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22 Chapter 2/Venous Embryology and Anatomy
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FIGURE 2.9 Common variations (a. −33%, b. −15%, c. −15%, d. −13%)
in the anatomy of the confl uence of inguinal veins (saphenofemoral
junction).
FIGURE 2.10 The small saphenous vein and lateral venous system of
the calf.
FIGURE 2.11 Deep veins of the foot and calf.
posterior-medial thigh. The sural nerve courses along the
SSV in the distal calf. Superfi cial veins of the lateral leg and
thigh form the lateral venous system. The lateral venous
system is drained through multiple small tributaries into the
GSV and SSV.
Deep veins of the foot form two divisions: the plantar
and the dorsal veins. The richly anastomosing deep plantar
venous arch drains the plantar digital veins through the
plantar metatarsal veins. The deep plantar venous arch drains
into the medial and lateral plantar veins, which in turn continue in the posterior tibial veins behind the medial ankle
(see Figure 2.11).25 On the dorsum of the foot the pedal vein
drains the deep dorsal digital veins through the dorsal metatarsal veins. The pedal vein continues in the anterior tibial
veins. Pairs of the posterior and anterior tibial and peroneal
veins accompany the corresponding arteries, and all drain
into the popliteal vein (see Figures 2.11 and 2.12). Large
soleal and gastrocnemius (medial, lateral, and intergemellar)
veins drain venous sinuses of calf muscles and join the
popliteal vein. Venous sinuses are closely related to deep
veins. They are embedded in the belly of calf muscles, such
Anatomy of the Lower Extremity Veins 23
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as the soleus and gastrocnemius, and are able to dilate and
hold a large amount of blood. With the contraction of calf
muscles at walking the blood is pumped to more proximal
deep veins (calf muscle pump). The popliteal vein continues
into the femoral vein as it is passing through the adductor
FIGURE 2.12 Deep veins of the leg.
canal. The popliteal and femoral veins are frequently duplicated.26 Distally the femoral vein runs lateral to the femoral
artery; however, more proximally it runs medial to it. The
deep femoral (profunda femoris) vein joins the femoral vein
to form the common femoral vein at about 9 cm below the
inguinal ligament.27 The common femoral vein is medial to
the common femoral artery and it becomes the external iliac
vein at the level of the inguinal ligament. The GSV joins the
common femoral vein at the confl uence of the superfi cial
inguinal veins. Other tributaries of the common femoral vein
are the circumfl ex femoral veins (lateral and medial). In the
distal thigh the femoro-popliteal segment frequently communicates through a large collateral with the deep femoral
vein providing an important alternative avenue for venous
drainage in case of femoral vein occlusion. The sciatic vein,
the main trunk of the primordial deep venous system, runs
along the sciatic nerve.
There are as much as 150 perforating veins (PVs) in the
lower extremity; however, only a few of these are clinically
important. Signifi cant variation exists in the location of individual PVs; however, distribution of clusters of PVs follows
a predictable pattern. Dorsal, plantar, medial, and lateral
foot perforators are the main groups of PVs in the foot.28 A
large PV runs between the fi rst and second metatarsal bones
and connects the superfi cial dorsal venous arch to the pedal
vein.29 Clusters of PVs at the ankle are the anterior, medial,
and lateral ankle perforators (see Figure 2.13).30 The medial
calf perforators have two groups: posterior tibial and paratibial PVs. Three groups (lower, middle, upper) of posterior
tibial PVs (Cockett I–III perforators) connect the posterior
accessory GSV to the posterior tibial veins (see Figures 2.8,
2.11, and 2.13).
31,32
The paratibial perforators drain the GSV
FIGURE 2.13 Relationship of the posterior tibial perforators to the deep and superfi cial posterior compartments (SPC)
of the calf (PTVs, posterior tibial veins).
24 Chapter 2/Venous Embryology and Anatomy
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into the posterior tibial veins.
33,34
Other perforators of the leg
below the knee are the anterior, lateral, medial, and lateral
gastrocnemius; intergemellar and Achillean PVs (see Figure
2.11). Infra- and suprapatellar and popliteal fossa PVs are
located around the knee. Perforators of the femoral canal
connect tributaries of the GSV to the femoral vein (see
Figure 2.8). Inguinal perforators drain into the femoral vein
in the proximal thigh.
Valves in superfi cial veins of the lower extremity usually
are located near to the termination of major tributaries. Some
valves are well developed with marked sinusoid dilation at
their base, others are more delicate in their structure. In the
GSV there are about six valves, with more valves located
below than above the knee. A nearly constant valve of GSV
is at 2–3 cm distal to its confl uence with the femoral vein.
Valves in the SSV are closer to each other than in the GSV.
Valves in communicating branches between the SSV and
GSV are oriented to direct blood from the small to the great
saphenous vein. Similar to superfi cial veins, deep veins have
more valves in the calf than in the thigh. Tibial veins are
densely packed with valves, whereas there are only one or
two valves in the popliteal vein. In the femoral vein there
are three to fi ve valves, with one of them located just distal
to the junction of the deep femoral vein. There is usually
one valve in the common femoral vein. Major PVs have one
to three valves, all located below the level of the fascia, that
direct fl ow toward the deep veins. Small PVs are usually
valveless. PVs of the foot are without any valves or with
valves that direct fl ow toward the superfi cial veins.
References
1. Caggiati A. Fascial relationships of the long saphenous vein, Circula-
tion. 1999. 100(25): 2547–2549.
2. Caggiati A, Bergan JJ, Gloviczki P, Jantet G, Wendell-Smith CP,
Partsch H. International Interdisciplinary Consensus Committee on
Venous Anatomical Terminology. Nomenclature of the veins of the
lower limbs: An international interdisciplinary consensus statement,
Journal of Vascular Surgery. 2002. 36(2): 416–422.
3. Carlson BM. The development of the circulatory system. In: Carlson
B, ed. Patten’s Foundation of Embryology, 5e. New York: McGrawHill. 1988. 586–627.
4. Nicholson CP, Gloviczki P. Embryology and development of the vas-
cular system. In: White RA, Hollier LH, eds. Vascular Surgery. Basic
science and clinical correlations. Philadelphia: JB Lippincott. 1994.
3–20.
5. Lundell C, Kadir S. Inferior vena cava and spinal veins. In: Kadir S,
ed. Atlas of normal and variant angiographic anatomy. Philadelphia:
Saunders. 1991. 187–202.
6. Hirsch DM, Chan K. Bilateral inferior vena cava, JAMA. 1963. 18S:
729–732.
7. Lundell C, Kadir S. Superior vena cava and thoracic veins. In: Kadir
S, ed. Atlas of normal and variant angiographic anatomy. Philadelphia:
Saunders. 1991. 163–175.
8. Mozes G, Carmichael SW, Gloviczki P. Development and anatomy of
the venous system. In: Gloviczki P, Yao ST, eds. Handbook of venous
disorders. London: Arnold. 2001. 11–24.
9. Parum DV. Histochemistry and immunochemistry of vascular disease.
In: Stehbens WE, Lie JT, eds. Vascular Pathology. London: Chapman
& Hall. 1995. 313–327.
10. Patrick JG. Blood vessels. In: Sternberg SS, ed. Histology for pathologist. New York: Raven Press. 1992. 195–213.
11. Hollinshead WH. The back and limbs. In: Hollinshead WH, ed.
Anatomy for surgeons. New York: Harper & Row Publishers. 1969.
617–631, 754–758, 803–807.
12. May R. Nomenclature of the surgically most important connecting
veins. In: May R, Partsch H, Staubesand J, eds. Perforating veins.
Baltimore: Urban & Schwarzenberg. 1981. 13–18.
13. Caggiati A. Fascial relationships of the short saphenous vein. Journal
of Vascular Surgery. 2001. 34(2): 241–246.
14. Negus D. The blood vessels of lower limb: Applied anatomy. In: Negus
D, ed. Leg ulcers: A practical approach to management. 2e. London:
Butterworth-Heinemann.
15. Braverman IM. The cutaneous microcirculation: Ultrastructure and
microanatomical organization, Microcirculation. 1997. 4(3): 329–
340.
16. Scultetus AH, Villavicencio JL, Rich NM. Facts and fi ction surrounding the discovery of the venous valves [comment], Journal of Vascular
Surgery. 2001. 33(2): 435–441.
17. Caggiati A, Bergan JJ. The saphenous vein: Derivation of its name and
its relevant anatomy, Journal of Vascular Surgery. 2002. 35(1): 172–
175.
18. Caggiati A, Bertocchi P. Regarding “fact and fi ction surrounding the
discovery of the venous valves” [comment], Journal of Vascular
Surgery. 2001. 33(6): 1317.
19. Gardner E, O’Rahilly R. Vessels and lymphatic drainage of the
lower limb. In: Gardner E, O’Rahilly R, eds. Anatomy, a regional
study of human structure. 5e. Philadelphia: W.B. Saunders. 1986.
190–196.
20. Thomson H. The surgical anatomy of the superfi cial and perforating
veins of the lower limb, Annals of the Royal College of Surgeons of
England. 1979. 61(3): 198–205.
21. Daseler EH AB, Reimann AF, Beaton LE. The saphenous venous
tributaries and related structures in relation to the technique of high
ligation: Based chiefl y upon a study of 550 anatomical dissections,
Surg Gynec and Obst. 1946. 82: 53–63.
22. Browse NL Burnand K, Irvine AT, Wilson NM. Embryology and
radiographic anatomy. In: Browse NL, Burnand K, Irvine AT, Wilson
NM, ed. Diseases of the veins, 2e. London: Arnold. 1999. 23–48.
23. Kosinski C. Observations on the superfi cial venous system of the lower
extremity, J Anat. 1926. 60: 131–142.
24. Bergan JJ. Surgical Management of primary and recurrent varicose
veins. In: Gloviczki P, Yao J, ed. Handbook of venous disorders,
Guidelines of the American Venous Forum. London: Chapman & Hall
Medical. 1996. 394–415.
25. White JV, Katz ML, Cisek P, Kreithen J. Venous outfl ow of the leg:
Anatomy and physiologic mechanism of the plantar venous plexus,
Journal of Vascular Surgery. 1996. 24(5): 819–824.
26. Zbrodowski A, Gumener R, Gajisin S, Montandon D, Bednarkiewicz
M. Blood supply of subcutaneous tissue in the leg and its clinical
application, Clinical Anatomy. 1995. 8(3): 202–207.
27. Dodd H, Cockett F. Surgical anatomy of the veins of the lower limb.
In: Dodd H, Cockett F, ed. The pathology and surgery of the veins of
the lower limb. London: E. & S. Livingstone. 1956. 28–64.
28. Kuster G, Lofgren EP, Hollinshead WH. Anatomy of the veins
of the foot, Surgery, Gynecology & Obstetrics. 1968. 127(4): 817–
823.
29. Stolic E. Terminology, division and systematic anatomy of the
communicating veins of the lower limb. In: May R, Staubesand J,
eds. Perforating veins. Baltimore: Urban & Schwarzenberg. 1981.
19–34.
References 25
https://t.me/med1917
30. May R. Nomenclature of the surgically most important connecting
veins. In: May R, Staubesand J, eds. Perforating veins. Baltimore:
Urban & Schwarzenberg. 1981. 13–18.
31. Mozes G, Gloviczki P, Menawat SS, Fisher DR, Carmichael SW,
Kadar A. Surgical anatomy for endoscopic subfascial division
of perforating veins, Journal of Vascular Surgery. 1996. 24(5): 800–
808.
32. Mozes G, Gloviczki P, Kadar A, Carmichael SW. Surgical anatomy of
perforating veins. In: Gloviczki P, Bergan J, ed. Atlas of endoscopic
perforator vein surgery. London: Springer-Verlag. 1998. 17–28.
33. Boyd AM. Discussion on primary treatment of varicose veins, Proc
Royal Soc Med. 1948. 61: 633–639.
34. Sherman RS. Varicose veins: Anatomic fi ndings and an operative procedure based upon them, Ann Surg. 1944. 120: 772–232.
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CHAPTER
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3
Epidemiology of Chronic
Peripheral Venous Disease
MICHAEL H. CRIQUI, JULIE O. DENENBERG, ROBERT D. LANGER,
ROBERT M. KAPLAN, and ARNOST FRONEK
INTRODUCTION
The term chronic venous disease, or more specifi cally of
interest here, chronic peripheral venous disease (CPVD) has
been used more generally to refer to either visible and/or
functional abnormalities in the peripheral venous system.
The most widely used classifi cation of such abnormalities is
the CEAP (Clinical, Etiological, Anatomic, Pathophysiologic), which includes both anatomic (superfi cial, deep, or
perforating veins) and pathophysiologic (refl ux, obstruction,
both) categories.
The CEAP classifi cation was created by an international
committee of clinical experts, and refl ects the clinical situation in patients typically referred to a vascular specialist for
clinically signifi cant venous disease. In contrast to the clinical situation, population studies of CPVD typically have
focused on broader categories determined by visual inspection only. The three major categories of interest have been
varicose veins (VV), chronic venous insuffi ciency (CVI),
and venous ulcers. However, there has not been a standard
defi nition of these categories. VV has been defi ned both
including and excluding telangiectasias (spider veins), and
at differing levels of visible disease severity. CVI typically
has been defi ned by skin changes and/or edema in the distal
leg. Venous ulcers, both active and healed, have been defi ned
by visual inspection and subjective inference as to etiologic
origin.
Two studies have now reported results on defi ned freeliving populations with simultaneous assessment of both
visible abnormalities and functional impairment by Duplex
ultrasound.
Population Study (SDPS) determined both obstruction and
refl ux, whereas the Edinburgh study determined only the
latter. These studies have rasied some questions regarding
1
2,3
The Duplex examination for the San Diego
the validity of the assumptions based on earlier population
studies and regarding the utility of the CEAP classifi cation,
at least as applied to largely healthy population samples.
Specifi cally, the general concept that visible disease necessarily implied underlying functional disease, and vice versa,
was true in the large majority of affected limbs, but not
universally so.
Although these discrepancies occurred in a minority of
cases, they were frequent enough to lead us to separately
classify visible and functional CPVD in each limb evaluated
in the SDPS. Specifi cally, we classifi ed each limb into
four visible categories: normal, telangectasias/spider veins
(TSV), VV, and trophic changes (TCS), the latter category
being one or more of hyperpigmentation, lipodermatosclerosis, or active or healed ulcer. The presence/absence of edema
was not by itself a criterion for TCS. For functional disease,
we determined the presence of obstruction and refl ux separately for the superfi cial, perforating, and deep systems. The
presence of either refl ux or obstruction in superfi cial or deep
veins was categorized as functional disease, and because of
small numbers, abnormalities of the perforating veins were
considered as deep disease. Three functional categories were
defi ned: normal, superfi cial functional disease (SFD), and
deep functional disease (DFD). Here, the term “functional”
is essentially interchangeable with “anatomic.” Also, in this
population study obstruction was uncommon, and virtually
all legs with obstruction also had refl ux, such that SFD and
DFD essentially refer to refl ux.
In addition to separately assessing edema, we asked about
a history of superfi cial venous thrombosis (SVT) and deep
venous thrombosis (DVT), with or without pulmonary
embolism.
Table 3.1 shows the prevalence of various manifestations
of CPVD in the SDPS by age, gender, and ethnicity. Spe-
The Vein Book
27
All rights of reproduction in any form reserved.
Copyright © 2006, Elsevier Inc.
28 Chapter 3/Epidemiology of Chronic Peripheral Venous Disease
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cifi cally, prevalence rates are given for TSV, VV, TCS,
SFD, DFD, edema on physical examination, and SVT and
DVT by history.
AGE AND CVPD
Using mutually exclusive categories for both visible and
functional CVPD, we found a graded relationship with
increasing age for VV, with those aged 70–79 years having
nearly twice the prevalence of those aged 40–49 years. TSV
also increased with age, but this difference was obscured by
the mutually exclusive categories with increasing numbers
of participants with TSV also having VV or TCS at older
ages. TCS showed the most dramatic age-related increase,
with the oldest age group having more than four times the
prevalence of the youngest.3 These fi ndings for visible
disease are consistent with most previous population studies,
which generally have found a linear increase in TSV or VV
with age (reviewed in Reference 4). Earlier studies typically
defi ned CVI only by venous (assumed) ulcers, and reported
exponential increases in CVI with age, fi ndings similar to
the dramatic age increase we reported for the broader TCS
category.
For functional CVPD, SFD was more than twice as
common and DFD was 64% more common in the oldest age
group. SFD showed both a higher prevalence and a steeper
age gradient than did DFD.3 The only other population data
on functional disease were from the Edinburgh study and
were limited to refl ux, and showed similar gradients with
2
age.
Edema was strongly age-related as expected, but history
of SVT and DVT were somewhat less so, perhaps refl ecting
selective recall bias in older participants.3 Nonetheless, our
data for DVT overall are quite similar to the lifetime prevalence in a large population-based study.
5
GENDER AND CPVD
For visible disease, we found nearly twice as much VV
in women as in men, but TCS were 50% more common in
men.3 These fi ndings for VV are consistent with earlier
studies, but earlier studies also have suggested a small excess
of CVI in women, in contrast to our fi ndings for the broader
category of TCS. However, more concordant with our fi ndings, the Edinburgh study reported that CVI was twice as
common in men as women. For functional CPVD, only the
Edinburgh study has comparable data, and only for refl ux,
and found a gender ratio for functional disease similar to the
SDPS.
Edema was about 50% more common in men than
women, consistent with a 50% greater history of DVT in
3
The Edinburgh group reported more edema in women,
men.
but a discordance with CVI being more common in men.2
In contrast, in our study a history of SVT was more than
twice as common in women, which has been linked to hormonal factors and pregnancy.
6,7
ETHNICITY AND CPVD
The SDPS reported data for four ethnicities, nonHispanic White, Hispanic, African-American, and Asian.
Non-Hispanic Whites showed the highest prevalence of
CPVD, with only 14.3% with a normal examination. NonHispanic Whites had the highest rates of TSV, TCS, and
DFD, and the second highest rates (after Hispanics) of VV
and SFD. African-Americans and Asians had a somewhat
lower prevalence of CPVD. Consistent with the visible and
functional fi ndings, Non-Hispanic Whites also had the
highest rates of edema and DVT by history, and Hispanics
the highest rate of SVT by history.
3
Several previous studies have suggested a higher prevalence in developed than developing countries, although
these studies are not entirely consistent (reviewed in Reference 4). The SDPS is the fi rst population study to evaluate
multiple ethnic groups who were residents of the same geographical area.
CONCORDANCE OF VISIBLE
AND FUNCTIONAL DISEASE
Figure 3.1 shows the concordance of visible and functional disease in the individual 4422 legs of the 2211 participants for this analysis. The majority of legs showed TSV,
but the majority of legs were also functionally normal. If we
consider TSV as a “normal” visible fi nding, visible disease
would be defi ned as VV or TCS, and functional disease as
SFD or DFD. The concordance between visible and functional disease was 92%, 17.4% concordant for disease presence and 74.6% concordant for disease absence. Discordance
was thus 8%, 4.9% of the legs with visible but not functional
disease, and 3.1% with functional but not visible disease.
Surprisingly, 21% of all legs with VV were normal functionally (3.7%/17.7%), as were 26% of all legs with TCS
(1.2%/4.6%). Thus, although the concordance was strong,
visible disease did not invariably mark underlying functional disease, and functional disease was sometimes present
in the absence of any visible venous disease.
3
CONCORDANCE OF CPVD
WITH EDEMA, SVT, AND DVT
Table 3.2 shows edema on examination and SVT and
DVT by history, cross-classifi ed by visible and functional
disease. Signifi cant differences from the normal/normal
Concordance of CPVD with Edema, SVT, and DVT 29
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TABLE 3.1 Visible and Functional Chronic Venous Disease, Edema, and Thrombotic Events by Strata of Sex, Age, and Ethnicity,
San Diego, California, 1994–1998
Edema and
Visible disease, % Functional disease, % thrombotic events, %
Study group N % NL TSV VV TCS NL SFD DFD Edema STE DTE
All subjects 2211 100 19.0 51.6 23.3 6.2 72.1 19.0 9.0 5.8 2.4 3.2
Men 780 35.3 33.6 43.6 15.0 7.8 75.6 13.1 11.3 7.4 1.5 4.0
Women 1431 64.7 11.0 55.9 27.7 5.3 70.1 22.2 7.8 4.9 2.8 2.7
Age, yrs <50 534 24.2 33.0 47.9 16.9 2.3 81.8 11.2 6.9 2.6 2.1 2.4
50–59 608 27.5 22.5 52.8 20.7 4.0 78.0 14.5 7.6 4.1 2.5 2.5
60–69 557 25.2 12.4 52.8 26.0 8.8 66.1 23.5 10.4 6.1 2.2 3.8
70+ 512 23.2 7.4 52.5 29.9 10.2 61.3 27.3 11.3 10.7 2.7 4.1
Ethnicity NHW 1282 58.0 14.3 54.8 24.0 6.9 69.7 20.0 10.3 7.8 2.6 4.4
Hispanic 338 15.3 18.9 50.0 26.3 4.7 71.0 22.8 6.2 1.8 3.6 1.5
Afr. Am. 318 14.4 27.7 45.3 20.8 6.3 76.7 16.4 6.9 4.1 0.9 1.9
Asian 273 12.4 31.1 45.4 18.7 4.8 78.8 12.5 8.8 3.3 1.5 1.1
Abbreviations: NL = normal, TSV = telangiectasias and spider veins, VV = varicose veins, TCS = trophic changes, SFD = superfi cial functional disease,
DFD = deep functional disease, NHW = Non-Hispanic White, Afr. Am. = African-American, STE = superfi cial thrombotic event, DTE = deep thrombotic
event.
NL
SFD
DFD
0
20
10
60
50
40
30
Percent
TCS
Visible disease
52.5
1. 0
2.4
1. 2
3.7
VV
TSV
NL
11. 9
22.1
NL
2.1
1. 7
0.5
0.8
0.1
DFD
SFD
Functional disease
FIGURE 3.1 Visible and functional chronic venous disease in 4422 legs
of 2211 persons, San Diego, California, 1994–1998.
reference group are noted. Edema was closely associated
with TCS. For limbs with TSV or VV, the presence of SFD
or DFD greatly increased the probability of edema, as did
DFD in legs visibly normal. Of legs with edema, 26% were
normal functionally and had either normal or TSV visible
fi ndings, providing an estimate of the minimum number of
legs on a population basis with edema of nonvenous etiology.
A history of SVT was not related to visible disease in legs
with normal function, but was increased similarly by both
SFD and DFD. This fi nding is consistent with the large proportion of DFD legs that also had SFD (48%). DVT was
TABLE 3.2 Prevalence of Edema, History of Superfi cial
Thrombotic Events and History of Deep Thrombotic Events
by Visible and Functional Disease, San Diego, California,
1994–1998
NL SFD DFD
Edema
NL 1.7* 0.6 6.6
TSV 1.8 14.9+ 10.5+
VV 3.9 7.4+ 15.6+
TCS 40.8+ 30.0+ 48.2+
Superfi cial Events
NL 0.6* 0.0 5.3+
TSV 0.4 10.0+ 0.0
VV 1.2 4.1+ 1.2
TCS 0.2 4.9+ 11.3+
Deep Events
NL 1.3* 0.0 5.4
TSV 1.7 0.0 5.4+
VV 3.0 2.4 6.6+
TCS 7.7+ 7.6+ 26.6+
Abbreviations: NL = normal, TSV = telangiectasias and spider veins,
VV = varicose veins, TCS = trophic changes, SFD =
superfi cial functional disease, DFD = deep functional
disease.
* = reference group.
+ = p < 0.005.
related to both TCS and DFD, but not to VV or SFD. By far
the highest pre valence of reported DVT, 25%, was in legs
with both TCS and DFD. Thus although edema, SVT, and
DVT were much more common in the presence of visible
and/or functional disease, they also sometimes occurred in
normal legs.
3
30 Chapter 3/Epidemiology of Chronic Peripheral Venous Disease
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TABLE 3.3 Signifi cant Odds Ratios in Multiple Logistic Regression Models for Visible and Functional Venous Disease, San
Diego, California, 1994–1998
Visible disease Functional disease
TSV VV TCS SFD DFD
Covariate M* W* M W M W M W M W
Age (10 years) 2.3 1.2 2.5 1.5 2.3 4.5 1.8 1.6 1.4 1.2
African-American/Asian 0.3 0.4 0.2 0.4 0.2 — — — — 0.5
Family History 1.8 3.0 4.2 5.8 2.9 12.0 3.5 2.1 2.6 2.0
Ankle Motility 1.3 1.2 — 1.4 — 1.4 0.8 1.3 — 0.9
Lower Limb Injury — — — — — — — — — 1.6
CVD-Related Factors 0.1 0.3 0.1 — — — 0.5 0.6 0.8 0.8
Walking/Standing — — 1.2 1.2 1.2 1.3 1.2 1.1 — —
Wt/Ht/BMI/Waist — — — 1.4 1.3 2.0 — 1.2 1.1 —
Exercise 0.3 — — — 0.8 — 0.2 — — —
Parity/HRT Duration Yrs — 1.1 — 1.2 — 1.3 — 1.2 — 1.2
*M = Men; w = Women; TSV = telangiectasias and spider veins; VV = varicose veins; TCS = trophic changes; SFD = superfi cial functional disease;
DFD = deep functional disease.
RISK FACTORS FOR CPVD
We have completed an extensive analysis of risk
factors for visible and functional CPVD.8 Table 3.3 summarizes this work and shows odds ratios for signifi cant
predictors of visible and functional venous disease in our
population.
Age was positively consistently related to all levels of
visible and functional disease in both sexes. In comparison
with non Hispanic whites (NHW), African-American Asian
had less TSV and VV in both sexes, less TCS in men, and
less DFD in women. Our results thus confi rm that older age
and NHW ethnicity are risk factors for CPVD.
Family history of venous disease based on subject recall
was a risk factor for all levels of visible and functional
disease. Although this fi nding could be biased, it is consistent with many other studies,
Ankle motility was a risk factor for visible disease
SFD in women and for TSV in men. It was protective for
women with DFD and men with SFD. The association of
increasing laxity in connective tissue with venous disease
corroborated previous research (reviewed in Reference 8).
The protective associations could refl ect increased ankle
motility leading to decreased venous pressure by increasing
pumping action.
Lower limb injury was a risk factor in women for DFD.
Coughlin et al., in a case-control study, found serious lower
limb trauma to be a risk factor for CVI.
CVD-related factors, such as angina, PTCA, hypertension, and diastolic pressure were associated with less
TSV, SFD, and DFD for men and women and less VV for
men. Although some studies have found a relationship
between atherosclerosis and venous disease (reviewed
in Reference 8), others have not.9 The reason for any protective effect of cardiovascular disease and hypertension
on CPVD is not readily apparent, although venous vaso-
9,10
although not all.
11
11
constriction and microthrombosis could conceivably be
involved.
Hours spent walking or standing was positively associ-
ated with VV, TCS, and SFD in men and women. Fowkes
12
et al.
found that walking was a risk factor for women with
venous insuffi ciency when age-adjusted, but less so when
multiply adjusted. They found walking to be related to lessened risk of venous insuffi ciency in men.12 Our data indicate
that standing was a strong risk factor for venous disease in
women. This is concordant with a number of studies,
contrasts with some other studies.
12
9,10
and
Weight, height, waist, and BMI, defi ned as weight in kg
divided by height squared in meters squared, were positively
asso ciated with TCS, and DFD in men and VV, TCS, and
SFD in women. Weight, waist circumference, the waist/hip
ratio, and body mass index are all measures of adiposity.
A number of studies have found an association of obesity with
venous disease. Gourgou et al.10 found a relationship in both
men and women with VV. Our fi nding of increased waist
circumference in men with TCS was consistent with fi ndings
that both obesity and male gender were associated with CVI
and with the fi nding that weight was an independent risk
factor for CVI in multivariate analysis (reviewed in Reference 8). In contrast, Coughlin et al. and Fowkes et al. both
found that obesity was not a factor in venous insuf fi ciency
11,12
among women.
Fowkes et al. extended this fi nding to men
as well.12 Other studies also have found no association
between obesity and venous disease.9 However, the Edinburgh group also found that for men and women combined,
persons with greater severity of varices (i.e., more segments
with refl ux) had higher body mass indices than those with
fewer segments involved. Additionally, Fowkes et al. found
that varicosities in the superfi cial system, but not in the deep
system, were related to body mass index in women.
12
Exercise was associated with lower rates of TSV, TCS,
and SFD in men. This is concordant with the fi nding of
Symptoms and CPVD 31
https://t.me/med1917
Gourgou et al. that physical activity is related to less VV.10
During exercise the venomuscular pump is activated, which
leads to a transient decrease in venous pressure, which
should be protective for venous disease. This is consistent
with our results in men.
HRT duration or parity was positively associated with all
levels of visible and functional disease in women. Gourgou
et al. found increasing VV prevalence with increasing
numbers of births.10 Coughlin et al. found that multiparity
was associated with varicose veins in pregnant women.11
Some studies have found that the changes are effected with
only one pregnancy.9 The increase of CPVD with HRT duration may indicate yet another underexamined systemic effect
of HRT.
Our data indicate that age and family history were the
strongest risk factors for CPVD, and neither is subject to
intervention. Other signifi cant fi ndings on inherent factors
included associations with connective tissue laxity and
height. CVD-related factors were associated with lower
rates of venous disease. Among volitional factors important
fi ndings were a relationship of CPVD with central adiposity,
positional factors such as hours spent standing or sitting,
exercise, and selected hormonal factors in women. In con-
trast with prior studies, we found no relationship with dietary
fi ber intake. In women but not men we confi rmed the importance of a previous lower limb injury for DFD.
SYMPTOMS AND CPVD
The SDPS reported data for ever having any of seven
symptoms of venous disease: aching, cramping, tired legs,
swelling, heaviness, restless legs, and itching.13 Aching legs
was the most commonly reported venous symptom, with an
overall prevalence of 17.7%. Cramping was present in 14.3%
of legs, tired legs in 12.8%, and swelling in 12.2%. Heaviness
and restless legs had similar prevalence at 7.5 and 7.4%.
Itching was the least commonly reported symptom, affecting
5.4% of legs. With the exception of restless legs, all these
symptoms increased in prevalence with increasing severity
of venous functional disease (see Figure 3.2). The rate was
lowest in normal legs, increased in legs with SFD, and highest
in legs with DFD. These differences were statistically signifi cant (p < 0.01) for all symptoms except for restless legs
(p = 0.56). Although each symptom was more common in
women than men, trends were similar in both sexes.
40
35
30
25
20
% Prevalence
15
10
5
0
Achin
MEN
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g
Itching
iness
v
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S
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SYMPTOM
g
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A
FIGURE 3.2 Symptoms by functional disease status, San Diego, California, 1994–1998.
t
I
ching
Heavines
WOMEN
s
Tire
Normal
SFD
DFD
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