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112 Chapter 11/Classifying Venous Disease
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• Preulcer condition of tissues
• Trophic ulcers
Etiology
• Primary venous dilatation
• Secondary (postthrombotic) occlusion and recanalization
• Congenital dysplasias
Central hemodynamics
• Compensation
• Decompensation
— Underloaded
— Overloaded
The same year,5 Pierchalla and Tronnier suggested differentiation between primary and secondary (postthrombotic)
disease, and between superfi cial, perforator, and deep venous
disease using objective measures.
In 1988,6 Porter et al. published reporting standards for
venous disease developed by an ad hoc committee for the
Society for Vascular Surgery (SVS) and the North American
chapter of the International Society for Cardiovascular
Surgery (ISCVS). This was similar to and based on the
Widmer classifi cation with the addition of etiology and
anatomic distribution. This was the stimulus for the CEAP
classifi cation that followed later.
In 1991,7 Cornu-Thénard et al. published a clinical classifi cation of the severity of varicose veins by inspection and
palpation and calculated the sum of maximum diameter at
7 sites of the leg.
In 1992,8 Enrici and Caldevilla published a clinical
classifi cation on the evolution of the postthrombotic
syndrome:
Stage 1: Early postthrombotic syndrome with painful swell-
ing of the leg with distal venous hypertension and veno-
graphically demonstrating residual obstruction of the
deep veins with competent perforators
Stage 2: Compensatory hypertrophy of the musculo-venous
calf muscle pump
Stage 3: Stage 2 plus appearance of secondary varicose
veins
Venography shows recanalization with varying refl ux with
incompetent perforators;
Stage 4: Advanced chronic venous insuffi ciency with
development of a vicious venous recirculation with
lipodermatosclerosis and ulceration due to venous
hypertension
Stage 5: Phlebo-arthrotic syndrome with immobilization of
the ankle
Leads to atrophy of the calf muscle with large circumferential ulcers
Stage 6: Secondary, postthrombotic lymphedema
In 1993,9 Miranda et al. published a clinical classifi cation:
Stage I: Dilatation of GSV 7 mm by duplex scanning
Stage II: Dilatation of GSV>7 mm without skin changes
Stage III: Stage II plus skin changes
Stage IV: Stage III plus active or healed ulcer
THE CREATION OF THE
CEAP CLASSIFICATION
At the fi fth annual meeting of the American Venous
Forum (AVF) in 1993, John Porter suggested using the same
approach as TNM for cancer to develop a classifi cation
system for venous diseases. Following a year of intense
discussions a consensus conference was held at the sixth
annual meeting of AVF in February 1994 on the island of
Maui, Hawaii, at which an international ad hoc committee,
chaired by Andrew Nicolaides, and with representatives
from Australia, Europe, as well as the United States, developed the fi rst CEAP consensus document.10 It contained
two parts, a classifi cation of CVD and a scoring system
of the severity of CVD. The classifi cation was based on
clinical manifestations (C), etiologic factors (E), anatomic
distribution of disease (A), and the underlying pathophysiologic fi ndings (P), thus the name CEAP. The severity
scoring system was based on three elements: the number
of anatomic segments affected, grading of symptoms and
signs, and disability. The CEAP consensus statement was
published in 26 journals and books in nine languages,
truly a universal document for CVD. It was endorsed by the
Joint Councils of the SVS and the North American Chapter
of the ISCVS, and its basic elements were incorporated
into venous reporting standards.11 Today most published
clinical papers on CVD use all or portions of the CEAP
classifi cation.
REVISION OF CEAP
Diagnosis and treatment of CVD were developed rapidly
in the 1990s and the need for an update of the classifi cation
logically followed. Now, it is important to stress that CEAP
is a descriptive classifi cation. Venous Severity Scoring
(VSS)12 was developed to allow longitudinal outcomes
assessment, but it became apparent that CEAP itself required
updating and modifi cation. In April 2002, an ad hoc committee on CEAP was appointed by AVF to review the classifi cation and make recommendations for change by 2004,
10 years after its introduction (see Table 11.1). An International ad hoc committee also was established to assure
continued universal utilization (see Table 11.2). The two
committees held four joint meetings in Hawaii, November
Terminology and New Defi nitions 113
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TABLE 11.1 Members of the American Venous Forum
hoc
Committee on Revision of CEAP classifi cation
Bo Eklof, chair
John Bergan
Peter Gloviczki
Robert Kistner
Mark Meissner, secretary
Gregory Moneta
Frank Padberg
Robert Rutherford
Thomas Wakefi eld
TABLE 11.2 The International
Revision of CEAP Classifi cation
The AVF ad hoc committee* plus:
Claudio Allegra, It
Pier Luigi Antignani, It
Patrick Carpentier, Fr*
Philip Coleridge Smith, UK*
André Cornu-Thenard, Fr
Ermenegildo Enrici, Ar
Jean Jerome Guex, Fr
Shunichi Hoshino, Jp
Arkadiusz Jawien, Pl
Nicos Labropoulos, USA
Fedor Lurie, USA
Mark Malouf, Au
Nick Morrison, USA
Kenneth Myers, Au*
Peter Neglén, USA
Andrew Nicolaides, Cy
Tomo Ogawa, Jp
Hugo Partsch, At
Michel Perrin, Fr*
Eberhard Rabe, Ge
Seshadri Raju, USA
Vaughan Ruckley, UK*
Ulrich Schultz-Ehrenburg, Ge
Jean Francois Uhl, Fr
Martin Veller, SA
Yuqi Wang, Ch
Zhong Gao Wang, Ch
*Editorial committee
ad hoc
Committee on
ad
2002; Cancun, Mexico, February 2003; San Diego, August
2003; and Orlando, February 2004.
The following passages summarize the results of these
deliberations, by describing the new aspects of the revised
13
CEAP.
The recommended changes, detailed next, include additions to or refi nements of several defi nitions used in describing CVD, refi nement of the C-classes of CEAP, addition of
the descriptor n (no venous abnormality identifi ed), incorporation of the date of classifi cation and level of clinical
investigation, and the description of basic CEAP, introduced as a simpler alternative to the full (advanced) CEAP
classifi cation.
TERMINOLOGY AND NEW DEFINITIONS
The CEAP classifi cation deals with all forms of chronic
venous disorders. The term chronic venous disorder (CVD)
includes the full spectrum of morphological and functional
abnormalities of the venous system from telangiectasias to
venous ulcers. Some of these, like telangiectasias, are
highly prevalent in the normal adult population, and in many
cases the use of the term “disease” is not appropriate. The
term chronic venous insuffi ciency (CVI) implies a functional abnormality of the venous system and usually is
reserved for patients with more advanced disease including
those with edema (C3), skin changes (C4), or venous ulcers
(C5–6).
It was agreed to maintain the overall structure of the
CEAP classifi cation, but to add more precise defi nitions.
The following recommended defi nitions apply to the clinical
C classes in CEAP:
Telangiectasia: A confl uence of dilated intradermal venules
of less than 1 mm in caliber. Synonyms include spider
veins, hyphen webs, and thread veins.
Reticular veins: Dilated bluish subdermal veins usually from
1 mm in diameter to less than 3 mm in diameter. They
usually are tortuous. This excludes normal visible veins
in people with thin, transparent skin. Synonyms include
blue veins, subdermal varices, and venulectasies.
Varicose veins: Subcutaneous dilated veins equal to or more
than 3 mm in diameter measured in the upright position.
These may involve saphenous veins, saphenous tributar-
ies, or nonsaphenous superfi cial leg veins. Varicose veins
usually are tortuous, but tubular saphenous veins with
demonstrated refl ux may be classifi ed as varicose veins.
Synonyms include varix, varices, and varicosities.
Corona phlebectatica: A fan-shaped pattern of numerous
small intradermal veins on the medial or lateral aspects
of the ankle and foot. This commonly is thought to be an
early sign of advanced venous disease. Synonyms include
malleolar fl are and ankle fl are.
Edema: A perceptible increase in volume of fl uid in the skin
and subcutaneous tissue characteristically indenting with
pressure. Venous edema usually occurs in the ankle
region, but it may extend to the leg and foot.
Pigmentation: A brownish darkening of the skin resulting
from extravasated blood, which usually occurs in the
ankle region but may extend to the leg and foot.
Eczema: An erythematous dermatitis, which may progress
to a blistering, weeping, or scaling eruption of the skin
of the leg. It is most often located near varicose veins but
114 Chapter 11/Classifying Venous Disease
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may be located anywhere in the leg. Eczema usually is
seen in uncontrolled CVD but may refl ect sensitization
to local therapy.
Lipodermatosclerosis (LDS): Localized chronic infl amma-
tion and fi brosis of the skin and subcutaneous tissues of
the lower leg, sometimes associated with scarring or contracture of the Achilles tendon. LDS is sometimes preceded by diffuse infl ammatory edema of the skin, which
may be painful and which is often referred to as hypo-
dermitis. This condition must be distinguished from lymphangitis, erysipelas, or cellulitis by their characteristically
different local signs and systemic features. LDS is a sign
of severe chronic venous disease.
Atrophie blanche or white atrophy: Localized, often circular
whitish and atrophic skin areas surrounded by dilated
capillaries and sometimes hyperpigmentation. This
fi nding is a sign of severe chronic venous disease and not
to be confused with healed ulcer scars. Scars of healed
ulceration also may have atrophic skin with pigmentary
changes but are distinguishable by history of ulceration
and appearance from atrophie blanche and are excluded
from this defi nition.
Venous ulcer: Full thickness defect of the skin most fre-
quently in the ankle region that fails to heal spontaneously and is sustained by CVD.
REFINEMENT OF C-CLASSES IN CEAP
The essential change here is the division of class C
4 into two subgroups that refl ect different severity of
disease, and carry a different prognosis in terms of risk of
ulceration:
C0: No visible or palpable signs of venous disease
C1: Telangiectasies or reticular veins
C2: Varicose veins—distinguished from reticular veins by
a diameter of 3 mm or more
C3: Edema
C4: Changes in the skin and subcutaneous tissue secondary
to CVD (now divided into two subclasses to better defi ne
the differing severity of venous disease):
C4a: Pigmentation and/or eczema
C4b: Lipodermatosclerosis and/or atrophie blanche
C5: Healed venous ulcer
C6: Active venous ulcer
Each clinical class is further characterized by a subscript for
the presence of symptoms (S, symptomatic) or absence of
symptoms (A, asymptomatic), for example, C2
Symptoms include aching, pain, tightness, skin irritation,
heaviness, and muscle cramps, as well as other complaints
attri butable to venous dysfunction.
or C5S.
A
REFINEMENT OF E, A, AND P IN CEAP
To improve the assignment of designations under E, A,
and P, a new descriptor n is now recommended for use
where no venous abnormality is identifi ed. This n could be
added to E (En: no venous etiology identifi ed), A (An: no
venous location identifi ed), and P (Pn: no venous pathophysiology identifi ed). Observer variability in assigning
designations in the past may have been contributed to by the
lack of a normal option. Further defi nition of the A and P
has also been afforded by the new venous severity scoring
system,12 which was developed by the ad hoc Committee on
Outcomes of the AVF to complement CEAP. It includes not
only a Clinical Severity Score but a Venous Segmental
Score. The latter is based on imaging studies of the leg veins,
for example, duplex scan, and the degree of obstruction or
refl ux (P) in each major segment (A) and forms the basis for
the overall score.
This same committee also is pursuing a prospective
multicenter investigation of variability in vascular diagnostic laboratory assessment of venous hemodynamics in
patients with CVD. The last revision of the venous reporting
11
standards
still cites changes in ambulatory venous pressure
or plethysmographically measured venous return time (VRT)
as objective measures of change. The current multicenter
study aims to establish the variability of, and thus limits of
“normal” for, the VRT and the newer noninvasive venous
tests as an objective basis for claiming signifi cant improvement as a result of therapy, and will hopefully provide
improved reporting standards for defi nitive diagnosis and
results of competitive treatments in patients with CVD.
DATE OF CLASSIFICATION
CEAP is not a static classifi cation; the patient can be
reclassifi ed at any point in time. Classifi cation starts with
the initial visit, but can be better defi ned after further investigations. A fi nal classifi cation may not be complete until
after surgery and histopathologic assessment. We therefore
recommend that any CEAP classifi cation be followed by the
date; for example, C4b,S,Ep,As,p,Pr (2003-08-21).
LEVEL OF INVESTIGATION
A precise diagnosis is the basis for correct classifi cation
of the venous problem. The diagnostic evaluation of the
patient with CVD can be logically organized into one or
more of three levels of testing, depending on the severity of
the disease:
Revision of CEAP: Summary 115
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Level I: The offi ce visit with history and clinical examina-
tion, which may include use of a hand-held Doppler
Level II: The noninvasive vascular laboratory, which now
routinely includes duplex color scanning, with some plethysmographic method added as desired
Level III: Invasive investigations or more complex imaging
studies including varicography, ascending and descending venography, venous pressure measurements, spiral
CT scan, or MRV
We recommend that the level of investigation (L)
should also be added to the classifi cation, for example,
C2,4b,S,Ep,As,p,Pr (2003-08-21,L II).
BASIC CEAP
A new basic CEAP is offered here. Use of all components
of CEAP is still encouraged but unfortunately many physicians merely use only the C-classifi cation, which is just a
modest advance beyond the previous classifi cations and is
based solely on the clinical appearance. Venous disease is
complex, but can be described by use of well-defi ned categorical descriptions. For the practicing physician, CEAP can
be a valuable instrument for correct diagnosis to guide treatment and assess prognosis. In modern phlebological practice
the vast majority of patients will have a duplex scan of the
venous system of the leg, which largely will defi ne the E,
A, and P categories.
Nevertheless, it is recognized that the merits of using the
full (advanced) CEAP classifi cation system hold primarily
for the researcher and for standardized reporting in scientifi c
journals. It allows grouping of patients so that the same
types of patients can be analyzed together, and such subgroup analysis allows their treatments to be more accurately
assessed. Furthermore, reports using CEAP can be compared with one another with much greater certainty. This
more complex classifi cation, for example, also allows any
of the 18 named venous segments to be identifi ed as the
location of venous pathology. Take a patient with pain,
varicose veins, and lipodermatosclerosis where duplex scan
confi rms primary refl ux of the GSV and incompetent perforators in the calf. The classifi cation here would be C2,4b,S,
Ep, As,p, Pr2,3,18.
Although the detailed elaboration of venous disease in
this form may seem unnecessarily complex, even intimidating, to some clinicians, it provides universal understandable
descriptions that may be essential to investigators in the
fi eld. To serve the needs of both, the full CEAP classifi cation, as modifi ed earlier, is retained as advanced CEAP, and
the following simplifi ed form is offered as basic CEAP.
In essence, Basic CEAP applies two simplifi cations: 1)
In basic CEAP, the single highest descriptor can be used for
clinical classifi cation. For example, a patient with varicose
veins, swelling, and lipodermatosclerosis would be C4b.
The more comprehensive clinical description, in advanced
CEAP, would be C2,3,4b.
2) In basic CEAP, where duplex scan is performed, E, A,
and P should also be classifi ed using the multiple descriptors
recommended, but the complexity of applying these to the
18 possible anatomic segments is avoided in favor of applying the simple s, p, and d descriptors to denote the superfi cial, perforator, and deep systems. Thus, using basic CEAP,
the same patient cited in a previous example (painful
varicosities plus lipodermatosclerosis and duplex scan
determined refl ux involving the superfi cial and perforator
systems) would be classifi ed as C4b,S, Ep, As,p Pr (rather
than C2,4b,S, Ep, As,p, Pr2,3,18).
REVISION OF CEAP: SUMMARY
Clinical Classifi cation
C0: No visible or palpable signs of venous disease
C1: Telangiectasias or reticular veins
C2: Varicose veins
C3: Edema
C4a: Pigmentation and/or eczema
C4b: Lipodermatosclerosis and/or atrophie blanche
C5: Healed venous ulcer
C6: Active venous ulcer
S: Symptoms including ache, pain, tightness, skin irritation, heaviness,
muscle cramps, as well as other complaints attributable to venous
dysfunction
A: Asymptomatic
Etiologic Classifi cation
Ec: Congenital
Ep: Primary
Es: Secondary (postthrombotic)
En: No venous etiology identifi ed
Anatomic Classifi cation
As: Superfi cial veins
Ap: Perforator veins
Ad: Deep veins
An: No venous location identifi ed
Pathophysiologic Classifi cation
Basic CEAP:
Pr: Refl ux
Po: Obstruction
Pr,o: Refl ux and obstruction
Pn: No venous pathophysiology identifi able
116 Chapter 11/Classifying Venous Disease
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Advanced CEAP
Same as basic, with the addition that any of 18 named venous segments
can be utilized as locators for venous pathology:
Superfi cial veins:
1. Telangiectasias/reticular veins
2. Great saphenous vein (GSV) above knee
3. GSV below knee
4. Small saphenous vein
5. Nonsaphenous veins
Deep veins:
6. Inferior vena cava
7. Common iliac vein
8. Internal iliac vein
9. External iliac vein
10. Pelvic: gonadal, broad ligament veins, other
11. Common femoral vein
12. Deep femoral vein
13. Femoral vein
14. Popliteal vein
15. Crural: anterior tibial, posterior tibial, peroneal veins (all paired)
16. Muscular: gastrocnemial, soleal veins, other
Perforating veins:
17. Thigh
18. Calf
Example: A patient presents with painful swelling of the leg and varicose
veins, lipodermatosclerosis, and active ulceration. Duplex scanning on
May 17, 2004, showed axial refl ux of GSV above and below the knee,
incompetent calf perforators, and axial refl ux in the femoral and popliteal
veins. No signs of postthrombotic obstruction.
• Classifi cation according to basic CEAP: C6,S, Ep, As,p,d, Pr
• Classifi cation according to advanced CEAP: C2,3,4b,6,S, Ep, As,p,d,
Pr2,3,18,13,14 (2004-05-17, LII)
REVISION OF CEAP—AN
ONGOING PROCESS
With improvement in diagnostics and treatment there will
be continued demands to adapt the CEAP classifi cation to
better serve future developments. There are several conditions that are not included in the CEAP classifi cation but
that can infl uence the management of the patients:
• Combined arterial/venous etiology
• Postthrombotic lymphedema
• Ankle ankylosis with atrophy of the calf
• Venous aneuryms
• Venous neuropathy
• Corona phlebectatica
• Pelvic congestion syndrome
• Morbid obesity
The role of corona phlebectatica (CP) was discussed during
the meetings and the Atlantic Ocean was a clear divider.
In parts of Europe CP has been used as an early indicator
of advanced CVD. Its scientifi c signifi cance is now under
investigation, particularly in France. There is a need to
incorporate appropriate new features without too frequent
disturbances of the stability of the classifi cation. As one of
the committee members (F. Padberg) stated in our deliberations, “It is critically important that recommendations for
change in the CEAP standard be supported by solid research.
While there is precious little that we are recommending
which meets this standard, we can certainly emphasize it for
the future. If we are to progress we should focus on levels
of evidence for changes rather than levels of investigation.
While a substantial portion of our effort will be developed
from consensus opinion, we should still strive to achieve an
evidence-based format.”
Acknowledgment
Part of this article was previously published in Eklöf B, Rutherford RB,
Bergan JJ, Carpentier P, Gloviczki P, Kistner RL et al., for the American
Venous Forum International Ad Hoc Committee for Revision of the CEAP
classifi cation. Revision of the CEAP classifi cation for chronic venous disorders: Consensus statement, J. Vasc. Surg. 2004. 40:1248–1252.
The author wishes to thank the Society for Vascular Surgery for permission to reproduce the relevant section.
References
1. Widmer LK. Peripheral venous disorders: Prevalence and socio-
medical importance: Observations in 4529 apparently healthy persons:
Basle III study. 1978. Bern, Switzerland: Hans Huber,
2. Hach W, Schirmers U, Becker L. Veränderungen der tiefen Leitvenen
bei inner Stammvaricose der V.saphena magna. In: Muller-Wiefel H,
ed. Microzirkulation und Blutrheologie. 1980. Baden, Germany:
Witzstrock. pp. 468–470.
3. Partsch H. “Betterable” and “nonbetterable” chronic venous insuffi -
ciency: A proposal for a practice oriented classifi cation. VASA. 1980.
9: 165–167.
4. Sytchev GG. Classifi cation of chronic venous disorders of lower
extremities and pelvis, Int. Angiol. 1985. 4: 203–206.
5. Pierchalla P, Tronnier H. Diagnosis and classifi cation of venous
insuffi ciency of the leg, Dtsch. Med. Wochenschr. 1985. 110: 1700–
1702.
6. Porter JM, Rutherford RB, Clagett GP, Cranley JJ, O’Donnell TF,
Raju S et al. Reporting standards in venous disease, J. Vasc. Surg.
1988. 8: 172–181.
7. Cornu-Thenard A, DeVincenzi G, Maraval M. Evaluation of different
systems for clinical quantifi cation of varicose veins, J. Dermatol. Surg.
Oncol. 1991. 17: 345–348.
8. Enrici EA, Caldevilla HS. Classifi cation de la insufi ciencia venosa
chronica. In: Enrici EA, Caldevilla HS, eds. Insufi ciencia Venosa
Cronica de los Miembros Inferiores. Buenos Aires, Argentina: Edito-
rial Celcius. 1992 pp. 107–114.
9. Miranda C, Fabre M, Meyer P, Marescaux J. Evaluation of a reference
anatomo-clinical classifi cation of varices of the lower limbs, Phlebologie. 1993. 46: 235–239.
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10. Bergan JJ, Eklof B, Kistner RL, Moneta GL, Nicolaides AN,
and the International ad hoc committee of the American Venous
Forum. Classifi cation and grading of chronic venous disease
in the lower limbs. A consensus statement, Vasc. Surg. 1996. 30: 5–
11.
11. Porter JM, Moneta GL, an International Consensus Committee on
Chronic Venous Disease. Reporting standards in venous disease: An
update, J. Vasc. Surg. 1995. 21: 635–645.
12. Rutherford RB, Padberg FT, Comerota AJ, Kistner RL, Meissner MH,
Moneta GL. Venous severity scoring: An adjunct to venous outcome
assessment, J. Vasc. Surg. 2000. 31: 1307–1312.
13. Eklöf B, Rutherford RB, Bergan JJ, Carpentier P, Gloviczki P,
Kistner RL et al., for the American Venous Forum International Ad
Hoc Committee for Revision of the CEAP classifi cation. Revision
of the CEAP classifi cation for chronic venous disorders: Consensus
statement, J. Vasc. Surg. 2004. 40: 1248–1252.
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CHAPTER
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12
Risk Factors, Manifestations,
and Clinical Examination of the
Patient with Primary Venous Insuffi ciency
JOHN BERGAN
Knowledge of the risk factors that enter into causation of
primary venous insuffi ciency provides an understanding that
aids in care of the patient. There are risk factors, such as
heredity, female gender, and aging, that cannot be altered
(see Table 12.1). There are others, such as pregnancy, that
are acquired but cannot be modifi ed, and there are those
with little or no infl uence, such as smoking, hypercholesterolemia, vitamin intake, and leg crossing. These and
the historical and largely abandoned physical tests of the
patient with venous insuffi ciency are the subject of this
chapter.
HEREDITY
Although development of varicose veins usually can be
ascribed to many conditions, conventional examinations
may not disclose the apparent source of the high-pressure
leak from the deep to the superfi cial system.1 Therefore
other inherent factors such as vein wall weakness, increased
primary valvular dysfunction or agenesis, and other genetic
factors may enhance the development of varicose veins.
In an extensive study in France, 134 families were
examined. Of these, 67 were families with patients with
varicose veins, and 67 were control families without familial varicose veins. A total of 402 subjects were examined
and the results demonstrated a prominent role of hereditary
in the development of varicose veins (p < .001). For the
children, the risk of developing varicose veins was 90%
when both parents were affl icted. When only one parent was
affected, the risk of developing varicose veins was 25% for
men and 62% for women. The overall risk of varicose vein
development is 20% when neither parent is affected by
varicosities.
2
A familial tendency toward the development of varicose
veins has been described in many population groups.
may also be demonstrated by the development over time of
varicose veins bilaterally when patients with unilateral varicose and telangiectatic veins are followed for 10 years.5 A
limited study of 50 patients with varicose veins in Great
Britain disclosed a simple dominant type of inheritance.6
Only 28% of patients had no family history of varicose
veins. In Scandinavia, questionnaires completed by 124
women with varicose veins disclosed a 72% prevalence
of varicose veins of an autosomal type in the women’s
siblings.7 Of these cases, 28% were of a recessive pattern.
Troisier and Le Bayon examined 154 families with 514
descendants. They found that if both parents had varicose
veins, 85% of children had evidence of varicose veins,
whereas 27% of the children were affected if neither parent
had varicose veins, and 41% of the children were affected
if one parent had varicosities. These authors conclude
that the inheritance of varicose disease is recessive. However, some studies have not found a signifi cant familial
tendency.
monozygotic pairs were concordant with regard to varicose
veins. Of 25 dizygotic, same-sexed pairs, 52% had varicose
veins.
itance. In a detailed study from Sweden of 250 probands of
patients with varicose veins requiring treatment, the overall
frequency of varicose veins in female relatives was 43%,
compared with 19% in male relatives.
femoral veins has been shown to be a marker of varicose
veins in a limited radiographic study of 12 male volunteers,
some with and some without varicose veins,12 and in a
8,9
A single study on unselected twins found that 75% of 12
10
Other studies have found more of a multifactorial inher-
11
The absence of venous valves in the external iliac and
3,4
This
The Vein Book
119
All rights of reproduction in any form reserved.
Copyright © 2006, Elsevier Inc.
120 Chapter 12/Risk Factors, Manifestations, and Clinical Examination of the Patient with Primary Venous Insuffi ciency
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TABLE 12.1 Risk Factors for Varicose Veins and
Telangiectasias
Certain
Heredity
Female Gender
Pregnancy
Aging
Conjectural
Diet
Abdominal Straining
Tight Clothing
Leg Crossing
venous Doppler study of 54 patients with varicose veins.12
In addition, a simple dominant mode of inheritance has been
reported in 14 patients with congenital partial or total absence
of venous valves of the leg.13 Thus this genetic predisposition may be the result of multiple factors, and the subsequent
development of varicose veins may depend on one or more
occupational or hormonal factors.
Recent studies on varicose and normal veins using gene
expression profi ling based on cDNA microarray analysis
suggest that pathways associated with fi brosis and wound
healing may be altered in varicose veins.14 Whether the upregulated varicose vein genes are a sequel to the changes in
the varicose vein wall rather than a primary contributing
factor to varicose pathogenesis awaits additional study.
PREGNANCY
Pregnancy typically is associated with secondary valvular incompetence. Many epidemiologic studies have found
a signifi cantly increased incidence of varicose veins in
women who have been pregnant.15 However, some epidemiologic studies have failed to confi rm this association
when the effect of age is controlled.16 Varices are often fi rst
noted during pregnancy and are exceedingly rare before
puberty. Indeed, population studies have found that only
12% of women with varicose veins have never been
pregnant.
for venous dilation. As many as 70% to 80% of patients
develop varicose veins during the fi rst trimester when the
uterus is only slightly enlarged. In the second trimester, 20%
to 25% of patients develop varicose veins, and 1% to 5% of
patients develop them in the third trimester.
six weeks into gestation, a time when the uterus is not yet
large enough to signifi cantly impede venous return from the
leg veins. Mullane20 notes that symptoms of varicose veins
can be the fi rst sign of pregnancy and can occur even before
the fi rst missed menstrual period. This confi rms observa-
17
In pregnancy, hormonal factors are primarily responsible
18,19
Varicose veins of the legs are fi rst apparent as early as
tions of many multiparous women and argues for a profound
infl uence of progesterone on venous dilation and valvular
insuffi ciency.
AGING
The incidence of varicose veins increases with age, therefore vein wall damage should be more pronounced in the
veins of older patients. An autopsy study of the popliteal
vein in 127 persons demonstrated diffuse changes, with an
increase in connective tissue in the media that become most
pronounced in the fi fth decade and are progressive thereafter. This is associated with the loss of muscle cells in the
media.21 The fi nding correlated with an abnormality in the
physical property of axial tension testing in 93 specimens of
saphenous veins from 22 patients harvested during coronary
bypass surgery.22 However, one study of 31 normal veins
and 41 varicose veins in patients and autopsy samples
ranging in age from 25 to 92 failed to disclose an age-related
difference.23 The latter study concluded that varicose veins
were a predetermined disease unrelated to aging effects.
THEORETICAL RISK FACTORS
One popular hypothesis for the development of varicose
veins is Western dietary and defecation habits, which cause
an increase in intraabdominal pressure. Population studies
have demonstrated that a high-fi ber diet is evacuated within
an average of 35 hours.24 In contrast, a low-fi ber diet has an
average transit time of 77 hours. An intermediate diet has a
stool transit time of 47 hours.
Defecatory straining induced by Western-style toilet seats
has also been cited as a cause of varicose veins, in contrast
to the African custom of squatting during defecation.
An association between prostatic hypertrophy, inguinal
hernia, and varicose veins may be caused by straining at
micturition with a resultant increase in intraabdominal
pressure.
Another mechanism for increasing distal venous pressure
by proximal obstruction is the practice of wearing girdles or
tight-fi tting clothing. A statistically signifi cant excess of
varicose veins is noted in women who wear corsets compared with women who wear less constrictive garments.
Leg crossing and sitting on chairs are two other potential
mechanisms for producing a relative impedance in venous
return. Habitual leg crossing is commonly thought to result
in extravenous compression, but this has never been scientifi cally verifi ed.
27
Most,
but not all,28 studies have found that obesity is
associated with the development of varicose veins. Careful
examination of some of these epidemiologic studies shows
that when the patient’s age is correlated with obesity, the
25,26
Symptoms of Primary Venous Insuffi ciency 121
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statistical signifi cance is eliminated. Varices may be secondary to decreased exercise and associated medical problems
specifi c to obesity such as hypertension, diabetes, hypercholesterolemia, and sensory impairment.
Finally, it commonly is noted that occupations that require
standing for prolonged periods have an increased incidence
of varicose veins. This may be exacerbated by tall height,
although this factor has not been supported by other studies.
VALVE REMODELING
Our interest and focus on the venous valve dysfunction
as a fundamental cause of distal venous hypertension began
with unpublished observations using angioscopy. The angioscope provided a direct view of the internal architecture of
saphenous veins. Patients taken to surgery who demonstrated preoperative refl ux verifi ed by duplex ultrasound
showed a variety of pathologic lesions in the valves themselves. The fi rst indication was a relative paucity of valves.
The observation of decrease in number of GSV valves was
reported by Cotton in 1961.29 Next, we encountered actual
valve lesions. These observations were an extension of those
reported by Hoshino et al.,30 who classifi ed valve damage in
the saphenous vein into three categories ranging from
stretched commissures to perforations and valve splitting.
From the preceding observations we suggest that the earliest valve defects are an increase in the commissural space,
which allows refl ux on the border of the vein. This may be
one of the earliest causes of refl ux in varicose veins. Later,
thinning, elongation, stretching, splitting, and tearing of the
valves develop. The latest stages are thickening, contraction,
and possibly even adhesion between valves. These observations have been confi rmed by Van Cleef et al.31 Although
we have proposed that this valve damage is acquired and
causes axial refl ux as well as outfl ow through check valves
in perforating veins, others have proposed that the cause of
primary venous insuffi ciency is an actual reduced number
of valves in the saphenous system.
The angioscopic observations could be confi rmed by
gross morphologic studies that, when extended to microscopic observations using monoclonal antibody labeling,
have demonstrated monocytic infi ltration into damaged
venous valves.33 Others have found leukocytic infi ltration
into varicose veins and have called attention to the fact that
the cells observed release vasoactive substances, including
histamine, tryptase, prostaglandins, leukotrienes, and cytokines. Observations in patients led to the conclusions that
venous hypertension was related to leukocytic infi ltration on
the cranial surfaces of the venous valve and venous wall and
that leukocytes there were greater in quantity than on the
caudal portion of valve leafl ets and venous wall.
Therefore a model of venous hypertension was developed
in which microvessels in rat mesentery were examined
32
34
microscopically. Venous occlusion and subsequent venous
hypertension were produced by pipette blockade of venules
about 40 μm in diameter. Videomicroscopy revealed early
signs of infl ammation, such as progressive leukocyte rolling,
adhesion, and subsequent migration as well as parenchymal
cell death.
This infl ammatory sequence occurred early during the
phase of venous hypertension and progressed further after
release of the occlusion. The model showed that venous
occlusion with elevation of the hydrostatic pressure caused
a highly injurious process for the surrounding tissues. It was
accompanied by formation of microhemorrhages on the
high-pressure side of the post capillary venule and rolling
and adhesion of leukocytes on the venular endothelium.
van Bemmelen et al.35 created a model of venous
hypertension by performing arteriovenous fi stulas in Wistar
rats using microsurgical techniques. Valvular incompetence
was seen as early as one day after creation of the arteriovenous fi stula, and valvular structural changes were noticeable
within two months of production of venous hypertension.
Elongation of the cusps was observed. Separation and
leakage of the cusps were encountered along the entire valvular free border, and, in later stages beyond four months,
valve areas became diffi cult to recognize because commissures were lost and bulging of the valve sinus disappeared.
We have pursued this line of investigation and have
reproduced the human observations in the animal
36,37,38
model.
Another model of venous hypertension has been produced by Lalka. This model creates venous hypertension by
ligation of the inferior vena cava, the common iliac veins,
and the common femoral veins. This preparation elevates rat
hind limb venous pressures compared with forelimb pressures. Myeloperoxidase assay indicates leukocyte trapping
in hindleg tissues just as it occurs in humans.
The observations just mentioned suggest that valve
damage in venous insuffi ciency is an acquired phenomenon
related to leukocyte and endothelial interactions and an
infl ammatory reaction. This observation is not universally
accepted. A study on 13 valve structures from varicose GSV
showed an absence of lymphomonocyte infi ltration in 85%,
and rare isolated “nonsignifi cant” infl ammatory cells in
15%. However, if this hypothesis is correct, pharmacologic
intervention to block leukocyte adhesion, activation, and
subsequent valve damage may be a possibility.
SYMPTOMS OF PRIMARY
VENOUS INSUFFICIENCY
It is well known that the presence and severity of symptoms do not correlate with the size or severity of the varicose
veins present. Symptoms usually attributable to varicose
veins include feelings of heaviness, tiredness, aching,
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