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Chapter
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1
Anatomy
103. Hamer JD, Malone PC, Silver IA. The
PO2 in venous valve pockets: its
possible bearing on thrombogenesis.
Br J Surg 1981;68:166.
104. Saphir O, Lev M. Venous valvulitis.
Arch Pathol 1952;53:456.
105. Saphir O, Lev M. The venous valve in
the aged. Am Heart J 1952;44:843.
106. Leu HJ, Vogt M, Pfrunder H.
Morphological alterations of
nonvaricose and varicose veins. Basic
Res Cardiol 1979;74:435.
107. Travers JP, Brookes CE, Evans J, et al.
Assessment of wall structure and
composition of varicose veins in
reference to collagen, elastin, and
smooth muscle content. Eur J Vasc
Endovasc Surg 1996;11:230.
108. Varty K, Jones L, Porte KE, et al. A
quantitative study of long saphenous
vein morphology in patients
undergoing arterial surgery.
Phlebology 1995;10:90.
109. Miani A, Rubertsi U. Collecting
venules. Minerva Cardioangiol
1958;41:541.
110. Benninghoff, quoted by Moretti G. In:
Jadassho J, editor. Handbuch der haut
und geschlechtskrangheiten. Berlin:
Springer-Verlag; 1968.
111. Bargmann W. Histologie und
mikroskopische anatomie des
meerschen. Stuttgart: Georg Thieme;
1956.
112. Goldman MP, Bennett RG. Treatment
of telangiectasia: a review. J Am Acad
Dermatol 1987;17:167.
113. Bean WB. Vascular spiders and related
lesions of the skin. Springfield, Ill:
Charles C Thomas; 1958.
114. Bodian EL. Sclerotherapy. Semin
Dermatol 1987;6:238.
115. de Faria JL, Moraes IN.
Histopathology of the telangiectasias
associated with varicose veins.
Dermatologia 1963;127:321.
116. Fried SZ, Lynfield L. Unilateral facial
telangiectasia macularis eruptiva
perstans. J Am Acad Dermatol
1987;16:250.
117. Azizkhan RG, Azizkhan JC, Zetter BR,
Folkman J. Mast cell heparin
stimulates migration of capillary
endothelial cells in vitro. J Exp Med
1980;152:931.
118. Folkman J. Regulation of
angiogenesis: a new function of
heparin. Biochem Pharmacol
1985;34:905.
119. Shepherd JT. Reflex control of the
venous system. In: Bergan JJ, Yao JST,
editors. Venous problems. Chicago:
year Book; 1978.
120. Kaiser GA, Ross J Jr, Braunwald E.
Alpha and beta adrenergic receptor
mechanisms in the systemic venous
bed. J Pharmacol Exp Ther
1964;144:156.
121. Johansson B, Ljung B. Role of
myogenic propagation in vascular
smooth muscle response to vasomotor
nerve stimulation. Acta Physiol Scand
1968;73:501.
122. Speden RN. Excitation of vascular
smooth muscle. In: Bülbring E, et al,
editors. Smooth muscle. Baltimore:
Williams & Wilkins; 1970.
123. Vanhoutte PM. Venous wall and
venous disease. In: Vanhoutte PM,
editor. Return circulation and
norepinephrine: an update. Paris:
John Libbey Eurotext; 1991.
124. Maleki M, Manley JC. Venospastic
phenomena of saphenous vein bypass
grafts: possible causes for unexplained
postoperative recurrence of angina or
early or late occlusion of vein bypass
grafts. Br Heart J 1989;62:57.
125. Vanhoutte PM, Shepherd JT.
Thermosensitivity and veins. J Physiol
(Paris) 1970;63:449.
126. Vanhoutte PM, Shepherd JT. Effect of
temperature on reactivity of isolated
cutaneous veins of the dog. Am J
Physiol 1970;218:187.
127. Wood JE, Eckstein JW. A tandem
forearm plethysmography for study of
acute responses of the peripheral veins
of man: the effect of environmental
and local temperature change and the
effect of pooling blood in the
extremities. J Clin Invest 1958;
37:41.
128. Thulesius O, Gjores JE. Reactions of
venous smooth muscle in normal
men and patients with varicose veins.
Angiology 1974;25:145.
129. Mellander S. Operative studies on the
adrenergic neuro-hormonal control of
resistance and capacitance blood
vessels in the cat. Acta Physiol Scand
1960;50:5.
130. Peterson LH. Some characteristics of
certain reflexes which modify the
circulation in man. Circulation
1950;2:351.
131. Watson WE. Distensibility of the
capacity blood vessels of the human
hand during sleep. J Physiol (Lond)
1962;161:392.
24
C H A P T E R
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Adverse Sequelae and Complications
of Venous Hypertension
2
Pathogenesis
Chronic venous insufficiency, which must be semantically distinguished from venous disease or disorder, may be defined
as relative impedance of venous flow back to the heart and
responsible for clinical consequences. When this occurs in the
lower extremities, the normal reabsorption of perivascular
fluids by osmotic and pressure gradients is impaired, resulting
in accumulation of perivascular and lymphatic fluid. This
leads to edema and impaired oxygenation of surrounding
tissue (Figs 2.1 and 2.2). This disruption of the normal vascular
and lymphatic flow of the lower extremities may result in
pain, cramping (especially at night), restlessness, pigmentary changes, dermatitis, and ulceration (Fig. 2.3).
association of abnormal venous flow with various signs
and symptoms has been noted for centuries: first by Hippocrates in the fourth century BC and by Wiseman in England
in 1676.
ciency will develop in almost 50% of patients with major
varicose veins.
4
It has been estimated that chronic venous insuffi-
5,6
Several alterations of normal venous flow cause venous
hypertension. Such hypertension in the lower extremities
is usually caused by a loss or disruption of the normal oneway valvular system. This may occur because of deep vein
thrombosis (DVT), thrombophlebitis, or a dilation of veins
from other causes.
7,8
When perforating vein valvular function
becomes incompetent, there may be shunting of blood flow
from the deep to the superficial venous system through the
incompetent perforating veins, with resultant adverse
sequelae.
9–11
The superficial veins respond by dilating to
accommodate the increased blood flow, which produces
superficial valvular incompetence leading to the development of varicosities.
12
In addition, with muscular movement
in the lower limbs, the high venous pressure normally occurring within the calf is transmitted straight to the superficial
veins and subcutaneous tissues.
13,14
Venous pressure in the
cuticular venules may greatly exceed the normal 100 mmHg
in the erect position.15 This causes venular dilation over the
whole area, resulting in capillary dilation, increased permea-
16–19
bility,
and increase in the subcutaneous capillary bed.
This is manifested as telangiectasia and venectasia (Fig. 2.4).
Venous hypertension has also been demonstrated to destroy
the venous valves that are present in the subcuticular vascular system.
21
This destruction promotes persistent and
pro gressive changes in the venous drainage system of the
skin and subcutaneous tissues. The greater the degree of
venous hypertension, the greater the risk of venous ulcer
development.
22,23
Fortunately, both sclerotherapy and sur gical
treatment are capable of normalizing abnormal venous
hypertension.
Venous hypertension and subsequent insufficiency may
also derive from venous obstruction, either at lower limb level
or at iliocaval level, usually associated with reflux.
1–3
The
17,20
24
Molecular Mechanisms
The molecular mechanisms involved in leukocyte adhesion
and activation in chronic venous disease (CVD) are beginning
to be elucidated. Circulating leukocytes and vascular endothelial cells express membrane adhesion molecules. For example,
binding of L-selectin on the leukocyte surface to E-selectin on
endothelial cells may be involved in leukocyte ‘rolling’ along
the endothelial surface (Fig. 2.5A). Then, when leukocytes are
activated, they shed L-selectin into the plasma and express
molecules of the integrin family, including CD11b, which
binds firmly to intercellular adhesion molecule-1 (ICAM-1).
Integrin binding can promote firm adhesion of leukocytes, the
starting point for their degranulation
the endothelium.
Several studies have looked at markers of leukocyte and
endothelial adhesion and activation in CVD. After venous
hypertension was induced by standing for 30 minutes, levels
of L-selectin and integrin CD11b on circulating neutrophils
and monocytes in CVD patients were found to decrease,
reflecting the trapping of these cells in the microcirculation.
At the same time, plasma levels of soluble L-selectin increased,
reflecting the shedding of these molecules from leukocyte
surfaces during leukocyte–endothelial adhesion.
basal plasma levels of the adhesion molecules ICAM-1,
endothelial leukocyte adhesion molecule-1 (ELAM-1), and
vascular cell adhesion molecule-1 (VCAM-1) were higher in
CVD patients than controls and increased significantly in
response to venous hypertension provoked by standing.
Baseline levels of plasma von Willebrand factor, a marker for
endothelial cell damage, were also higher in patients with
lipodermatosclerosis than in those without skin changes.
Lactoferrin and neutrophil elastase are enzymes released from
neutrophil granules. Plasma levels of these molecules are
therefore markers of neutrophil activation, and both were
found to be higher in patients with CVD than in age- and sexmatched controls.
27
In most of these studies, prolonged standing induced
venous hypertension. However, in patients with chronic
venous insufficiency, increases in plasma levels of ICAM-1
and VCAM-1 can be induced by walking,28 presumably in
response to hydrodynamic pressure increases generated by the
musculovenous pump being transmitted to subcutaneous and
cutaneous small vessels through incompetent perforating
veins.
In addition to local factors operating in relation to venous
hypertension, CVD patients have a tendency for systemically
elevated leukocyte adhesion. Venous hypertension in the
upper limb (where the local vessels and tissues are presumably
normal) produced by means of a pressure cuff causes greater
leukocyte accumulation in patients with venous leg ulcers
than in normal subjects.
29
Evidence has been found for an
activation factor in the plasma of CVD patients.
8
and migration through
24
Similarly,
15
25
26
Plasma
Chapter
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2
Hormonal
venous dilation
Deep vein
thrombosis
Thrombo-
phlebitis
Pelvic
obstruction
Arterial
Figure 2.1 Schematic diagram showing the normal resorption of
pericapillary fluid in response to precapillary and postcapillary pressure and
interstitial pressure.
Adverse Sequelae and Complications of Venous Hypertension
Interstitial edema
↓cutaneous and subcutaneous
oxygenation and nutrition
Venous
Arteriovenous
malformation
↑pressure transmitted
to superficial veins
Development of
varicose veins
↑pressure transmitted
to cutaneous venules
↑capillary permeability
Interstitial
edema
Figure 2.2 Flowchart showing etiology of cutaneous venous hypertension.
GravityValvular incompetence
Extravasated
red blood cells
↑Fibrinogen
Subcutaneous
fat necrosis
Subcutaneous
lipodermatosclerosis
Dermatitis
Pruritus
Cutaneous ulceration
Figure 2.3 Flowchart showing etiology of cutaneous manifestations of
venous hypertension.
and/or
white blood
cell activation
26
Figure 2.4 Telangiectasia in the medial ankle/pedal area in a patient with
chronic venous insufficiency, referred to as corona phlebectasia.
A
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Macrophage
Rolling, adhesion
migration
Molecule expression
(ICAM-1, E-selectin)
B
Shear stress
Antigrowth
Low mean shear
Progrowth
Figure 2.5 A: Leukocyte-endothelial interactions on a venous valve.
ICAM-1, intercellular adhesion molecule-1.
Bergan JJ, Schmid-Schönbein GW: Ann Vasc Surg 14:427, 2000 and from Coleridge Smith PD,
Bergan JJ: Inflammation in venous disease: In Schmid-Schönbein GW, Granger N, editors,
Molecular basis for microcirculatory disorders, Paris, 2003, Springer-Verlag, pp 489–500, with
permission.)
(upper panel) and turbulent or reversing shear stress (lower panel) on vessel
walls. NO, nitric oxide; PGI
TGF-β, transforming growth factor beta; MCP-1, monocyte chemotactic
protein-1; VCAM-1, vascular cell adhesion molecule-1; ANG II, angiotensin II;
PDGF, platelet-derived growth factor.
Thromb Vasc Biol 18:677, 1998, with permission.)
B: Summary of contrasting effects of steady, laminar shear stress
Valve
sinus
Proximal wall
Venous wall
Steady laminar blood flow
Antithrombic
NO
PGI
2
IPA
Thrombomodulin
NO
TGF-β
Prothrombic
ANG II
PDGF
Endothelin-1
, prostacyclin; t-PA, tissue plasminogen activator;
2
Direction of flow
Valve
cusp
Venous valve
Distal wall
Antimigration
NO
Flow reversal
Promigration
MCP-1
VCAM-1
Atherosclerotic lesion
(Modified from Takase S,
(Modified from Traub O, Berk BC: Arterioscler
Pro-survival
Endothelium
Smooth muscle
Pro-apoptosis
Endothelium
Smooth muscle
obtained from CVD patients induced greater degrees of activation as shown by oxygen-free radical production and pseudopod formation in healthy, naive granulocytes than did plasma
taken from normal subjects. Also, there was a trend towards
more activation in more severe cases of chronic venous
insufficiency. The nature of the plasma factor responsible for
leukocyte adhesion and activation is presently unknown.
Inflammation and Skin Changes
There has also been progress in linking the chronic inflammatory state seen in CVD patients with the specific skin changes
typical of the condition. In lipodermatosclerosis, the skin capillaries become elongated and tortuous, giving the appearance
in histologic sections of elevated capillary density.
advanced skin disease especially in the ulcerative stages, the
capillaries may take on a glomerular appearance,
seems clear that substantial proliferation of the capillary
endothelium occurs. Several factors could contribute to
endothelial proliferation, but vascular endothelial growth
factor (VEGF) is an obvious candidate. VEGF is known to be
involved in inflammatory and healing processes in the skin
and has been shown to increase microvascular permeability
both acutely and chronically.
32
Plasma levels of VEGF have
been shown to increase during the venous hypertension
induced by 30 minutes of standing both in normal subjects
and in CVD patients. Both supine and standing VEGF levels
are higher in patients than in normal controls.
33
Furthermore,
plasma VEGF levels are higher in CVD patients with skin
changes than in CVD patients with normal skin.
Another feature of the skin changes associated with CVD is
dermal tissue fibrosis. Transforming growth factor-β1 (TGF-β1)
is a known fibrogenic cytokine. Detailed analysis of punch
biopsy specimens has shown that skin from the lower calf of
CVD patients had significantly elevated active TGF-β1 levels
compared with normal skin. In addition, this was true relative
to skin taken from the lower thigh region of the same patients.
Immunohistochemistry and immunogold labeling showed
the TGF-β1 to be located in leukocytes, fibroblasts, and on
collagen fibrils. Pappas el al
36
proposed that activated leuko-
cytes migrate out of the vasculature and release TGF-β1, which
stimulates increased collagen production by dermal fibroblasts. Over an extended period, such a process could contribute to the typical dermal fibrosis seen in CVD.
Altered collagen synthesis has also been reported for dermal
fibroblasts taken from apparently healthy areas of skin in
patients with varicose veins.
37
It has been possible to correlate
altered levels and distributions of growth factors, including
basic fibroblast growth factor (bFGF), transforming growth
factor-3 (TGF-3), and the receptor for epidermal growth
factor (EGF), with different types of skin change, including
venous eczema, pigmentation, lipodermatosclerosis, and
ulceration.
38
Advanced cutaneous changes of lipodermatosclerosis
appear as an erythematous, telangiectatic, edematous plaque
with mottled hyperpigmentation. Histologic examination
shows advanced stasis changes, including zones of ischemic
necrosis in the central part of fat lobules. Septal fibrosis, fat
microcysts, membranous fat necrosis, and sclerosis occur later.
This advanced clinical–histologic change is termed sclerosing
panniculitis.
39
With superficial venous insufficiency alone,
changes in the histologic appearance of capillaries are moderate. The combination of deep venous insufficiency, with or
without superficial venous insufficiency, produces more profound changes.
40,41
Venous hypertension is not a benign condition. The cutaneous chain of events following the onset of venous stasis is
thought to occur in the following temporal order: localized
edema, induration, pigmentation, dermatitis, atrophie
blanche, and, in untreated cases, eventual ulceration, infection, scarring, lymphatic obstruction and sensitization to
applied medications.
Labropoulos et al42 studied 255 limbs in 217 patients.
These had superficial venous insufficiency alone, with normal
perforating veins and deep veins. The color-flow duplex
imaging techniques were used. The researchers concluded that
aching, ankle edema and skin changes in limbs with reflux
34
30
31
and it
In
35
Inflammation and Skin Changes
27
Chapter
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2
Adverse Sequelae and Complications of Venous Hypertension
confined to the superficial venous system were associated predominantly with reflux in veins below the knee. An important
finding was that ulceration occurred only when the entire
great saphenous vein (GSV) was involved or when reflux was
extensive in both the great and small saphenous systems.
Classification of Venous Disease
An international ad hoc committee of the American Venous
Forum developed the CEAP classification for CVD in 1994.
The goal was to stratify clinical levels of venous insufficiency.
The four categories selected for classification were: clinical
state (C), etiology (E), anatomy (A), and pathophysiology (P).
The CEAP classification has been endorsed worldwide despite
its acknowledged deficiencies. It has been adopted as a standard in many clinics in Europe, Asia and South America and is
considered the only modern method for reporting data in the
United States.
The first step in evaluating a patient with CVD is to establish his or her clinical class. The patient’s clinical class will
dictate the need for further evaluation.
The CEAP classes are shown in Box 2.1. Each clinical class
is further characterized by a subscript for the presence of
symptoms (S, symptomatic) or their absence (A, asymptomatic). Symptoms include aching, pain, tightness, skin irritation, heaviness, and muscle cramps, as well as other complaints
attributable to venous dysfunction. A basic CEAP is suggested.
For the practicing physician, CEAP is an instrument for correct
diagnosis, to guide the treatment and assess the prognosis.
Venous disease is complex, but can be described. In modern
phlebologic practice, the vast majority of patients will undergo
a duplex scan of the venous system of the leg, which will
provide data on E, A and P. In basic CEAP where a duplex scan
is performed, E, A and P should be utilized. For the anatomical
classification A in basic CEAP, the simple s = superficial, p =
perforator and d = deep descriptors should be used. Multiple
descriptors should be permitted for all four components in
basic CEAP; for example a patient could be classified as C234s
Ep Asd Pr. Use of all components of CEAP is encouraged.
Definitions that apply to the CEAP classification are shown in
Box 2.2.
But the CEAP is a description of the disease, not an assessment of its severity. It serves for classification, not evaluation.
For this reason, several scores have been added to the CEAP,
such as the VCSS (venous clinical severity score).
a physician reported outcome such as the VCSS is influenced
by the ‘experimenter-expectancy effect’ and so the need for the
application of patient reported outcomes (PROs) to clinical
trials is now recognized.
Box 2.1
CEAP classes of clinical state
C0: No visible or palpable signs of venous disease.
C1: Telangiectasias or reticular veins.
C2: Varicose veins – separated from reticular veins by a diameter
of 3 mm as the upper limit of size of a reticular vein.
C3: Edema.
C4: Changes in the skin and subcutaneous tissue secondary to
chronic venous disease are divided into two subclasses to
better define the differing severity of venous disease:
C4a: Pigmentation and eczema (commonly occur and do not
C4b: Lipodermatosclerosis and atrophie blanche (commonly
C5: Healed venous ulcer is usually associated with skin changes.
C6: Active venous ulcer.
43–45
47
Revicki summarizes: ‘… the patient’s
need to predict the appearance of ulcers);
predict the development of ulcers).
46
However,
perspective and patient-reported HRQL (health related quality
of life) is the ultimate outcome for health care interventions.’48
Basically, a PRO will increase the validity of randomized controlled trials (RCTs) especially when they cannot be double or
even single blinded. The influence of the experimenter’s
opinion about the efficacy of a treatment significantly changes
the RCT results in many different fields of medicine.
49
An
additional precaution for outcome evaluation could be the use
of an external evaluation, but this would not take into account
the patient’s point of view and self-appraisal.
The patient’s opinion is a point that, albeit obvious, has
been too long neglected. Several Quality of Life questionnaires, generic (e.g. SF12
already exist and have been successfully used.
50
) and specific (e.g. CIVIQ,51 AVVQ)
52
However, they
have not take into account the only sure thing we could ever
Box 2.2
CEAP definitions
Telangiectasia: a confluence of dilated intradermal venules of
less than 1 mm in caliber. Synonyms include spider veins,
hyphen webs, and thread veins.
Reticular veins: dilated bluish intradermal veins, usually from
1 mm in diameter to less than 3 mm in diameter. They are
usually tortuous. This excludes normal visible veins in people
with transparent skin. Synonyms include blue veins,
intradermal varices, and venulectasias.
Varicose veins: subcutaneous dilated veins equal to or more
than 3 mm in diameter in the upright position. Varicose veins
are usually tortuous, but refluxing tubular veins may be
classified as varicose veins. These may involve saphenous
veins, saphenous tributaries, or nonsaphenous veins.
Synonyms include varix, varices, and varicosities.
Corona phlebectatica: fan-shaped pattern of numerous small
intradermal veins on the medial or lateral aspects of the ankle
and foot. Its significance is unclear, but commonly thought to
be an early sign of advanced venous disease. Synonyms
include malleolar flare and ankle flare.
Edema: perceptible increase in volume of fluid in the skin and
subcutaneous tissue characterized by indentation with
pressure. Venous edema usually occurs in the ankle region,
but it may extend to the leg and foot. It can be difficult to
differentiate from lymphedema which usually involves the
toes.
Pigmentation: brownish darkening of the skin initiated by
extravasated blood which usually occurs in the ankle region
but may extend to the leg and foot.
Eczema: erythematous dermatitis, which may progress to a
blistering, weeping, or scaling eruption of the skin of the leg.
It is often located near varicose veins but may be located
anywhere in the leg. Eczema is usually caused by chronic
venous disease (CVD) or by sensitization to local therapy.
Synonyms include venous dermatitis and stasis dermatitis.
Lipodermatosclerosis: localized chronic inflammation and
fibrosis of the skin and subcutaneous tissues, sometimes
associated with scarring or contracture of the Achilles
tendon. It is sometimes preceded by diffuse inflammatory
edema of the skin, which may be painful and which is often
referred to as hypodermitis. The absence of lymphangitis,
lymphadenitis and fever differentiates this condition from
erysipelas or cellulitis. Lipodermatosclerosis is a sign of severe
CVD.
Atrophie blanche or white atrophy: circumscribed, often
circular, whitish, and atrophic skin areas surrounded by
dilated capillary spots and, sometimes, hyperpigmentation.
This is a sign of severe CVD. Scars of healed ulceration are
excluded in this definition.
Venous ulcer: chronic defect of the skin most frequently around
the ankle that fails to heal spontaneously because of CVD.
28
state: if the patient is not happy with the result of the treatment,
Percent population
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it means it (you) failed. Therefore, the need to assess the patient’s
own appraisal in detail, with satisfactory sensitivity and specificity, appears of utmost importance. Guex et al addressed
this point and observed that CVD patients had one main
concern belonging to one of the following five groups:
discomfort/pain, appearance/attractiveness, risk/threat to
health, restriction of movements/activities, emotional dis-
53
tress.
They have therefore constructed a novel PRO (the
SQOR-V), specially dedicated to CVD and based on these five
patient concerns.54 Its values range from 20 to 100, 20–30
being normal, 30–50 moderate consequences of CVD and >50
being severe CVD. This questionnaire is free to use and is
available in several languages, including French, English and
Spanish.
Pittaluga et al have established a classification of venous
refluxes based on the extent of saphenous vein reflux.55 They
noted a positive correlation between age and progression of
superficial venous insufficiency.
Incidence
Varicose veins have been noted to increase in incidence with
age and have been estimated to occur in 7% to 60% of the
adult population in the United States.
occur in 8% of women aged of 20 to 29 years, increasing to
41% in the fifth decade and 72% in the seventh decade of
57,61,62
life.
A similar rate of increase in the incidence of varicose
veins occurs in men: 1% in the third decade, increasing to 24%
in the fourth decade and 43% in the seventh decade.
Basle study III found that the greatest correlation between age
and incidence of varicose veins occurred in those with varicose
veins only, rather than in those with the presence of telangiectasias (hyphenwebs) or reticular veins (Fig. 2.6).
Framingham study,
63
curiously, showed no difference in the
incidence of varicose veins with age.
Varicosities in childhood are rare, occurring almost exclusively in association with congenital vascular malformations
(see Chapter 3). When varicosities occur, they usually appear
as a subtle physical finding, such as a slight bulge over the
popliteal fossa (Fig. 2.7). One estimation on the incidence of
telangiectasias in children was performed by Oster and
Nielsen
64
in Denmark. Of 2171 Danish schoolchildren exam-
5,15,56–60
Varicose veins
57,61
The
5
The
ined, 46.2% of the girls and 35.1% of the boys had telangiectasias on the nape of the neck; 1% of these children had
pronounced telangiectasias elsewhere; that is, on the shoulders, thorax, cheeks and ears. No mention was made of the
occurrence of telangiectasias on the legs. An examination of
403 children in the former East Germany, aged 8–18 years,
disclosed a 50% incidence of ‘very discrete’ venous abnormalities of leg veins. Of the children examined, 15% had clear
symptoms (without visible varices) that could be assigned to
a prospective varicose disease. Only between the ages of 17
and 18 years could reticular varicose veins be identified. In the
403 children studied by venous Doppler, 2.3% had incompetent communicating veins and 3.2% had an incompetent
saphenofemoral junction.
65
An epidemiologic study of 419
Czechoslovakian children aged 8 to 13 years, with clinical
examination plus digital photoplethysmography, showed clinically apparent varices in 8.7% and an impairment of venous
function in 14.3% of the examined extremities.
66
The most recent and complete studies of 518 children aged
10 to 20 years, using photoplethysmography in addition to
venous Doppler, are the Bochum I, II, and III studies. This
continuing investigation initially demonstrated a 10.2% incidence of reticular varicose veins without other venous abnormalities in children who were 10 to 12 years of age.
67
When
these children were examined 4 years later, the incidence
of reticular veins was 30.3%; 2% of the children had developed varicose veins and 4% had developed incompetent
communicating veins. When they were examined another
4 years later, the frequency of saphenous refluxes and large
varices was still increasing (19.8% saphenous refluxes, 3.3%
truncal varices, 5% tributary varices, and 5.2% incompetent
perforators). The incidence of reticular veins increased to
35.5%, and the incidence of telangiectasia increased to
Incidence
30
20
10
0
30
Figure 2.6 Risk of varicosity by age. Increasing age best correlated with the
development of varicose or reticular veins. (From Widmer L: Peripheral venous
disorders: prevalence and socio-medical importance: observations in 4529 apparently
healthy persons, Basle Study III, Bern, Switzerland, 1978, Hans Huber.)
40 50 60 70
Truncal
varicose veins
Telangiectasias
or reticular veins
Telangiectasias
Age
Figure 2.7 Subtle, asymptomatic varicosity of the great saphenous vein at
the junction in the popliteal fossa of an 11-year-old girl. There is no
significant family history of varicose veins.
29
Chapter
Percent of subjects with complaints
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2
Adverse Sequelae and Complications of Venous Hypertension
12.9%.68 Therefore, venous disease can be demonstrated in a
small number of children, its progression can be documented,
and saphenous reflux is a risk factor for the development of
truncal varices.
Symptoms
Varicose veins may be symptomatic in addition to being large
and unsightly (Box 2.3). A study of 4280 town and country
inhabitants of Tübingen, Germany, found symptoms in 98%
of patients with clinically relevant venous alterations.
American health survey found that nearly 50% of those with
varicose veins were bothered by their symptoms once in a
while, and 18% noted frequent to continuous symptoms.
71
Galen
described the symptoms of varicose veins as ‘a heavy
and depressing pain’. Pain is related most likely to pressure on
the dense network of somatic nerve fibers present in the subcutaneous tissues adjacent to the affected nerve. Alternatively
(or in addition), pain may occur from the dilated vein compressing adjacent nerves or from lactic acid accumulation that
results from retrograde, circular, or slower venous blood flow
clearance. Symptoms may precede the clinical appearance of
the varicosity and are proportional to the presence of intermittent edema. At this point, discomfort usually occurs during
warm temperatures when the patient is standing for prolonged
periods.
72
These patients may respond to systemic hydroxyrutosides, which decrease inflammation of the vein wall.
Paroven – a mixture that mainly consists of mono-, di-, tri-,
and tetra-O-β-hydroxyethyl rutosides containing at least 45%
troxerutin (Zyma, United Kingdom) – 250 mg three or four
times a day has been reported to help.76 Reduction in venous
hypertension or excision of the involved segment usually
causes prompt relief of pain.
4
Almost all patients with postthrombotic obstruction complain of ‘bursting’ calf pain that is exacerbated by exercise.
Venous claudication is an appropriate term to use in this situation to emphasize the relationship of exercise to pain. Pain
during exercise may be due to nociceptor stimulation of the
distended vein wall.
78
Alternatively, exercise pain may be due
to an accumulation of tissue metabolites or an increase in
interstitial pressure. Patients with acute DVT have an increased
intramuscular pressure that is proportional to the degree of
thrombosis.
79,80
Kistner81 has found that perforator incompetence leads to
indurated skin with ulceration, whereas incompetence of the
tibial, popliteal, or femoral system produces aching and swelling in the leg. There are patients who have a significant amount
of valvular incompetence without symptoms. Clinical symptoms vary based on the effectiveness of the calf muscle pump
to compensate for venous hypertension. Young, thin, and
more athletic patients have fewer symptoms than older and
obese patients.
69
One
70
73–75
77
Varicose vein pain is described usually as a dull aching of
the legs, particularly after prolonged standing or during certain
times of the menstrual cycle (especially during menses).
small number of women also experience painful varicose veins
after sexual intercourse.
venous pressure with distension of the varicose vein contributes to heaviness and tightness of the lower legs.
83
It is proposed that the increase in
4,84
The Basel
study III found a similar range of complaints in both men and
women (Fig. 2.8) and an increased incidence of complaints
among women and older patients.
study III had complaints without evidence of peripheral vascular disease. Strandness and Thiele
5
Many patients in the Basel
4
suggest that symptoms
specifically caused by varicose veins improve with aging as the
level of activity declines.
Symptoms in varicose veins are often disproportionate to
the amount of actual pathologic change. Patients with small,
early-stage varices may complain more than those with large,
longstanding varicosities.
85–89
A survey of 350 patients who
presented for sclerotherapy treatment of veins that were less
than 1 mm in diameter noted that 53% of these patients
complained of swelling, burning, throbbing and cramping of
the legs, in addition to a ‘tired feeling’.
90
A retrospective analysis of 401 patients who sought treatment solely for telangiectasia showed 69% with various symptoms, including pain,
cramping, burning, throbbing and heaviness.
91
These symptoms are so insidious that most patients fail to realize how
good their legs can feel until after treatment of these blood
vessels by either compression sclerotherapy or by wearing
lightweight (20 mmHg) graduated compression stockings.59
Patients with nonsaphenous reflux had twice the incidence
of painful legs (43%) than did patients with saphenous
reflux (22%).
92
The increased incidence of symptomatic varicose veins in
women may have a hormonal etiology. It has been estimated
that 27.7% of women with varicose veins have premenstrual
pain in their varices.
93
Varicose veins during pregnancy appear
to be more symptomatic than those unassociated with pregnancy. In a study of 150 pregnant women with varicose veins,
125 noted pain and 26 were unable to stand for more than 1
to 2 hours because of the pain.
94
Warm weather tends to increase the severity of pain, as does
continual standing. Cooling the legs with water immersion or
compresses, or raising the legs, relieves the symptoms.
30
25
20
2102 men
434 women
82
A
Box 2.3
Symptoms of varicose vein/venous stasis disease (chronic
venous insufficiency)
• Cosmetic
• Aches and pains
• Night cramps
• Edema
• Cutaneous pigmentation
• Dermatitis
• Ulceration
• Hemorrhage
• Superficial thrombophlebitis
30
15
10
5
0
Restless
legs
Figure 2.8 Type of complaint according to sex. Except for an increase in
the complaint of ankle swelling, men with varices have complaints similar to
those of women.
socio-medical importance: observations in 4529 apparently healthy persons, Basle Study III,
Bern, Switzerland, 1978, Hans Huber.)
Leg pains Cramps Heaviness Swelling
(From Widmer L: Peripheral venous disorders: prevalence and
Box 2.4
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Differential diagnosis of leg pain
• Varicose veins
• Thrombophlebitis
• Osteoarthritis
• Rheumatoid arthritis
• Malignancy
• Osteomyelitis
• Meniscal tear
• Achilles tendonitis or tear
• Intermittent (arterial) claudication
• Venous claudication
• Spinal claudication
• Myalgia
• Peripheral neuropathy
• Lymphedema
From Browse NL, Burnand KG, Thomas ML: Diseases of the veins: pathology,
diagnosis, and treatment, London, 1988, Edward Arnold.
Box 2.5
Venous stasis disease signs
• Ankle edema
• Dilated veins and venules
• Telangiectasias
• Corona phlebectasia
• Pigmentation
• Venous dermatitis
• Atrophie blanche
• Ulceration
ulcers. A study of 2404 employees of the University of California, San Diego Medical Center, also found an adverse effect
on QOL in patients with CVD.
is more on the functional scale (what a person can do) and
does not seem to affect the well-being aspects (how a person
feels). Thus, venous disease is more than simply a cosmetic
problem to most patients.
100
The effect of venous disease
Signs
The differential diagnosis of leg pain is extensive and not
necessarily attributable to a patient’s varicosities (Box 2.4).
Symptoms derived from varicose veins can usually be distinguished from arterial symptoms. Pain associated with arterial
diseases often disappears at rest and is exacerbated with
walking. Pain associated with varicosities is dull, vague and
localized on the medial side of the legs. It is usually relieved
with walking. In addition to the dull aching, varicose veins
associated with venous hypertension may produce cramping
or painful spasms of the legs and an increase in leg fatigue
and restless legs, especially at night. Unfortunately, a patient’s
perception and reporting of pain are subjective in nature and
difficult to document. Browse et al95 advocate the use of compression hosiery as a diagnostic test to determine if the pain
is of venous origin. The authors have found that if a patient’s
symptoms are alleviated with 20 mmHg graduated compression stockings, sclerotherapy treatment also alleviates the
symptoms.
In a study that compared groups matched by age as well as
gender, it was found that subjects with venous disease were
markedly symptomatic compared with control individuals.
Symptoms specific to venous disease were found to correlate
with the presence of both small vein and large vein disease.
Vein size did not predict the presence or severity of symp-
96
toms.
A study of 1366 people in Edinburgh, Scotland, found
that women were more likely than men to report a wide range
of lower limb symptoms.
97
In men, only itching was significantly related to the presence of varicose veins. In women,
there was a significant relation between varicose veins and
heaviness or tension, aching and itching.
Using the Aberdeen varicose vein questionnaire, a prospective cohort of 137 patients was studied and the results compared with the well-accepted short form (SF-536). The two
questionnaires correlated highly. Both showed the patients
having worse health preoperatively than postoperatively. After
surgery, all domains of health were improved and reached
significance, chiefly in mental health. The conclusion of the
authors of this study was that persons with varicose veins have
a reduced quality of life (QOL) compared with the general
population and that this discrepancy is significantly improved
at 6 weeks after surgery.
98
Two recent QOL studies were conducted on people with
varicose veins. An analysis of 5688 consecutive outpatients in
Belgium, Canada, France, and Italy found that the QOL in
patients with varicose veins is associated with concomitant
venous disease, rather than the presence of varicose veins per
99
se.
Sixty-five percent of patients with varicose veins also have
concomitant venous diseases such as edema, skin changes or
Signs
In addition to the direct symptoms of varicose and telangiectatic veins, varicose veins may be a cutaneous marker for
venous insufficiency, where they occur in more than 50% of
patients (Box 2.5).
a result of valvular incompetence is the major etiologic factor
for the cutaneous manifestations of chronic venous insufficiency. In fact, when descending venography was used to
examine patients with chronic venous insufficiency, reflux
occurred in the superficial system alone in only 2% of the 644
examined limbs. Eighteen percent of the limbs had combined
deep and superficial reflux.
raphy have shown that more than 20% of patients with chronic
venous insufficiency have isolated perforator incompetence as
the only demonstrable abnormality.
group of patients has superficial venous insufficiency alone
(13–38%) or in combination with deep venous insufficiency
(28–78%).
ing the incompetent superficial venous system with ligation
and stripping the GSV to the knee with stab avulsion of distal
varices restored competency to the femoral vein. Therefore,
identification of patients with superficial venous insufficiency
is important because they may respond to sclerotherapy or
surgical treatment of the superficial venous system alone.
It has been estimated that between 17% and 50% of the
population with varicose veins have cutaneous findings.
Approximately 70% of limbs with chronic venous insufficiency have clinical findings.
between the severity of clinical signs (described later in this
chapter) and superficial venous incompetence.
patients with cutaneous abnormalities have incompetence of
perforator veins and all patients with either active or healed
venous ulcerations have evidence of perforator incompe-
114
tence.
The cutaneous manifestation appears as edema,
hyperpigmentation, dermatitis or ulceration. More than a
million Americans suffer from skin ulcers caused by abnormal
circulation that results from varicose veins, and nearly 100,000
Americans are totally disabled by this condition.
cose and telangiectatic leg veins are not merely of cosmetic
concern but represent a widespread and potentially serious
medical problem.
Edema
Ankle edema is usually the first manifestation of chronic
venous insufficiency.
101–104
Certainly, deep venous insufficiency as
104,107–112
In addition, Walsh et al
115
Ankle edema tends to be worse in
105
Studies using ascending venog-
106
However, a significant
113
found that treat-
108
There is a strong association
108
Almost all
57
Thus, vari-
2,114
31
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2
Adverse Sequelae and Complications of Venous Hypertension
32
Box 2.6
Differential diagnosis of ankle edema
• Cardiac failure
• Renal failure
• Deep vein thrombosis
• Venous obstruction from other causes
• Hypoalbuminemia
• Fluid retention syndromes
• Lymphedema
• Lipodystrophy
• Hemihypertrophy (Klippel–Trénaunay syndrome)
• Venous valvular agenesis
2
warm weather
common in persons who stand a great deal.
edema is rare,
sis present in lipodermatosclerosis. The edema usually found
is restricted to a limited area drained by capillaries that empty
directly into the varicose or incompetent perforating veins.
This area has been termed the gaiter area and refers to the
ankle and lower calf. (In the 1800s it was commonly covered
by a cloth or leather material (gaiter) to protect the ankle and
instep from the environmental elements. Such protection is
still used today by cross-country skiers.) Ankle edema caused
by venous hypertension and varicose veins must be differentiated from that caused by other conditions (Box 2.6). However,
as previously described, lymphatic edema may also be present
in patients with chronic venous leg ulcers.
The incidence of leg edema may not be related to the extent
of varicose vein disease. A statistical study of 9100 civil servants
in the German cities of Düsseldorf and Essen disclosed a statistically significant increase only in leg swelling in those with
leg veins less than 1 mm in diameter compared to in those
without such veins.
cramps, restless legs, and itching. Pain was not evaluated.
The protein-rich edema fluid stimulates fibroblastic activity,
which entangles blood vessels and lymphatics into a fibrous
119
mass.
120
seen.
polysaccharides, is probably the main reason for the lack of
nutrition of the skin.
hypertrophy of the skin and subcutaneous tissues disrupt the
flow of cutaneous nutrition. In women with venous stasis and
fat, hairless, erythrocyanoid-type ankles, the resulting decrease
in nutrition for the sizable fatty subcutaneous tissue and the
decrease in local tissue oxygenation may cause sudden and
massive fat necrosis of the subcutaneous tissue.
area may then appear erythematous, indurated, and tender to
the touch.
Guex et al have correlated ankle circumference, symptoms
and quality of life scores in 1036 patients with venous symp-
123
toms.
swelling to be secondary to chronic venous insufficiency.
Treatment of ankle edema caused by increased venous pressure, with or without lipodermatosclerosis, is directed primarily towards the prevention of trauma and alleviation of
superficial venous hypertension.
include leg elevation, systemic diuretics and localized compression bandaging.
normalize lymphatic flow over time. Thus this ‘conservative’
form of treatment is actually therapeutic as well (see Chapter
6). Recently, fibrinolytic enhancement has reportedly been
successful in improving symptoms, induration and cutaneous
thickening in patients with lipodermatosclerosis.
authors of that report used stanozolol (5 mg by mouth, twice
daily) in 14 patients with longstanding lipodermatosclerosis
resulting from venous disease. Of these 14 patients, 11 noted
and towards the end of the day.59 It is especially
85
perhaps resulting from increased dermal fibro-
118
There was no difference in muscle
59
True ‘pitting’
117
116
Histologically, a microedema around capillaries is
The edema, which contains fibrin, proteins and neutral
121,122
The resulting lymphedema and the
2,15
The affected
They demonstrated the relevance of moderate ankle
19
Temporizing treatments
19
Graduated compression bandaging can
124
The
Figure 2.9 Hyperpigmentation around dilated telangiectasias and venules
in a 70-year-old man. There had been no history of cutaneous trauma.
improvement within 3 months. Long-term follow-up was not
given, nor has this treatment been accepted elsewhere.
Pigmentation
Pigmentation (Fig. 2.9) is a sign of venous stasis disease. The
elongated, distended vascular system underlying areas of
stasis is more susceptible to trauma than are normal vessels.
Even minor blunt injuries may cause rupture of the vascular
wall with extravasation of erythrocytes into the cutis.
Histologically, cutaneous hyperpigmentation represents
increased melanin early on and extravasated erythrocytes and
hemosiderin-laden macrophages interspersed between dilated
and tortuous capillaries in later stages and in inflammatory
12,125,126
stages.
become fragmented during their passage (Fig. 2.10). Extravasation appears to be due to increased intravascular pressure and
not chemotaxis, as occurs with white blood cells.
Extravasated erythrocytes may be found in the deep dermis
around adnexal structures (Fig 2.11). When present clinically,
they are a reliable guide to the existence of microangiopathy.
A more acute ‘eruptive’ cutaneous pigmentation has also been
noted as a ‘blow-out’ of erythrocytes into the dermis as a result
of tremendous back pressure within the cutaneous microvasculature.
of lichen aureus (Fig. 2.12).
condition is correction of the underlying venous hypertension
(sclerotherapy and/or surgery), including graduated compression stockings and leg elevation. Fortunately, when venous
hypertension is treated, dark pigmentation gradually fades.
After correction of the etiology for the venous hypertension,
a Q-switched laser specific for hemosiderin can then be used
to remove or minimize the pigmentation (see Chapter 8). In
addition, a noncoherent intense pulsed light source has also
Erythrocytes appear either intact or to have
125
127
This phenomenon has been ascribed as the cause
128
The only treatment for this
12,18,119
Figure 2.10 Two deformed erythrocytes wind through an intercellular
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space (E) into the pericapillary tissue. (Osmium-cacodylate ×18,100.) (From
Wenner A et
been demonstrated to lighten pigmentation in one case
report.
al: Exp Cell Biol 48:1, 1980.)
129
Venous (stasis) dermatitis
The next dermatologic manifestation to occur in the chain of
events following venous hypertension–stasis is ‘stasis’ dermatitis. This dermatitis has been given many names, including
stasis eczema, varicose eczema, stasis syndrome, hypostatic
eczema, congestive eczema and dermatitis hypostatica. Because
there may not be a true ‘stasis’ in the lower leg with venous
insufficiency, but rather venous hypertension, this condition
is best referred to as ‘venous’ dermatitis. Venous dermatitis
occurs more frequently in women, obese people, middle-aged
men and women and those with a history of DVT and thrombophlebitis.
cutaneous venous circulation to a high pressure system with
increased vascular permeability, is the precursor of this
dermatitis.
A random sample of 476 people over the age of 65 years
in Sheffield, England, found an incidence of venous dermatitis
of 21% in men and 25% in women.
dence in a random sample of people in homes for the aged
(55–106 years old; mean age, 80 years) was 6.9%.
authors speculated that the difference was due to better nutrition in the Danish population. A similar incidence of venous
dermatitis (5.9%) was found in a randomized examination of
noninstitutionalized volunteers aged 50 to 91 years (average
age, 74 years) in Boston, Massachusetts.
survey of dermatologic patients in the Filipino population
aged 60 years and over disclosed a 12% incidence of venous
dermatitis, with 49% of all patients having varicosities.
is contrary to the popular belief (see Chapter 3) that there is
a lower incidence of venous disease in non-Western races.
The dermatitis usually begins in the medial paramalleolar
region. This region is particularly vulnerable because the vascular supply, skin nutrition and subcutaneous tissue are less
abundant here than in other areas of the lower extremity.
Venous dermatitis appears clinically as a sharply marginated,
erythematous, crusted plaque (Fig. 2.13). With time and cutaneous trauma resulting from pruritus, overlying lichenifica-
3
Edema, which causes the change from the normal
128–132
133
In Denmark, the inci-
134
135
Interestingly, a
62
The
This
136
A
B
Figure 2.11 Skin biopsy specimen taken from the medial malleolar area of
a 38-year-old man with ankle-pedal telangiectasias and venulectases with
associated hyperpigmentation. Note hemosiderin-laden macrophages
interspersed among eccrine glands in the deep dermis. (Hematoxylin–eosin;
A, ×50; B, ×200.)
tion may occur,3 as well as exudation, depending on the extent
of the inflammation and associated edema. However, an indolent venous flow may make the skin assume a much paler
color with less moisture.
a result of an increase in melanocytic postinflammatory hyperpigmentation and dermal hemosiderin (Fig. 2.14).
matitis may also be complicated by a generalized systemic
hypersensitivity or ‘ID’ reaction.
137
The color of the lesion darkens as
2,138
The der-
2
Venous dermatitis may manifest as a solitary lesion in 7%
of patients and may mimic neoplasms including squamous
cell carcinoma and basal cell carcinoma.
139
Early recognition
of the solitary venous dermatitis lesion should lead to appropriate treatment of venous hypertension, which may prevent
further morbidity.
Recently, an association of venous dermatitis with amlodipine (a long-acting calcium channel blocker used in the
treatment of hypertension, chronic stable angina and vasospastic angina) has been reported.
amlodipine use may predispose those with venous insuffi-
140
It is thought that
ciency to leg edema and venous hypertension. Therefore, it is
prudent to question patients with new onset stasis dermatitis
about medication use.
Signs
33
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