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Table10.1 MEMBERS OF THE AMERICAN VENOUS
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FORUM AD HOC COMMITTEE ON REVISION OF CEAP
CLASSIFICATION
Bo Eklof, chair
John Bergan
Peter Gloviczki
Robert Kistner
Mark Meissner, secretary
Gregory Moneta
Frank Padberg
Robert Rutherford
omas Wake eld
e two committees held four joint meetings in Hawaii,
November 2002; Cancun, Mexico, February 2003; San
Diego, August 2003; and Orlando, February2004.
e following passages summarize the results of these
deliberations, by describing the new aspects of the revised
13
CEAP.
e recommended changes, detailed next, include additions to or re nements of several de nitions used in describing CVD, re nement of the C-classes of CEAP, addition
of the descriptor n (no venous abnormality identi ed),
incorporation of the date of classi cation and level of clinical investigation, and the description of basic CEAP, introduced as a simpler alternative to the full (advanced) CEAP
classi cation.
Table10.2 THE INTERNATIONAL AD HOC COMMIT
TEE ON REVISION OF CEAP CLASSIFICATION
e AVF ad hoc committee* plus:
Claudio Allegra, It
Pier Luigi Antignani, It
Patrick Carpentier, Fr*
Philip Coleridge Smith, UK*
André Cornu- enard, 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
TERMINOLOGY AND NEW
DEFINITIONS
e CEAP classi cation deals with all forms of chronic
venous disorders. e 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. e term
“chronic venous insu 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–C6).
It was agreed to maintain the overall structure of the
CEAP classi cation, but to add more precise de nitions.
e following recommended de nitions apply to the clinical C classes inCEAP:
Telangiectasia :Acon uence of dilated intradermal
venules of less than 1mm in caliber. Synonyms
include “spider veins,” “hyphen webs,” and “thread
veins.”
Reticular veins :Dilated bluish subdermal veins
usually from 1mm in diameter to less than 3mm
in diameter. ey usually are tortuous. is
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 3mm in diameter measured in the
upright position. ese may involve saphenous
veins, saphenous tributaries, or nonsaphenous
super cial leg veins. Varicose veins usually are
tortuous, but tubular saphenous veins with
demonstrated re ux may be classi ed as varicose
veins. Synonyms include “varix,” “varices,” and
“varicosities.”
Corona phlebectatica :Afan-shaped pattern of
numerous small intradermal veins on the medial or
lateral aspects of the ankle and foot. is commonly
is thought to be an early sign of advanced venous
disease. Synonyms include “malleolar are” and
“ankle are.”
Edema :Aperceptible increase in volume of 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 andfoot.
Pigmentation :Abrownish darkening of the skin
resulting from extravasated blood, which usually
occurs in the ankle region but may extend to the leg
andfoot.
88 • BASIC CONSIDERATIONS
Eczema :An erythematous dermatitis, which may
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progress to a blistering, weeping, or scaling
eruption of the skin of the leg. It is most o en
located near varicose veins but may be located
anywhere in the leg. Eczema usually is seen in
uncontrolled CVD but may re ect sensitization to
local therapy.
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
or C5 S .
A
Symptoms include aching, pain, tightness, skin irritation,
heaviness, and muscle cramps, as well as other complaints
attributable to venous dysfunction.
Lipodermatosclerosis (LDS) :Localized chronic
in ammation and 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
di use in ammatory edema of the skin, which
may be painful and which is o en referred to as
hypodermitis . is condition must be distinguished
from lymphangitis, erysipelas, or cellulitis by their
characteristically di erent 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 finding 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
definition.
Venous ulcer :Full thickness defect of the skin most
frequently in the ankle region that fails to heal
spontaneously and is sustained byCVD.
REFINEMENT OF CCLASSES INCEAP
e essential change here is the division of classC4 into two
subgroups that re ect di erent severity of disease, and carry
a di erent prognosis in terms of risk of ulceration:
REFINEMENT OF E, A, AND P
INCEAP
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 identi ed. is n could be added to E
(E n :no venous etiology identi ed), A(A n :no venous loca-
tion identi ed), and P (P n :no venous pathophysiology iden-
ti ed). In the past, the lack of a “normal” option may have
contributed to observer variability in assigning designations.
Further de nition of the Aand P has also been a orded by
12
the new venous severity scoring system,
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. e latter is based on
imaging studies of the leg veins, for example, duplex scan,
and the degree of obstruction or re ux (P)in each major
segment (A)and forms the basis for the overallscore.
is same committee also is pursuing a prospective multicenter investigation of variability in vascular diagnostic
laboratory assessment of venous hemodynamics in patients
with CVD. e last revision of the venous reporting stan-
11
still cites changes in ambulatory venous pressure or
dards
plethysmographically measured venous return time (VRT)
as objective measures of change. e 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 signi cant improvement as a result of therapy, and will hopefully provide
improved reporting standards for de nitive diagnosis and
results of competitive treatments in patients withCVD.
DATE OF CLASSIFICATION
C0: No visible or palpable signs of venous disease
C1: Telangiectasies or reticularveins
C2: Varicose veins—distinguished from reticular
veins by a diameter of 3mm ormore
C3: Edema
C4: Changes in the skin and subcutaneous tissue
secondary to CVD (now divided into two sub-
classes to better de ne the di ering severity of
venous disease):
C4a: Pigmentation and/oreczema
C4b: Lipodermatosclerosis and/or atrophie blanche
C5: Healed venousulcer
C6: Active venousulcer
CEAP is not a static classi cation; the patient can be reclassi ed at any point in time. Classi cation starts with the
initial visit, but can be better de ned a er further investigations. A nal classi cation may not be complete until a er
surgery and histopathologic assessment. We therefore recommend that any CEAP classi cation be followed by the
date; for example, C4b,S, Ep, As,p, Pr (August 21,2003).
L E V E L O F I N V E S T I G A T I O N
A precise diagnosis is the basis for correct classi cation
of the venous problem. e diagnostic evaluation of the
CLASSIFYING VENOUS DISEASE • 89
patient with CVD can be logically organized into one or
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more of three levels of testing, depending on the severity of
the disease:
Level I : e o ce visit with history and clinical
examination, which may include use of a hand-held
Doppler
Level II : e 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,orMRV
We recommend that the level of investigation (L)should
also be added to the classi cation, for example, C2,4b,S, Ep,
As,p, Pr (2003-08-21,LII).
B A S I C C E A P
A new basic CEAP is o ered here. Use of all components
of CEAP is still encouraged, but unfortunately many physicians merely use only the C-classi cation, which is just a
modest advance beyond the previous classi cations and is
based solely on the clinical appearance. Venous disease is
complex, but can be described by use of well-de 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 de ne the
E, A, and P categories.
Nevertheless, it is recognized that the merits of using the
full (advanced) CEAP classi cation system hold primarily
for the researcher and for standardized reporting in scienti 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. is
more complex classi cation, for example, also allows any
of the eighteen named venous segments to be identi ed as
the location of venous pathology. Take a patient with pain,
varicose veins, and lipodermatosclerosis where duplex scan
con rms primary re ux of the GSV and incompetent perforators in the calf. e classi cation here would be C2,4b,S,
Ep, As,p, Pr2,3,18.
Although the detailed elaboration of venous dis-
ease 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 eld. To serve the needs of both, the
full CEAP classi cation, as modi ed earlier, is retained
as advanced CEAP, and the following simpli ed form is
o ered as basicCEAP.
In essence, Basic CEAP applies two simpli cations:(1) In basic CEAP, the single highest descriptor can
be used for clinical classi cation . For example, a patient with
varicose veins, swelling, and lipodermatosclerosis would
be C4b. e 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 classi ed using the multiple descriptors recommended,
but the complexity of applying these to the eighteen possible anatomic segments is avoided in favor of applying the
simple s , p , and d descriptors to denote the super cial, per-
forator, and deep systems. us, using basic CEAP, the same
patient cited in a previous example (painful varicosities plus
lipodermatosclerosis and duplex scan–determined re ux
involving the super cial and perforator systems) would be
classi ed as C4b,S, Ep, As,p Pr (rather than C2,4b,S, Ep,
As,p, Pr2,3,18).
REVISION OF CEAP:SUMMARY
CLINICAL CLASSIFICATION
C0:No visible or palpable signs of venous disease
C1:Telangiectasias or reticularveins
C2:Varicoseveins
C3:Edema
C4a:Pigmentation and/oreczema
C4b:Lipodermatosclerosis and/or atrophie blanche
C5:Healed venousulcer
C6:Active venousulcer
S: Symptoms including ache, pain, tightness, skin
irritation, heaviness, muscle cramps, as well
as other complaints attributable to venous
dysfunction
A:Asymptomatic
ETIOLOGIC CLASSIFICATION
Ec:Congenital
Ep:Primary
Es:Secondary (postthrombotic)
En:No venous etiology identi e d
ANATOMIC CLASSIFICATION
As:Super cialveins
Ap:Perforatorveins
Ad:Deepveins
An:No venous location identi e d
90 • BASIC CONSIDERATIONS
PATHOPHYSIOLOGIC
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CLASSIFICATION
calf perforators, and axial re ux in the femoral and popliteal veins. No signs of postthrombotic obstruction.
BasicCEAP:
Pr:Re ux
Po:Obstruction
Pr,o:Re ux and obstruction
Pn:No venous pathophysiology identi able
ADVANCEDCEAP
Same as basic, with the addition that any of eighteen named
venous segments can be utilized as locators for venous
pathology:
Super cialveins:
1. Telangiectasias/reticularveins
2. GSV aboveknee
3. GSV belowknee
4. Small saphenousvein
5. Nonsaphenousveins
Deepveins:
6. Inferior venacava
7. Common iliacvein
8. Internal iliacvein
9. External iliacvein
10. Pelvic:gonadal, broad ligament veins,other
11. Common femoralvein
12. Deep femoralvein
13. Femoralvein
14. Poplitealvein
15. Crural:anterior tibial, posterior tibial, peroneal veins
(all paired)
16. Muscular:gastrocnemial, soleal veins,other
Perforatingveins:
17. igh
•
C l as s i cation according to basic CEAP:C6,S, Ep, As,p,d,Pr
•
C l a s s i 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 CEAPAN
ONGOING PROCESS
With improvement in diagnostics and treatment there will
be continued demands to adapt the CEAP classi cation to
better serve future developments. ere are several conditions that are not included in the CEAP classi cation but
that can in uence the management of the patients:
•
Combined arterial/venous etiology
•
Postthrombotic lymphedema
•
Ankle ankylosis with atrophy of thecalf
•
Venous aneurysms
•
Venous neuropathy
•
Corona phlebectatica
•
Pelvic congestion syndrome
•
Morbid obesity
e 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 scienti c signi cance is
now under investigation, particularly in France. ere is a
need to incorporate appropriate new features without too
frequent disturbances of the stability of the classi 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 e ort will
be developed from consensus opinion, we should still strive
to achieve an evidence-based format.”
18. Calf
Example:Apatient presents with painful swelling of
the leg and varicose veins, lipodermatosclerosis, and active
ulceration. Duplex scanning on May 17, 2004, showed
axial re ux of GSV above and below the knee, incompetent
ACKNOWLEDGMENT
Part of this article was previously published in Eklof B,
Rutherford RB, Bergan JJ, etal.; for the American Venous
Forum International Ad Hoc Committee for Revision of
CLASSIFYING VENOUS DISEASE • 91
the CEAP classi cation. Revision of the CEAP classi ca-
https://t.me/med1917
tion for chronic venous disorders: Consensus statement,
JVasc Surg . 2004. 40:1248–1252.
e 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 . Bern, Switzerland : Hans Huber . 1978 .
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 . Baden, Germany : Witzstrock .
1980 . 468–470 .
3. Partsch H . “Betterable” and “nonbetterable” chronic venous insu -
ciency: Aproposal for a practice oriented classi cation , Vasa . 1980 .
9 : 165–167 .
4. Sytchev GG . Classi cation of chronic venous disorders of lower
extremities and pelvis , Int Angiol . 1985 . 4 : 203–206 .
5. Pierchalla P , Tronnier H . Diagnosis and classi cation of venous insuf-
ciency of the leg, Dtsch Med Wschr . 1985 . 110 : 1700–1702 .
6. Porter JM , Rutherford RB , Clagett GP , etal. Reporting standards in
venous disease , J Vasc Surg . 1988 . 8 : 172–181 .
7 . C o r n u - énard A , DeVincenzi G , Maraval M . Evaluation of di er-
ent systems for clinical quanti cation of varicose veins, J Derm Surg
Onc . 1991 . 17 : 345–348 .
8. Enrici EA , Caldevilla HS . Classi cation de la insu ciencia venosa
chronica. In: Enrici EA , Caldevilla HS , eds. Insu ciencia venosa
cronica de los miembros inferiores . Buenos Aires, Argentina : Editorial
Celcius . 1992. 107–114 .
9. Miranda C , Fabre M , Meyer P , Marescaux J . Evaluation of a reference anatomo-clinical classi cation of varices of the lower limbs ,
Phlebologie . 1993 . 46 : 235–239 .
10. Bergan JJ , Eklof B , Kistner RL , Moneta GL , Nicolaides AN ; and the
International Ad Hoc Committee of the American Venous Forum.
Classi cation and grading of chronic venous disease in the lower
limbs:Aconsensus statement , Vasc. Surg. 1996 . 30 : 511 .
11. Porter JM , Moneta GL ; 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 , et al. Venous severity
scoring: An adjunct to venous outcome assessment , J. Vasc . Surg .
2000 . 31 : 1307–1312 .
13. Eklöf B , Rutherford RB , Bergan JJ , etal.; for the American Venous
Forum International Ad Hoc Committee for Revision of the CEAP
classi cation. Revision of the CEAP classi cation for chronic venous
disorders:Consensus statement , J. Vasc. Surg . 2004 . 40 : 1248–1252 .
92 • BASIC CONSIDERATIONS
P A R T I I
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PRIMARY SUPERFICIAL VENOUS
INSUFFICIENCY
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11.
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RISK FACTORS, MANIFESTATIONS, AND CLINICAL
EXAMINATION OF THE PATIENT WITH PRIMARY
VENOUS INSUFFICIENCY
J o h n J . B e r g a n
nowledge of the risk factors that enter into causation of primary venous insu ciency provides an
K
risk factors, such as heredity, female gender, and aging, cannot be altered (see Table11.1). Others, such as pregnancy,
are acquired but cannot be modi ed. And there are those
with little or no in uence, such as smoking, hypercholesterolemia, vitamin intake, and leg crossing. ese and the historical and largely abandoned physical tests of the patient
with venous insu ciency are the subject of this chapter.
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 super cial system.
other inherent factors such as vein wall weakness, increased
primary valvular dysfunction or agenesis, and other genetic
factors may enhance the development of varicoseveins.
ined. Of these, 67 were families with patients with varicose
veins, and 67 were control families without familial varicose
veins. Atotal of 402 subjects were examined and the results
demonstrated a prominent role of hereditary in the development of varicose veins (p < 0.001). For the children, the
risk of developing varicose veins was 90% when both parents were a icted. When only one parent was a ected, the
risk of developing varicose veins was 25% for men and 62%
for women. e overall risk of varicose vein development is
20% when neither parent is a ected by varicosities.
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 10years.
Alimited study of y patients with varicose veins in Great
Britain disclosed a simple dominant type of inheritance.
Only 28% of patients had no family history of varicose
understanding that aids in care of the patient. Some
H E R E D I T Y
1
erefore
In an extensive study in France, 134 families were exam-
2
A familial tendency toward the development of varicose
3,4
is
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.
Of these cases, 28% were of a recessive pattern. Troisier and
Le Bayon examined 154 families with 514 descendants.
ey found that if both parents had varicose veins, 85% of
children had evidence of varicose veins, whereas 27% of the
children were a ected if neither parent had varicose veins,
and 41% of the children were a ected if one parent had
varicosities. ese authors conclude that the inheritance of
varicose disease is recessive. However, some studies have not
found a signi cant familial tendency.
A single study on unselected twins found that 75% of
twelve monozygotic pairs were concordant with regard to
varicose veins. Of 25 dizygotic, same-sexed pairs, 52% had
varicose veins.
Other studies have found more of a multifactorial inheritance. 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.
e absence of venous valves in the external iliac and
femoral veins has been shown to be a marker of varicose
veins in a limited radiographic study of twelve male volunteers, some with and some without varicose veins,
and in a venous Doppler study of y-four patients with
varicose veins.
inheritance has been reported in fourteen patients with
congenital partial or total absence of venous valves of the
13
us this genetic predisposition may be the result
leg.
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 pro ling based on cDNA microarray analysis
suggest that pathways associated with brosis and wound
5
healing may be altered in varicose veins.
upregulated varicose vein genes are a sequel to the changes
6
in the varicose vein wall rather than a primary contributing
factor to varicose pathogenesis awaits additionalstudy.
10
12
In addition, a simple dominant mode of
8,9
11
14
Whether the
7
12
95
Table11.1 RISK FACTORS FOR VARICOSE VEINS AND
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TELANGIECTASIAS
Certain
Heredity
Female Gender
Pregnancy
Aging
Conjectural
Diet
Abdominal Straining
Tight Clothing
Leg Crossing
P R E G N A N C Y
Pregnancy typically is associated with secondary valvular
incompetence. Many epidemiologic studies have found a
signi cantly increased incidence of varicose veins in women
15
who have been pregnant.
However, some epidemiologic
studies have failed to con rm this association when the
16
e ect of age is controlled.
Varices are o en rst noted
during pregnancy and are exceedingly rare before puberty.
Indeed, population studies have found that only 12% of
17
women with varicose veins have never been pregnant.
In pregnancy, hormonal factors are primarily responsible for venous dilation. As many as 70 to 80% of patients
develop varicose veins during the 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
18,19
patients develop them in the third trimester.
Varicose veins of the legs are rst apparent as early as six
weeks into gestation, a time when the uterus is not yet large
enough to signi cantly impede venous return from the leg
20
veins. Mullane
notes that symptoms of varicose veins can
be the rst sign of pregnancy and can occur even before the
rst missed menstrual period. is con rms observations
of many multiparous women and argues for a profound
in uence of progesterone on venous dilation and valvular
insu ciency.
A G I N G
e 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 di use changes, with an
increase in connective tissue in the media that become most
pronounced in the h decade and are progressive therea er. is is associated with the loss of muscle cells in the
21
media.
e nding correlated with an abnormality in the
physical property of axial tension testing in ninety-three
specimens of saphenous veins from twenty-two patients
22
harvested during coronary bypass surgery.
However, one
study of thirty-one normal veins and forty-one varicose
veins in patients and autopsy samples ranging in age from
twenty- ve to ninety-two failed to disclose an age-related
di erence.
23
e latter study concluded that varicose veins
were a predetermined disease unrelated to aging e ects.
THEORETICAL RISK FACTORS
One popular hypothesis for the development of varicose
veins is Western dietary and defecation habits, which cause
an increase in intra-abdominal pressure. Population studies
have demonstrated that a high- ber diet is evacuated within
24
an average of 35 hours.
In contrast, a low- ber diet has an
average transit time of 77 hours. An intermediate diet has a
stool transit time of 47hours.
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
25,26
defecation.
An association between prostatic hypertrophy, inguinal hernia, and varicose veins may be caused by straining
at micturition with a resultant increase in intra-abdominal
pressure.
Another mechanism for increasing distal venous pressure by proximal obstruction is the practice of wearing
girdles or tight- tting clothing. A statistically signi 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 scienti cally veri 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
statistical signi cance is eliminated. Varices may be secondary to decreased exercise and associated medical problems
speci 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. is may be exacerbated by
tall height, although this factor has not been supported by
other studies.
V A L V E R E M O D E L I N G
Our interest and focus on the venous valve dysfunction as a
fundamental cause of distal venous hypertension began with
unpublished observations using angioscopy. e angioscope
provided a direct view of the internal architecture of saphenous veins. Patients taken to surgery who demonstrated
96 • PRIMARY SUPERFICIAL VENOUS INSUFFICIENCY
preoperative re ux veri ed by duplex ultrasonography
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showed a variety of pathologic lesions in the valves themselves. e rst indication was a relative paucity of valves.
e observation of decrease in number of great saphenous
29
vein (GSV) valves was reported by Cotton in 1961.
Next,
we encountered actual valve lesions. ese observations
were an extension of those reported by Hoshino et al.,
30
who classi 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 re ux on the border of the vein. is may be
one of the earliest causes of re ux in varicose veins. Later,
thinning, elong ation, stretching, splitting, and tearing of the
valves develop. e latest stages are thickening, contraction,
and possibly even adhesion between valves. ese observa-
31
tions have been con rmed by Van Cleef etal.
Although we
have proposed that this valve damage is acquired and causes
axial re ux as well as out ow through check valves in perforating veins, others have proposed that the cause of primary
venous insu ciency is an actual reduced number of valves
32
in the saphenous system.
e angioscopic observations could be con rmed by
gross morphologic studies that, when extended to microscopic observations using monoclonal antibody labeling,
have demonstrated monocytic in ltration into damaged
33
venous valves.
Others have found leukocytic in 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 in ltration
on the cranial surfaces of the venous valve and venous wall
and that leukocytes there were greater in quantity than on
34
the caudal portion of valve lea ets and venous wall.
erefore a model of venous hypertension was developed in which microvessels in rat mesentery were examined
microscopically. Venous occlusion and subsequent venous
hypertension were produced by pipette blockade of venules
about 40m in diameter. Videomicroscopy revealed early
signs of in ammation, such as progressive leukocyte rolling,
adhesion, and subsequent migration as well as parenchymal
celldeath.
is in ammatory sequence occurred early during the
phase of venous hypertension and progressed further a er
release of the occlusion. e 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 postcapillary venule and rolling
and adhesion of leukocytes on the venular endothelium.
35
van Bemmelen etal.
created a model of venous hypertension by performing arteriovenous stulas in Wistar rats
using microsurgical techniques. Valvular incompetence was
seen as early as one day a er creation of the arteriovenous
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 di 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 model.
Another model of venous hypertension has been produced by Lalka. is model creates venous hypertension by
ligation of the inferior vena cava, the common iliac veins,
and the common femoral veins. is preparation elevates
rat hind limb venous pressures compared with forelimb
pressures. Myeloperoxidase assay indicates leukocyte trapping in hind leg tissues just as it occurs in humans.
e observations just mentioned suggest that valve
damage in venous insu ciency is an acquired phenomenon
related to leukocyte and endothelial interactions and an
in ammatory reaction. is observation is not universally
accepted. Astudy on thirteen valve structures from varicose
GSV showed an absence of lymphomonocyte in ltration in
85%, and rare isolated “nonsigni cant” in 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, burning, throbbing, itching, and cramping in the legs (see
Table11.2). ese symptoms are generally worse with prolonged sitting or standing and are improved with leg elevation or walking. Apremenstrual exacerbation of symptoms
is also common. Generally, patients nd relief with the use
of compression in the form of either support hose or an elastic bandage. Weight loss or the commencement of a regular
program of lower extremity exercise may also lead to a diminution in the severity of varicose vein symptoms. Clearly,
these symptoms are not speci c, as they may also be indicative of a variety of rheumatologic or orthopedic problems.
However, their relationship to lower extremity movement
and compression is usually helpful in establishing a venous
origin for the symptoms. Signi cant symptoms suggestive
of venous disease should prompt further evaluation for valvular insu ciency and calf muscle pump dysfunction. If a
venous etiology is suspected but all examinations are negative, repeat examination during a symptomatic period is
warranted and o en fruitful.
36,37
RISK FACTORS, MANIFESTATIONS, AND CLINIC EXAMINATION • 97
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