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of 13–15 mmHg. During inspiration, the volume of the veins of the thorax increases and
the pressure decreases in response to reduced intrathoracic pressure (12,13). Expiration
leads to the opposite effect, with decreased venous volume and increased pressure. The
venous response to respiration is reversed in the abdomen, where the pressure increases
during inspiration because of the descent of the diaphragm, and decreases during
expiration as the diaphragm ascends. Increased abdominal pressure during inspiration
decreases pressure gradients between peripheral veins in the lower extremities and the
abdomen, thus reducing flow in the peripheral vessels (14). During expiration, when intra-
abdominal pressure is reduced, the pressure gradient from the lower limbs to the abdomen
is increased and the flow in the peripheral veins rises correspondingly. The respiratory
effects are usually associated with clear phasic changes in venous flow in the extremities.
These can be detected by various instruments, including many forms of plethysmography
and Doppler flow detectors. The respiratory changes in venous velocity may be
exaggerated by respiratory manoeuvres, such as the Valsalva manoeuvre, which increases
intra-thoracic and abdominal pressures and decreases, abolishes, or even reverses flow in
some peripheral veins.
From the Supine to the Upright Position
When the subject moves from the supine position to the upright position, the influence
of the respiratory cycle changes and the effect on the venous blood flow patterns has
been demonstrated in the common femoral vein using duplex ultrasonography with
simultaneously recordings of the cardiac and respiratory cycles using an electro-
cardiogram (ECG) monitor and a respiratory monitor (2). The subject was placed in the
non weightbearing supine position and on a tilt table and gradually moved until fully
upright. At minus 10 degrees head down, the weight of the abdominal viscera presses on
the diaphragm and this is sufficient to counteract the descent of the diaphragm during
inspiration. In this position, the outward movement of the chest wall generates the
negative intra-thoracic pressure that is required for inspiration with little change in the
intra-abdominal pressure. The venous blood flow patterns were shown to be primarily
dependent upon the cardiac cycle but virtually independent of the respiratory cycle.
Blood leaving the legs essentially flows downhill into the passively dilating right atrium
until it is stopped by the onset of the cardiac contraction. As the subject becomes more
upright, the influence of the cardiac cycle on the venous return rapidly diminishes as the
respiratory cycle becomes more important. It has been shown in the study above that
with the subject in the non weightbearing and 30 degree head-up position on a tilt table,
the respiratory monitor indicated presence of flow in the common femoral vein during
expiration and flow ceased with normal inspiratory effort.
In the Fully Upright Position
In the upright position, the column of blood between the level of the manubrium sterni,
the point used as the zero reference for the pressure measurement, and the foot exerts a
gravitational force known as the hydrostatic pressure. The pressure in the foot vein then
becomes 15 mmHg plus the hydrostatic pressure (Fig. 1). In this position, the expiratory
promotion of venous flow is not enough to overcome the gravitational hydrostatic forces
and promote adequate venous return. The contraction of the calf muscles is required to
overcome this gravitational forces and promote venous return.
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THE RETURN OF BLOOD TO THE HEART
Blood returning from the lower extremity must flow against the forces of gravity to return
to the right atrium. The foot vein pressure in the supine position is about 100 mmHg, so
in order for blood to return from the foot, it has to reach this pressure to ensure adequate
return. Since the vascular system is a closed series of tubes, the return pressure on the
venous side is balanced by an equal hydrostatic arterial pressure supplying the limb. The
pumping force of the heart results in the blood leaving the capillary system having
a small residual pressure of 15–20 mmHg. This is sufficient to ensure venous return
whether in the supine or erect position. In the supine position, the venous return takes
place at the expense of a high venous pressure in the extremity. A highly specialised
pumping mechanism has been evolved to actively pump venous blood back to the heart
from the lower limb. It is thought that the principal participants in the pumping
mechanism are the calf veins, gastrocnemius and soleus, within the calf muscles. Failure
of this system results in symptoms ranging from varicose veins to severe ulceration of the
lower limb.
THE CALF MUSCLE PUMP
It is thought that the principal participants in the pumping mechanism are the veins of the
calf within the calf muscles, gastrocnemius and soleus. These contain as much as 250 ml
of blood (15). Additional muscle pumps are also recognized in the thigh and foot (9,16).
The latter has a much smaller capacity (about 25 ml), but assists in the return of blood from
the foot. It may have a “pump priming” effect on the calf muscle pump. The calf pump is
often referred to as the peripheral heart. Venous flow is also dependent upon the contractile
force of the heart, static filling pressure and gravity. During calf contraction, the pressure
within the deep fascia becomes raised to as much as 250 mmHg resulting in all the intra-
muscular veins becoming completely compressed (Fig. 4). Blood that was present in these
veins is emptied into the outflow tract, the first part of which is the popliteal vein. The large
veins within the gastrocnemius and soleus muscles form the main chamber of the pump
but the venae comitantes of the posterior tibial and peroneal veins and all other deep veins
participate (16). Distal deep venous valves prevent axial reflux and functional or
physiological valves in the communicating veins prevent reflux from the deep venous
system to the superficial venous system (17). With continuous exercise, the calf blood
volume is reduced by 1.5–2.0 ml/100 ml mainly as a result of the compression of the veins
in the pump chamber and the average expelled volume is approximately 100–120 ml, that
is, about 50% of all the blood within the pump. The pump will normally expel this volume
in four or five contractions though one single sustained contraction can expel as much. The
popliteal vein is a large bore vein which offers virtually no resistance to outflow. As the
gradient of 10–15 mmHg between the small veins and the heart is sufficient to ensure
venous blood flow in the supine position, the increase in gradient produced by the calf
muscle pump during contraction is more than enough to ensure an adequate rapid venous
return to the heart during vigorous erect muscle exercise.
As the calf muscles relax, valves cephalad to the muscle pump close and prevent
reflux of blood from more proximally in the axial veins. The pressure within the muscle
fascia falls to low levels. The valves in the communicating veins open and allow normal
blood flow from the superficial to the deep venous system. In addition, arterial inflow from
the lower extremity capillary beds re-primes the calf muscle pump for a subsequent
Physiology of the Veins and Lymphatics 29
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contraction. At the moment when the calf muscles relax, their contained veins are empty, at
low pressure and as yet unfilled by arterial inflow. As the veins are collapsed, they are
unaffected by hydrostatic pressure. On the other hand, the superficial veins are full and
subjected to hydrostatic pressure plus the remnant of cardiac generated pressure, the “vis a
tergo.” The pressure gradient between the two compartments becomes 100–110 mmHg
resulting in blood immediately flowing from the superficial to the deep compartment
through the many communicating veins (18). This empties the superficial compartment and
reduces its pressure (19).Therefore, the function of the calf muscle pump is vitalin ensuring
venous return from the lower limbs during exercise and the reduction of the superficial
venous pressure, thus removing the damaging effects of the hydrostatic pressure ever
present as a result of man’s upright posture.
The effectiveness of the calf muscle pump can be investigated by air
plethysmography and ambulatory venous pressure measurement technique which
measures deep venous pressure directly by placing a needle in a dorsal foot vein and
connecting it to a standard pressure transducer and a recording device during rest
and exercise.
30
40
50
60
70
80
90
100
mm. Hg. from right atrium
Soleal
Sinusoids
140
140 ml
250
100
0
30
100
60
70
90
110
20
30
20
10
0
150
100
0
100
0
Post-tibial vein
Dorsal foot vein
Popliteal vein
Upper femoral vein
REST EXERCISE
Figure 4 The physiological events during the operation of the calf muscle pump.
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LOWER LIMB VENOUS PATHOPHYSIOLOGY
In venous disease some components of the venous system become damaged, and the
well-organized physiology described above becomes less efficient. The most commonly
affected structure is the venous valve. In varicose veins the valves of the superficial veins
spontaneously become incompetent permitting reverse flow in the GSV, SSV and their
tributaries. This does not normally cause any problem since the pumping capacity of
the muscle pumps can usually compensate for incompetent superficial veins. Should
the superficial veins become very dilated then the volume of venous reflux may be
considerable resulting in ankle edema, skin changes or even leg ulceration. The valves of
the deep veins may also be damaged, most commonly as a consequence of deep vein
thrombosis. In some patients spontaneous incompetence of the deep vein valves may
occur. Veins may also become temporarily or permanently occluded by venous
thrombosis. In the major axial veins this results in considerable disturbance of normal
flow with large collateral channels of venous drainage developing. The pressure in the
lower limb remains permanently elevated and edema is a common clinical problem in
these patients.
VALVULAR REFLUX OR RETROGRADE FLOW
Venous reflux is the flow of blood in the opposite direction from physiological flow. This
reflux may be natural, physiological or pathological. The duration of the reflux flow
depends on the physiological or pathological state of the valvular apparatus. There have
been studies (20) to show that the duration of reflux in the deep venous trunks in normal
subjects was less than 0.5 sec in 95% of subjects scanned. Other studies (21,22) have also
shown that reflux is significant if the duration of the retrograde flow within the veins
exceeds 0.5 sec. Although it is not necessarily correlated to the development of varicose
disease, this minimum duration of 0.5 sec does seem to be universally recognised as
indicative of pathological reflux (23–25). Kistner proposed a classification of deep vein
reflux according to the level of descent of radiological contrast medium, during
descending venography (26). He defined four classes in increasing order of severity, with
class 1 corresponding to reflux descending to mid-thigh, class 2 corresponding to reflux
descending to the knee, class 3 corresponding to reflux descending to the mid-calf and
class 4 corresponding to reflux descending to the ankle.
There are several ways of eliciting reflux flow in the lower limb venous system, and
the most effective ones include manual compression of the calf by means of a cuff.
Compression with the cuff placed on the calf and inflated to 120 mmHg and then rapidly
deflated, thus mobilizing the blood from the superficial and deep veins, is the method that
is easy to reproduce systematically since automatic cuffs that can inflate and deflate
rapidly are available.
The accurate quantification of venous reflux in individual veins has not yet been
fully established. Several methods of quantifying venous reflux in individual veins have
been described using duplex scanning. These include measurements of valve closure time
(27), venous reflux index or the Doppler efficiency index (EId) (28), velocity at peak
reflux, and quantitative volume flow measurements by calculating the cross-sectional area
of the vessel and the time-averaged velocity.
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EDEMA
Starling Forces and How Edema Is Formed
Edema is described as a perceptible expansion of the interstitial fluid volume. While
the clinical importance of edema is usually that of its underlying cause, the accumulation
of edema fluid and elevation of tissue pressure may directly interfere with various
physiological activities.
Most of the fluid that enters the tissue space by ultrafiltration from the arterial end of
the capillary bed is absorbed back into the circulation at the venous end of that network
(Fig. 5). Ernest Starling, in 1896, described interstitial fluid formation and absorption in
terms of the pressure gradients acting across the capillary endothelium, the surface area
available for fluid transfer and the permeability of the capillary membrane to protein. The
direct and immediate causes of edema are alterations in the Starling forces that lead to an
increase in the capillary-absorption ratio and a decrease in lymphatic drainage.
In the capillary circulation the capillary endothelium is slightly permeable to plasma
proteins allowing a small amount to enter the interstitial space. In general, there is little
protein in extracellular fluid compared to blood and the colloid osmotic pressure due to the
plasma proteins (which amounts to about 25 mmHg) favors reabsorption of fluid into the
capillaries. At the arterial end of the capillary bed the capillary pressure may be as high as
50 mmHg. This would favor egress of water into the tissues, since this exceeds, the colloid
osmotic pressure. Near the venous end of the capillary, when the pressure is 15 mmHg,
the osmotic pressure is higher than the capillary pressure and fluid is reabsorbed by the
capillary. This situation is summarized by Fig. 5. It must be recognized that this diagram
is a considerable simplification of what actually happens in the capillary network but it
depicts the net consequences of many complex events.
Edema is observed in a wide variety of diseases in which one or more of the Starling
forces are modified by the disease process. In most cases, there is a complex interaction
among the factors that control transcapillary fluid exchange and interstitial volume.
A simple example of edema is the orthostatic edema that occurs in the dependent parts of
the body. In this case, gravity acts to impair venous return resulting in increased capillary
filtration rate as a result of increased capillary volume and capillary pressure. The single
affected element of the system is the capillary pressure. Any procedure that will facilitate
Starling equilibrium
Arteriolar inflow
50 mm Hg
Venular
outflow
Fluid
Fluid reabsorption
Figure 5 Diagrammatic representation of the Starling equilibrium.
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venous return, such as muscle activity or compression stockings, will alleviate the
condition. It is clear from this consideration that if capillary pressure was allowed to rise to
that of the potential hydrostatic pressure in the veins at the ankle, considerable edema
would develop. The need for an efficient pumping system which maintains a low pressure
in the superficial veins of the leg becomes obvious.
In lower limb chronic venous insufficiency, edema may occur as a result of increased
capillary pressure, secondary to an elevation in venous pressure due to venous obstruction,
or increased venous hypertension due to valvular incompetence. Other causes of clinical
edema include pregnancy, congestive heart failure, and renal or hepatic insufficiency.
Edema may also occur in inflammatory conditions of any type since these tend to increase
the amount of protein escaping into the tissues. This reduces the difference in colloid
osmotic pressure between the interstitial fluid and the capillaries favoring the development
of edema.
Plasma proteins that escape into the interstitial fluid cannot be reabsorbed by the
capillaries since there is no active mechanism to achieve this. In order to prevent a steady
rise in interstitial protein levels, these must be removed continuously. Failure to do this
would result in the development of edema as the osmotic pressure rose in the interstitial
fluids. The lymphatic system is responsible for removing plasma proteins from the
interstitial fluid. The volumetric flow in these vessels is very small in comparison to the
arterial inflow. For example, at rest the flow of blood to the lower limbs is about 1 L per
minute whereas the total flow of lymph returning via the thoracic duct is 100 mL per hour.
This small volume of fluid contains much protein (40–60 gL
K1
) and it is this which is of
great importance to the tissues. These proteins would otherwise remain trapped in the
interstitial tissues (29).
LYMPHATIC SYSTEM
In most tissues of the body a network of lymphatic “capillaries” is present. These comprise
a single layer of endothelial cells that are held together by connective tissue structures.
The junctions between lymphatic cells are not tight junctions but formed by overlapping
cells. These permit entry of interstitial fluid, including large protein molecules, into the
lumen of the lymphatic vessels. It is considered that the junctions between endothelial
cells act as flap valves preventing exit of fluid from within the vessels. The pressure within
the lymphatics is approximately 1 mmHg, similar to that of the interstitial space. The
lymphatic capillary endothelial cell contains myoendothelial fibres which contract
rhythmically allowing the vessels to pump lymph proximally toward the larger lymphatic
vessels. During pumping the overlapping endothelial cells provide a valve mechanism
which prevents lymph from returning to the interstitial space. The connective tissue fibers
anchoring the endothelial cells pull the lymphatic capillary open again after contraction,
allowing it to refill with interstitial fluid.
The small lymphatic capillaries join to form larger lymphatic vessels. These have an
inner endothelial layer and an outer muscle layer conferring contractility on these vessels.
The walls of these vessels are impermeable to protein and contract rhythmically actively
pumping lymph more proximally. The pressures with the larger lymphatic vessels reach as
much as 25 mmHg. The lymphatic vessels are also compressed by adjacent structures such
as muscle, arterial pulsation and compression by clothes. Immobilisation of a limb may
result in swelling due to loss of this extra impetus to lymphatic propulsion. The lymphatic
vessels contain many tiny bicuspid valves which ensure that lymph is pumped in the
correct direction.
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In the lower limbs the lymphatics are arranged in two distinct layers which run
separately. One set lies in the superficial tissues outside the investing fascia of the limb. The
other set lies deeply beneath the fascia draining the muscles and other deep structures (30).
At intervals along the lymphatic vessels lymph nodes are present. Lymph flows
through the lymph nodes in order to reach more proximal lymphatic vessels. These vary in
size between 0.2 mm and 20 mm in length. Collections of lymph nodes are found in the
axilla and inguinal region, the neck and in the thorax and abdomen. These structures
facilitate interaction of the immune system with the lymph. This is a further function of the
lymphatic system and is crucially important in protection of the body against infection and
tumors, functions which are provided by the complex components of the immune system.
The lymphatic vessels unite to form large vessels. Those from the lower limb enter
the posterior wall of the abdomen after leaving the inguinal lymph nodes and eventually
reach the cysterna chyli, a sac-like dilation situated in front of the bodies of the first and
second lumbar vertebrae. From here the lymph enters the thoracic duct which also receives
lymphatic flow from the left side of the thorax, left arm and left side of the head and neck.
The thoracic duct enters the venous system at the junction of the left subclavian vein and
left internal jugular vein. The right lymph duct drains lymph from the right side of the
thorax, the right side of the head and neck and the right arm. The normal total return of
lymph to the venous system is about 2–4 litres per day.
The lymph is similar in electrolyte composition to other extracellular fluids but
contains substantial amounts of protein (40–60 gL
K1
) of which albumin is the main part
(23–34 gL
K1
). The white cell count in peripheral lymph is about 5!10
8
cells per litre of
which half are lymphocytes. The lymph entering the thoracic duct contains about 1!10
10
lymphocytes per litre, emphasising the role of this system in the immune response.
The return of lymph from the peripheral tissues maintains the interstitial fluid protein level
at about 15 g L
K1
, which is usually sufficiently low to ensure that edema does not arise.
This has a low colloid osmotic pressure (about 5 mmHg) ensuring that a substantial
gradient exists between the interstitial tissues and capillary lumen favoring reabsorption
of water from the tissues.
LYMPHEDEMA
Lymphedema arises when the lymphatic system fails to drain lymphatic fluid and
interstitial fluid contains increased amounts of protein. This may arise as a congenital
deficiency when lymphatic channels are absent or ineffective. More commonly this is seen
as a secondary problem arising following trauma, such as surgery, radiation or infection.
The lymphatics may become blocked by parasitic infection such as filariasis or by
malignant disease. The distribution of the resulting lymphedema will depend upon the
anatomical location of the affected vessels.
REFERENCES
1. Evans CJ, Fowkes FG, Ruckley CV, Lee AJ. Prevalence of varicose veins and chronic venous
insufficiency in men and women in the general population: Edinburgh Vein Study. J Epidemiol
Community Health 1999; 53:149–153.
2. Moneta GL, Bedford G, Beach K, Strandness DE. Duplex ultrasound assessment of venous
diameters, peak velocities, and flow patterns. J Vasc. Surg 1988; 8:286–291.
3. Moreno AH, Katz AI, Gold LD, Reddy RV. Mechanics of distension of dog veins and other
thin walled tubular structures. Circ Res 1970; 27:1069–1080.
Smith34
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4. Ackroyd JS, Pattison M, Browse NL. A study of the mechanical properties of fresh and
preserved human femoral vein wall and valve cusps. Br J Surg 1985; 72:117.
5. Cotton LT. Varicose veins. Gross anatomy and development. Br J Surg 1961; 48:589.
6. Powell T, Lynn RB. The valves of the external iliac, femoral and upper third of the popliteal
vein. Surg Gynec Obstet 1951; 92:453.
7. Basmajian JV. Distribution of valves in femoral, external iliac and common iliac veins and
their relationship to varicose veins. Surg. Gynecol. Obstet 1952; 95:537–542.
8. Ludbrook J, Beales G. Femoral venous valves in relation to varicose veins. Lancet 1962; 1:79.
9. Gardner AMN,Fox RH. The venous pump of the human foot. Bristol Med Chir J 1983; 109:112.
10. Pegum JM, Fegan WG. Physiology of venous return from the foot. Cardiovasc Res 1967; 1:249.
11. van Bemmelen PS, Beach K, Bedford G, Strandness DE. The mechanism of venous valve
closure. Its relationship to the velocity of reverse flow. Arch Surg 1990; 125:617–619.
12. Moreno AH, Burchell AR, Vanderwonde R, Burke JH. Respiratory regulation of splanchnic
and systemic venous return. Am J Physiol 1967; 213:455.
13. Moreno AH, Katz AI, Gold LD. An integrated approach to the study of the venous system with
steps toward a detailed model of the dynamics of venous return to the right heart. IEEE Trans
Biomed Eng 1969; 16:308.
14. Duomarco JL, Rimini R. Energy and hydraulic gradients along systemic veins. Am J Physiol
1954; 178:215.
15. Ludbrook J, Louchlin J. Regulation of volume in posarteriolar vessels of the lower limb.
Am Heart J 1964; 67:493–507.
16. Gardner AMN, Fox RH. The return of blood to the heart: venous pumps in health and disease.
London: John Libbey & Co Ltd, 1989.
17. Almen T, Nylander G. Serial phlebography of the normal lower limb during muscular
contraction and relaxation. Acta Radiol Scand 1962; 57:264.
18. Bjordal R. Simultaneous pressure and flow recordings in varicose veins of the lower extremity.
Acta Chir Scand 1970; 136:309.
19. Pollack AA, Wood EH. Venous pressure in the saphenous vein at the ankle in man during
exercise and changes in posture. J Appl Physiol 1949; 1:649.
20. Van Bemmelen PS, Beach K, Bedford G, Strandness DE. The mechanism of venous valve
closure. Its relationship to the velocity of reverse flow. Arch Surg 1990; 125:617–619.
21. Neglen P, Raju D. A comparison between descending phlebography and duplex Doppler
investigation in the evaluation of reflux in chronic venous insufficiency: A challenge to
phlebography as the ‘gold standard’. J Vasc Surg 1992; 16:687–693.
22. Neglen P, Raju S. A rational approach to detection of significant reflux with duplex Doppler
scanning and air plethysmography. J Vasc Surg 1993; 17:590–595.
23. Sarin S, Scurr JH, Coleridge Smith PD. Mechanism of action of external compression on
venous function. Br J Surg 1992; 79:499–502.
24. Moulton S, Bergan JJ, Beeman S, Poppiti R. Gravitational reflux does not correlate with
clinical status of venous stasis. Phlebology 1993; 8:2–6.
25. Coleridge Smith PD. How should we investigate patients with venous disease? Phlebology
1993; 8:1.
26. Kistner RL. Transvenous repair of the incompetent femoral vein valve. Chicago: Year Book
Medical Publishers, 1978 (Bergan JJ, Yao JST, eds. Venous Problems).
27. Welch HJ, Faliakou EC, McLaughlin RL, Umphrey SE, Belkin M, O’Donnell TF. Comparison
of descending phlebography with quantitative photoplethysmography, air plethysmography,
and duplex quantitative valve closure time in assessing deep venous reflux. J Vasc Surg 1992;
16:913–920.
28. Beckwith TC, Richardson GD, Sheldon M, Clarke GH. A correlation between blood flow
volume and ultrasonic Doppler waveforms in the study of valve efficiency. Phlebology 1993;
8:12–16.
29. Pflug JJ. The lymphatic system and lymphedema. Br J Hospital Medicine 1972;270–363.
30. Pflug JJ, Calnan JS. The normal anatomy of the lymphatic system in the human leg. Br J Surg
1971; 58:925–930.
Physiology of the Veins and Lymphatics 35
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4
Epidemiology of Venous Disorders
F. G. R. Fowkes
Wolfson Unit for Prevention of Peripheral Vascular Diseases, University of Edinburgh,
Edinburgh, U.K.
Venous disorders in the legs are extremely common and can range from minor
asymptomatic incompetence of venous valves to severe chronic leg ulceration. In this
chapter on epidemiology, the frequency of varicose veins, asymptomatic venous
insufficiency, venous skin changes and chronic ulceration in the general population will
be described. Epidemiological evidence on risk factors for varicose veins and ulceration
will also be discussed.
VARICOSE VEINS: PREVALENCE AND INCIDENCE
The prevalence of varicose veins observed in selected studies (1–20) conducted during the
last 40 years is shown in Table 1. The study populations varied widely because they were
based in different countries, were often derived from selected groups in the population,
used different methods of assessment, and had slightly different age ranges. There was no
standard definition of varicose veins. Some authors included varices of all sizes (“all
varicosities”) while others only included trunk (stem) varices and excluded some of the
smallest, e.g., telangiectasia or reticular varices. Given these study differences it is not
surprising that the prevalences varied markedly, even in the same country. In Switzerland,
for example, the prevalence in females in three surveys (4,5,7) ranged from 29% to 68%.
In order to obtain a reasonable estimate of the prevalence of varicose veins in
Western populations, the data from studies based on general population samples in the
United States (6), New Zealand (8), Israel (11), Turkey (16), Scotland (17), Finland (18)
and Italy (19) are of interest. Although the definitions of disease and methods of
measurement were slightly different, Figure 1 shows that the prevalence of varicose veins
in females was remarkably consistent with around one-quarter to one-third of
women affected.
There is little doubt from the majority of epidemiological studies that a higher
prevalence of varicose veins has been observed in females than in males (Table 1).
Prevalences derived from earlier surveys in the general population between 1973 and 1981
(6,8,11), suggest that the female:male ratio was approximately 2:1. However, in two
studies, one in Switzerland (7) and one in the Rarotongan Cook Islanders (21), no sex
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