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be followed by contrast MRI or CT scan aiming to be able to image distension of the left
renal vein as it is compressed between the aorta and the superior mesenteric artery, as
well as identifying renal congestion. This clearly defines the anatomical abnormality.
Direct venous pressure measurement and the demonstration of a gradient across the
obstruction is desirable but obtaining accurate readings is difficult due to variation in
measurements when readings are taken in the supine and erect positions. False negative
results are also likely in the prone and supine positions. Duplex scanning has a place but
the morphology of the patient will affect the imaging (51). Once the problem is defined
treatment should be directed by a multidisciplinary group involving vascular,
gynaecological and renal specialists. Its aim is to minimize further renal damage by
relieving the compression.
The treatment options for this condition include open surgery and transposition of
the vein, auto transplantation of the kidney, external stenting of the vein with external
supported PTFE and internal stenting (2,51–53). Each of these has pros and cons and
selection must be tailored to the individual patient’s clinical case. Internal stenting has
great attractions due to its less invasive nature but may be complicated by fibromuscular
hyperplasia and further obstruction or even occlusion of the left renal vein. The potential
for embolisation of endovascular devices are well known in the arterial system and this is
likely to be so in the venous system. Deteriorating renal function will be a strong
indicator to intervene but vascular specialists must be rigorous in selecting patients
for intervention.
Ovarian Vein Reflux
Dilation of the veins in the pelvis and their association with CPP has been demonstrated
clinically and at autopsy on many occasions (54–57). Hobbs described ovarian vein reflux
and its association with the clinical presentation of vulval and buttock varicosities which
develop during gestation and disappear after parturition (59). New imaging technology,
which is now both safer and more easily available, is allowing clinicians to investigate
patients as never before. These investigations are demonstrating abnormalities in the
venous system which are now being associated with chronic conditions not normally
considered to be the vascular domain of the vascular specialist. The possibility of being
able to treat them is highly seductive but should be approached carefully especially as in a
review of CT scans performed for reasons other than investigating ovarian veins, a dilated
ovarian venous system was found more often than expected in women without symptoms
attributable to CPP (60). Vascular experts will be sent patients who will have a long
history of symptoms and who are desperate for a cure.
Intervention for Ovarian Vein Reflux
The traditional treatment for ovarian vein reflux is open surgery to ligate the ovarian
vein (59). The procedure may now be carried out minimally invasively and this must be
the first choice for surgical intervention in the twenty first century. The question of
whether ligation is adequate when compared with excision of the ovarian vein has been
raised (3). A claim for the relief of symptoms during pregnancy with phlebotonic agents
has been made but is probably of very limited value (61).
Cordts et al. used their standard duplex test with a tilt of twenty degrees reversed
Trendelenberg, to illicit reflux in the ovarian and pelvic veins of eleven women with
CPP (62). All of the women underwent venography, which is essential in defining the
anatomy and patency of the ovarian vein, and was also essential in this study to characterize
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the ovarian veins that could not be imaged by duplex. CT or MRI was not performed
to exclude the “nutcracker syndrome,” which may have been a contributing factor to the
occluded ovarian veins. Nine cases underwent endovenous embolization of refluxing
ovarian veins were carried out. Follow up was short at 13.4 months, but early results are
promising, although the authors are honest enough to call for caution in interpreting them.
It is a good feasibility study and they call for a randomized study. This will be difficult
to do because of the different forms of presentation and the variety of treatments that may
be offered. Meticulous recording of important clinical data may contribute more to the
understanding of how to manage these conditions especially when combined with pre-
and post-assessment questioning of the patients. Agreed datasets should be constructed
and there may even be a case for a national registry. Endovenous ovarian vein oblation is
possible, however, with minimum morbidity. The greatest challenge to vascular specialists
will be to know how to select who to treat. The seductive rush to intervene must be
tempered by wise deliberation.
Review of the published literature indicates a multiplicity of possible therapeutic
options and the paucity of large studies to create a consistency of approach to treatment
(2). The review identified 13 different forms of treatment including: ovarian function
suppressing hormones, vasoactive agents, local excision or sclerotherapy of vulval
varices, several types of gynecologic surgery, gonadal embolization with coils, glues,
balloons, and sclerosants, selective surgical division or catheter embolization of the
hypogastric vein tributaries, and extraperitoneal or laparoscopic resection of the gonadal
plexus. Long-term follow up, however, is lacking and remains a gap in the knowledge
needed to advise and guide treatment in these unfortunate women. The studies to date
indicate that patients with mild to moderate symptoms and small vulval varicosities do
well with sclerotherapy and gonadal vein resection. The complications of coiling and
other endoluminal obliterative therapies are probably underestimated. In this potential
huge area of need for treatment there is also a big potential for creating problems rather
than resolving them and clinicians need to be systematic in their approach.
The 25 year experience of treating 57 woman with PCS by one unit emphasizes
the complexity of the clinical presentations and the many ways of treating them (3).
This has led the authors to develop a classification to guide assessment and treatment.
It is based on clinical presentation, hemodynamics, and pathophysiology. The four types
proposed are:
1. Vulval varices without symptoms of PCS
2. Venous insufficiency of the hypogastric vein and its tributaries (internal
pudendal, obturator, round ligament, and gluteal veins)
3. Predominantly gonadal venous insufficiency
4. Obstructed gonadal veins (nutcracker syndrome)
Their range of treatments included injection sclerotherapy and local excision for
vulval varices, gonadal vein embolisation for type 2, and gonadal vein resection combined
with other modalities for type 3. The management of type 4 has been covered previously
(2); physicians intent on treating these conditions should read this paper.
What is obvious from reading the U.S. literature and listening to the experiences
of U.S. vascular specialists, is that the U.S. experience is different from that in the United
Kingdom. The British literature has few papers on the subject which may either be
a reflection of a different clinical need or on the lack of imaging to identify these
conditions in the United Kingdom. The clinical presentation in some papers suggests
a different population of patients (2,3).
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Challenges to Vascular Specialists with Respect to
Pelvic Congestion Syndrome
Vascular specialists need to be aware of current understanding with respect to venous
abnormalities and their association with PCS. Much of the interventions proposed are
untried territories and new knowledge about these conditions is still emerging. There is
a need to ensure that interventions are not carried out just because they can be done. The
literature does not reveal a standard form of treatment even for the classification offered
above. A literature review revealed a lack of uniformity and consensus in the diagnosis
and management of patients with pelvic venous disorders. Most series are single cases and
there are no randomized studies. The challenges to vascular specialists include:
† Creating a multidisciplinary approach to include vascular surgeons, radiologists,
gynecologists, and in the case of renal vein obstruction, urologists
† Approaching interventions in a systematic way and refining the classifica-
tion above
† Creating a database of known cases and of new ones treated and considering
a national registry
† Learning to understand the natural history of the condition in order to learn when
to and when not to intervene
† Considering the use of randomized studies once a classification of the venous
presentation been has been achieved
Since venous surgery is often considered a cosmetic procedure it is incumbent upon
vascular surgeons to lead the way in researching and providing evidence for beneficial
interventions. Without such an approach, patients—especially women—will be denied
treatments. Used indiscriminately vascular interventions may fall into disrepute. Vascular
specialists have a responsibility to their patients and to their profession to get it right.
KEY POINTS
† Advice given to women in the child bearing age group about varicose veins
relies on myth rather than fact. There is a need to improve the knowledge and
understanding of professional on the known facts.
† Normal lower limb veins dilate during gestation returning to their normal size
after delivery but do not develop reflux.
† Refluxing veins of the lower limbs dilate during gestation the maximum changes
occurring at about 34 weeks. Many fail to return to their pre-pregnancy size
especially after many pregnancies. They are responsible for the appearance of
varicose veins following pregnancy.
† PTE remains the most common direct cause of maternal death in the UK with
56 women dying of PE in the five years up to 2002.
† Superficial thrombophlebitis in pregnancy may be a cause of PE and even death
in pregnant women.
† PCS is a complex problem requiring a careful history, clinical examination and
multidisciplinary approach involving vascular surgeons, vascular radiologist
and gynecologists to customizing each individual patient’s care.
† PCS presents twice as frequently in women compared with men. It has two broad
causes, left renal vein obstruction (“nutcracker syndrome”) and gonadal vein reflux
(valvular dysfunction or absence), and has a wide range of clinical presentations.
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† Doppler of vaginal and vulval varices in steep reversed Trendelenberg using
Valsalva’s maneuvre is useful to illicit reflux, which may indicate the presence
of pelvic and ovarian vein reflux.
† CT and/or MRI is necessary in PCS to distinguish the “nutcracker syndrome” from
ovarian vein reflux and cinevideo angiography may be useful to vizualise venous
connections in the pelvis.
† Pregnancy probably exacerbates the problem of venous reflux in PCS in a similar
way to that described in lower limb veins.
† Treatment for PCS, which may include open surgery with transposition of the vein,
auto transplantation of the kidney, external stenting of the vein with external
supported PTFE, and internal stenting, must be customised for each
individual patient.
† Ovarian vein reflux is common in women without symptoms of PCS.
† Symptomatic ovarian vein reflux may be treated with open or minimally invasive
surgical intervention or by endovenous techniques. Patient selection is vital.
† Vascular specialists need to develop a system for collecting data on the selection
of patients for interventional treatment and of the outcomes achieved.
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25
Superficial Vein Thrombosis:
Natural History and Clinical Significance
Athanasios D. Giannoukas
University of Thessaly Medical School and Division of Vascular Surgery,
University Hospital of Larissa, Larissa, Greece
Nicos Labropoulos
Vascular Laboratory, Division of Vascular Surgery, New Jersey Medical School, Newark,
New Jersey, U.S.A.
Superficial thrombophlebitis (STP) or superficial vein thrombosis most often affects the
veins of the lower extremities although it may be found in any superficial vein of the body.
Because most physicians consider it as a benign condition, its treatment is usually
conservative with elastic stockings (ES), ambulation, antibiotics, and nonsteroidal anti-
inflammatory drugs (NSAIDS) (1–4). Patients with STP near to the deep veins have been
treated with anticoagulation or ligation.
The main symptoms of STP are pain, erythema, and swelling around a superficial
vein. Accessory veins and tributaries with STP become solid and on palpation feel like
a cord. However, thrombosis of the main saphenous trunks may be missed on palpation, as
they are located in the saphenous canal. STP is often found in patients with varicose veins
probably due to blood stasis in these veins, but multiple factors have been implicated with
its development (5–10). Its diagnosis can be made based solely on clinical assessment, but
the use of duplex ultrasound imaging (DUS) has enabled the accurate detection of its
extent and progress (6,11–14).
Additionally, in contrast to the common perception among the physicians that it is
a benign condition, this is not always true as there is evidence in the literature suggesting
that STP may precipitate or may be associated with deep venous thrombosis (DVT), and it
could cause pulmonary embolism (PE). Nevertheless, because there are only a few
prospective studies dealing with this condition, the strength of these associations
remain unknown.
DEMOGRAPHIC CHARACTERISTICS
The incidence of STP has been reported to be in the range of 3–11% in the general
population (15), and in another report the rate clinically recognized STP was 123,000
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patients per year with a preponderance of the female gender (78%) (16). It is important to
mention that both of these studies are old and the diagnosis was clinical, and thus the STP
prevalence is probably underestimated because in many patients, the symptoms of
STP can be minor and not present for medical attention. Preponderance of females with
a ratio of 6 to 4 has been reported in the literature (17–22), attributing this to the higher
prevalence of varicose veins in pregnancy (22). Previous thromboembolic episodes, long-
haul flight, pregnancy, oral contraceptives, hormone replacement therapy, immobilization,
obesity, recent surgery, trauma, and sclerotherapy all have been implicated as potential
risk factors. Nevertheless, it is of importance that more than one risk factor has to be
present for the development of thrombosis. Of notice is that age is an important factor; the
older the patient, the fewer factors are needed (23). In multiple reports the mean age of
presentation is around 60 (20,21,24–28).
VARICOSE VEINS, LOCATION, AND STP
The most common location of STP is the saphenous veins and their tributaries in the lower
limb. This is followed by the superficial vein system in the upper limb (cephalic and basilic
vein), whereas it is uncommon in veins of other parts of the body (20). Patients with
varicose veins may develop STP, which in the literature has a wide range varying from 4%
to 59% (6,18,22). It appears that the great saphenous vein (GSV) is more often involved
(60–80%) than the small saphenous vein (SSV) (10–20%) but none of the lower limbs has
a predilection (6). Bilateral involvement is not very common (5–10%) (6,20) but it may be
associated with a higher number of complications (8%). GSV thrombosis may also
be associated with more complications than thrombosis in other locations (6). In most of
the cases STP develops in varicose tributaries rather than in the saphenous trunk (18).
As potential pathophysiologic mechanism has been considered the presence of localized
defects in the fibrinolysis and platelet aggregation but the current evidence is not definitive
and further work is needed (29).
HYPERCOAGULABLE STATES AND STP
While STP confined to varicose tributaries is considered as a complication of varicose vein
disease, saphenous trunk thrombosis is often a more significant thromboembolic process
(12,24). Many coagulation abnormalities have been reported to be associated with
saphenous thrombosis (8,9,24,30). When STP occurs in the absence of varicose veins,
autoimmune diseases or malignancy, the risk of STP was found to be six-fold for the
Factor V Leiden mutation, 4-fold for the factor II G20210A mutation and 13-fold for
antithrombin III, protein C and S deficiencies taken together (7). Anticardiolipin
antibodies and increased levels of factor VIII seem to be more prevalent in patients with
recurrent STP (30,31). Although there is lack of large studies evaluating the prevalence of
hypercoagulable states in different cohorts of patients with STP, it is clear that patients
with STP have high prevalence of hypercoagulable states (Table 1) (7,8,24,30–35).
Therefore, the development of STP in the absence of varicose veins, or STP extension to
the main trunk of the GSV, denotes a possible underline hypercoagulable state, which
should be investigated.
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PREGNANCY AND STP
There are only two studies in this area and both are of retrospective nature. The first
investigated 30,040 pregnancies, from which only 14 cases (0.05%) of STP were
diagnosed by ultrasonography, mostly presenting within 48 hours of delivery (36). In the
other one an incidence of 0.068% (49/72,200 deliveries; 95% CI 0.048–0.088) was found;
ten of these cases occurred prior to delivery and the rest (nZ39, 0.054%, 95%
CI 0.037–0.071) within seven days postpartum (10). A small number of patients with STP
(nZ24) were tested for thrombophilia, and only one was positive for a Factor V mutation.
The limited information on this topic does not allow any meaningful associations.
MALIGNANCY AND STP
The current literature on vascular disorders that preceded the diagnosis of malignancy
reveals that the relationship between STP and cancer remains weak (37), and it has
been derived from two retrospective studies (13,38). In the first study, the prevalence of
malignancy was 13% (14/106), and in 11 patients the malignancy was already diagnosed
(13). In the second study, which included 398 limbs, 56 had STP of which only 10 had
malignant disease (38). In daily practice when association of STP and cancer is found,
Table 1 STP and Hypercoagulable States
Author Patients State Prevalence (%)
Odds ratio
(95% CI) STP
Engesser
1987 (32)
71 Protein S
deficiency
72
Pabinger
1996 (34)
230 Coagulation
inhibitor
deficiency
[ in Protein C
and S
deficiency
– First episode
and recur-
rent
De Moerloose
1998 (8)
112 Factor V
Leiden
14.3 2.51 (1.04–6.24) First episode
Factor
IIA20210
3.6 3.28 (0.46–36.84)
Martinelli
1999 (7)
63 Factor VA1691 15.9 6.1 (2.6–14.2) First episode
Factor
IIG20210A
9.6 4.3 (1.5–12.6)
ATIII, Protein
CorS
deficiency
10.2 12.9 (3.6–46.2)
de Godoy
2001 (31)
45 Anticardiolipin
antibodies
33.3 6.64 (2.48–17.82) Recurrent
de Godoy
2003 (35)
36 Protein S
deficiency
5.2 Recurrent
(R2)
Schonauer
2003 (30)
45 High factor
VIII
24% (pZ0.004) 4 (2.0–8.6) Recurrent VTE
Abbreviations: ATIII, antithrombin III deficiency; STP, superficial vein thrombosis.
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