial veins
has been thought to lead to the development of varicose veins. Several longitudinal studies
have been set up to examine this theory (19,21). They have not been able to demonstrate
the phenomenon of a normal venous valve becoming incompetent during pregnancy. This
remains the case in over 200 women now investigated for this phenomenon in our vascular
laboratory (22). It is largely unrecognized by the healthcare community and even by many
vascular specialists. The conclusions to be drawn from these studies are that new venous
valve reflux is not created during pregnancy and duplex scanning can identify the problem.
The traditional idea that all women with varicose veins should postpone treatment until
they have completed their family is therefore inappropriate. Clinical judgement and the
opinion of the woman must be taken into account for each case. Obviously not every
woman with refluxing valves will either want or even need treatment for their venous
reflux.
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The physical effects of the growing uterus on the pelvic and abdominal veins are well
known to midwives and gynecologists. When a woman in the third trimester of pregnancy
lies on her back the enlarged uterus compresses the inferior vena cava and the common iliac
veins and even the aorta in what is known as the aorto-caval compression syndrome (23).
As a result, venous pressure is increased in the legs and venous flow patterns become less
responsive to respiration thus impairing the abdominal and respiratory components of
venous return. More significantly, a reduced venous return to the heart created by this effect
may cause fainting. The clinical observation of this led to the practice of placing a women on
their left side during delivery to avoid this compression. More recent studies have also
shown marked velocity changes in lower limb deep veins in the supine position indicating
vena cava obstruction (24,25). These obstructive effects however probably have nothing to
do with the development ofpermanent venous problems leading to varicose veins. They are
more relevant to the obstetric health of the mother than any vascular problems.
Treatment of Varicose Veins in Women During Pregnancy
In 1964 George Fegan, a pioneer in both injection sclerotherapy and treatment of varicose
veins wrote:
We have been using an injection technique for 14 years for treating varicose veins on
15,000 patients—one-fourth of whom were pregnant at the time (26).
This must be the largest series of pregnant women (3750) who were given inter-
ventional treatment during gestation. Today, I believe that vascular specialists do not aim
to actively treat varicose veins during pregnancy but aim only to minimize the symptoms
of suffering women. An exception to this may be the need to perform a sapheno-femoral or
a sapheno-popliteal disconnection for superficial thrombophlebitis which threatens to
extend into the deep venous system. This has rarely been reported.
Fegan justified his course of action for treating women when they were pregnant by
claiming to deal with their painful problem immediately and further, taking away their
need to return to the hospital at a later date for treatment. He further justified his actions
by the fact that he had had no thromboembolic complications with this approach. His
meticulous bandaging techniques may have contributed to this; however, he provided
no evidence to support this statement (27). His treatment was obviously appreciated by his
patients and his clinics were full.
Today the most common treatment for symptomatic varicose veins during pregnancy
is the prescription of support hosiery. Stansby pointed out that, “the idea that varicose
veins may be treated with support hosiery is likely to be costly and to fail” (28). Coughlin
presented her findings of a randomized study designed to explore acceptability, compliance
and control of the symptoms and venous dilation with the wearing of Class One support
tights by pregnant women with venous reflux (14). Eighty-three women with superficial
venous reflux and no other identified venous abnormality were randomized. Increasing
numbers of women rejected the tights as their pregnancy progressed with the last trimester
being the final straw for most. Similar to another study, it showed that Class One support
hosiery failed to control completely the superficial and the deep vein dilatation which
developed as pregnancy progressed (29). The conclusions by the research team were that
careful selection of women was needed before prescribing tights and exploration of other
types of garments such as stocking “hold ups” should be considered. Support for the mother
by a dedicated team of stocking experts might increase compliance (30).
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Pregnancy, Pulmonary Thromboembolism, and Varicose Veins
Pulmonary thromboembolism (PTE) remains the most common direct cause of maternal
death in the UK (31) with 56 women dying of PE in the five years up to 2002. It was
highest in the 25 to 39 years age group. In the latest report of the Confidential Enquiry
into Maternal and Child Health (CEMAC), it is reported that in the last 20 years,
a demonstrable reduction in other causes, eg., hypertension and anaesthesia have been
reported but no such improvement in the rates of death from PTE. Postpartum deaths
following Caesarean section have fallen, however, and it is suggested that the adoption of
published recommendations on the use of anti-DVT prophylaxis may have contributed
to this.
Recommendations for prophylaxis against DVT are published by the Royal College
of Obstetricians and Gynecologists (32). These guides indicate three levels of risk Low,
Moderate and High for Cesarean section and these are presented in Table 1. Interestingly,
these include intheir moderate risk group “gross varicose veins,” butthey offer no reference
to the criteria for such a description or reasons for why they are there. As mentioned below,
the risk of superficial thrombophlebitis and its potential development into a DVT needs to be
considered further.
Table 1 RCOG UK Risk Factors for Venous Thromboembolism in Pregnancy and the
Puerperium
Pre-existing New onset or transient
Previous VTE Surgical procedure in pregnancy or
puerperium, e.g., evacuation of retained
products of conception, postpartum
sterilization
Thrombophilia
Hyperemesis
Congenital
Dehydration
Antithrombin deficiency
Ovarian hyperstimulation syndrome
Protein C deficiency
Severe infection, e.g., pyelonephritis
Protein S deficiency
Immobility (O 4 days bed rest)
Factor V Leiden
Pre-eclampsia
Prothrombin gene variant
Excessive blood loss
Acquired (antiphospholipid syndrome)
Long-haul travel
Lupus anticoagulant
Prolonged labour
Anticardiolipin antibodies
Midcavity instrumental delivery
Age over 35 years
Immobility after delivery
Obesity (BMI O 30 kg/m
2
) either
pre-pregnancy or in early pregnancy
Parity O 4
Gross varicose veins
Paraplegia
Sickle cell disease
Inflammatory disorders, e.g., inflammatory
bowel disease
Some medical disorders, e.g., nephrotic
syndrome, certain cardiac diseases
Myeloproliferative disorders, e.g., essential
thrombocythemia, polycythemia vera
Source: Modified from Ref. 32.
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Factors Contributing to Venous Thrombosis
Venous thromboembolic disease is complex and stimulated by abnormalities of systemic
factors and local venous conditions (33,34). It was Virchow who first linked abnormalities
of the vein wall, flow and blood constituents as the three things which contribute to venous
thrombosis. It is worth considering the vein wall and its contribution to thrombosis with
respect to varicose veins because they have an abnormal morphology and do have an
association with the body’s fibrinolytic system.
The fibrinolytic system is the body’s natural defence mechanism against thrombosis
and relies on the release of tissue plasminogen activator (TPA), mainly from the vein wall,
which then activates circulating plasminogen to plasmin which breaks down fibrin into its
soluble fibrin degradation products (FDPs). The presence of FDPs in the blood when
a thrombotic process is being lysed is the principle behind the commonly used screening
test for DVT, the D Dimer test.
Plasminogen activator was convincingly shown to be present in the vein wall by
Todd in 1958 (35). But it was Nilsson who in 1968 postulated the important clinical
relationship between thrombosis and the level of plasminogen activator in the vein
wall (36). Later with Isacson she suggested that there was a defective release of
plasminogen activator in patients with idiopathic thrombosis and went on to hypothesize
that deficient supplies of TPA in the vein wall may be a factor in the potential development
of thrombosis (37).
The 1960s and 1970s saw extensive research on the vein wall and its relationship to
TPA. The demonstration of a fibrinolytic deficiency in patients with venous leg ulcers led
to the development offibrinolytic drugs to treat venous leg ulcers, but they enjoyed a short
lifetime of success. The key findings of the time were that lower limb veins had
a significantly lower TPA concentration than hand veins; varicose veins had less activity
than normal veins, and dilatation of the veinwall depleted it of its TPAreserves (38). This is
summarized by de Cossart in her thesis “Plasminogen Activator and Vascular Disease” (39).
During pregnancy, a dilated varicose vein, which already has an abnormal wall as well as a
reduced TPA level, is subjected to dilatation and significant changes in flow, especially in
late pregnancy, when the dilatation is at its peak. These factors all contribute to a thrombo-
genic environment in the varicose vein, which is therefore a vein waiting to thrombose.
When a varicose vein thromboses, it presents clinically as the painful condition
known as superficial thrombophlebitis, and this is a recognized complication of pregnancy.
The increasing evidence that superficial thrombophlebitis may extend into the deep
veins and even cause pulmonary embolism indicates that it is not the benign condition
once thought (40). Superficial thrombophlebitis is commonly recorded as a condition
experienced by pregnant women but I have been unable to find any published case which
links such events with DVT or PE during pregnancy. I would speculate, however, that some
PE deaths in pregnancy may be associated with this condition. The obstetric community
needs to be awareof these facts and advise women with varicose veins,especially if they are
very dilated to seek advise from a vascular specialist between pregnancies.
Vulval Varicosities
Vulval varicosities are a benign condition, which is usually worse during the last trimester
of the pregnancy. They often cause alarm when lumps appear spontaneously on the vulva
and defy inspection because of a large abdomen. However, they rarely cause harm and,
despite the theoretical risk, do not cause bleeding problems at delivery. Episiotomy,
however, is contraindicated. Surprisingly, they rarely thrombose and they usually
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disappear following delivery. Detailed documentation of their prevalence in different
societies is lacking. Before the advent of modern imaging vulval phlebography was
pioneered as a useful means of planning a surgical treatment for them. They are associated
with PCS, a condition that is very common and multifactorial in etiology.
Challenges to Vascular Specialists Concerning Varicose Veins
and Pregnancy
Vascular specialists need to raise awareness in the healthcare community caring for
pregnant women about varicose veins and their cause. This is particularly true with respect
of the facts that:
† Venous valvular reflux causes varicose veins.
† Research has been unable to demonstrate pregnancy as a cause of valvular
reflux.
† Superficial thrombophlebitis may lead to DVT and PE.
† Women are intolerant of support tights.
† There is a need to create a classification of varicose veins with respect to their
size as an indicator for treatment to prevent phlebitis.
PELVIC CONGESTION SYNDROME
A Scenario
Recently a 38-years-old woman consulted a vascular surgeon and declared that she had
been assured by another doctor that her CPP was most likely be caused by refluxing
varicosities in the ovarian veins, which could now be treated successfully by surgery
or interventional radiology. She wished to be treated by one of these methods as she had
been seeking a cure for many years and had been extensively investigated by the
gynecologists who were unable to offer help.
Chronic Pelvic Pain
CPP is common in woman of child bearing age. It falls within the expertise of
gynecologists and is reported as being at least ten percent of their outpatient practice.
It leads to a significant number of laparoscopies and hysterectomies (41) and is
characterized by chronic complaint of lower abdominal/pelvic pain often exacerbated by
long periods of standing. Sexual intercourse too is often painful and when dyspareunia is
part of the syndrome this tends to reduce the chance of a beneficial outcome from
treatment. The exclusion of other pelvic conditions is essential before making the
diagnosis and this leads to the high laparoscopic rates in gynecological practice. Absence
of a precise cause of this chronic condition limits therapeutic options but high dose
progestogen treatment using medroxyprogesterone acetate seems to offer some women
symptomatic relief (42). As in many conditions where an objective cause for the
symptoms is elusive there is a tendency to disbelieve and even dismiss the woman as
a chronic complainer (43). A multidisciplinary approach to the problem which widens
deliberation and discussion with these women about their problems has been associated
with better management of the condition. Two key papers and a review are recommended
for surgeons who would be wise to explore this topic further (4,5,41). PCS is one cause of
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CPP and with the emergence of new imaging techniques and potential vascular solutions,
is growing in its relevance to vascular specialist (44).
Pelvic Congestion Syndrome
Pelvic Conjestion Syndrome (PCS), also known as pelvic venous incompetence, is
a condition resulting from ovarian vein dysfunction either due to reflux caused by
abnormal ovarian vein valves or ovarian vein obstruction caused by compression of the
left renal vein between the aorta and the superior mesenteric artery, the “nutcracker
syndrome” (2). Both of these conditions will result in abnormal venous flow and distal
venous hypertension. It will often manifest itself as a plexus of dilated veins around the
pelvic structures which can be seen on ultrasound and at laparoscopy. It may also present
as varicosities in the lower limbs where no long saphenous or short saphenous valvular
reflux can be demonstrated. In the case of renal vein obstruction the venous hypertension
may lead to renal failure in this kidney. PCS is one of the recognized causes of chronic
pelvic congestion syndrome (41).
The symptoms of PCS are usually thought of as a female problem. The anatomical
abnormalities described however are not gender specific. While the condition is twice
as common in women, it was in males that the varices were identified as the cause of
indentations in the ureter (45,46). Pregnancy undoubtedly imposes its effects on these
veins too and probably stimulates further abnormal dilatation of the veins in a similar way
to that previously described in the lower limbs (18).
The “Nutcracker Syndrome”
Grant the anatomist first described the obstruction of the ovarian vein by the mesenteric
artery. In 1950 this was described more precisely by El Sadr and Mina (47). Later it
became known as the “nutcracker syndrome” reflecting the crushing of the renal vein by
the artery and likening it to the of action of a nutcracker (48,49). In addition to suffering
from symptoms suggestive of PCS, patients with this problem may also suffer renal
damage as a complication of renal hypertension. This is characterized by the finding of
microscopic hematuria.
The repeated crushing injury to the renal vein also causes physical damage to the
vein wall and the development of thickenings and spurs on the outside of the vein wall at
the site of the compression (2). Inside the vein, the intimal damage caused by the repeated
crushing creates luminal webs surprisingly similar to the changes described by Cockett
with respect to the left iliac vein compressed by the right iliac artery in the “iliac vein
compression syndrome” (50). Sculteus et al. have elegantly reported an illustrated history
of the effects of the “nutcracker” phenomenon and reported a range of interventional
therapeutic options (2). Selection of patients for intervention, however, requires a very
careful history and examination and good clinical judgement by the vascular specialist
about when to intervene and in whom.
Investigation and Treatment of the “Nutcracker Syndrome”
The combined symptoms of PCS with microscopic hematuria and the demonstration of
pelvic varices in the female, or a varicocele in the male, are essential to the diagnosis.
Thorough investigation of renal function is important because of the likelihood of renal
cell damage due to the venous hypertension. Clinical suspicion of the condition should
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