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Chapter
https://t.me/med1917
3
Pathophysiology of Varicose Veins
Accordingly, dilation of varicose veins, at times only in certain
areas of the vein, must be caused by a vein wall defect – not
merely by the presence of high venous pressure. A generalized
increase in venous distensibility was found in superficial
forearm and hand veins in patients with a saphenous varicosity as compared with patients without varicosities.
285,286
Abnormal distensibility curves were found to be similar
regardless of the age and sex of the patient. This may be related
to a reported decrease in collagen content in the saphenous
veins of patients with varicosities, which occurs even in vein
segments that are not varicose.
22,32
The decrease in venous
distensibility may also be related to a constitutional decrease
in venous α-adrenergic receptor responsiveness in patients
with varicosities. Patients with varicose veins require significantly higher doses of norepinephrine for vasoconstriction
than do control subjects. This finding applies to both varicose
and normal veins in the same individual.
287
The neural regulatory network in the saphenous vein also consists of acetylcholinergic and peptidergic neurons, as well as both circulating
and endothelium-derived vasoactive substances.
288
Thus,
neural and hormonal factors are important regulators of
venous distensibility.
The decreased collagen content in varicose vein walls has
been related physically to its viscoelastic properties, with varicose veins breaking at lower pressures than normal veins.
289
This may occur in certain patients from a genetic defect affecting the biosynthesis of certain collagen types. One example is
type 4 Ehlers-Danlos syndrome (vascular type), in which
patients have a deficiency in collagen 3, normally present in
the skin, arteries and gut. These patients also frequently have
varicose veins.
surgery also have an increased incidence of varicose veins suggesting that ligamentous laxity may be a risk factor.
290
In addition, patients with previous hernia
135
However,
this theory does not explain why correction of proximal valvular dysfunction with a tourniquet can correct abnormal
venous pressures distally if, indeed, it is the vein wall that is
abnormally distensible.
291
Generalized dystrophic changes in the vein wall were confirmed histologically through biopsy of normal dorsal foot
veins in 97.3% of patients with varicose veins.
zation of venous wall changes from superficial to deep veins
was also demonstrated.
22
The authors speculate that this
292
The generali-
generalized trend may allow improvement of sclerotherapy
techniques by choosing a stronger sclerosing agent when a
peripheral venous biopsy demonstrates severe dystrophy (see
Chapter 9).
Another interesting relationship is the recently described
association of varicose veins with the ABO blood group
system. Numerous studies have demonstrated a relationship
between blood groups of the ABO system and DVT of the
lower limbs.
293–296
These studies indicate an increased incidence of DVT in patients with blood type O, particularly when
associated with pregnancy or the use of oral contraceptive
296
agents.
of thromboembolism in people with blood group A.
However, one study found an increased incidence
297
A
study of 569 French men and women showed the risk of varicose veins in patients with type A blood to be double that of
patients with all other blood groups.
298
Varicose veins were
defined as the presence, in the standing position, of a permanent dilation of at least one leg vein with a diameter of 3 mm
or more with reflux. The risk of varicose veins persisted after
adjustment for age, sex, paternal or maternal history and a
personal history of DVT. No association was found between
Rhesus factor and varicose veins. Therefore, a patient’s blood
group may be taken into account when assessing the need for
Table 3.3 Development of varicose veins (percentage of study
population)
Age (Years)
Telangiectasia 0 3.7 12.9 50.4
Reticular 10.2 30.3 35.3 74.3
Perforating 0 4.1 5.2 25.7
Tributary varicose 0 0.8 5.0 17.7
Truncal varicose 0 1.7 3.3 12.5
Junctional reflux 0 12.3 19.8 26.5
Adapted from: Schultz-Ehrenberg U, Reich-Schupke S, Robak-Pawelczyk B et al:
Prospective epidemiological study on the beginning of varicose veins (Bochum
Study I-IV). Phlebologie 2009; 38:17–25.
10–12 14–16 18–20 29–31
prophylactic treatment of varicose veins or assessing the risk
of postoperative venous thrombosis.
Recent studies on varicose and normal veins using gene
expression profiling based on cDNA microarray analysis
suggest that pathways associated with fibrosis and wound
healing may be altered in varicose veins.
299
Whether the upregulated varicose vein genes are a sequel to the changes in the
varicose vein wall rather than a primary contributing factor to
varicose pathogenesis awaits additional study.
Aging
The incidence of varicose veins increases with age (Table 3.3);
therefore, vein wall damage should also be more pronounced
in the veins of older patients. Superficial venous reflux also
sed a marked increase with age.
popliteal vein in 127 persons demonstrated diffuse changes,
with an increase in connective tissue in the media, which
became most pronounced in the fifth decade and are progressed thereafter. This is associated with the loss of muscle
cells in the media.
302
The finding correlated with an abnormality in the physical property of axial tension testing in 93 specimens of saphenous veins from 22 patients harvested during
coronary bypass surgery.
303
veins and 41 varicose veins in patients and autopsy samples
ranging in age from 25 to 92 years failed to disclose an agerelated difference.
304
The latter study concluded that varicose
veins were a predetermined disease unrelated to aging effects.
In conclusion, both the influence of genetic and environmental factors in the development of varicose veins has been
clearly demonstrated. Although the FOXC2 gene is likely to
be involved, the heredity of varicose veins appears to be
multigenic. Identification of the different components is
crucial for the understanding of the pathogenesis of the
disease. However, environmental factors also play a crucial
role; as they are strongly associated with the lifestyle of industrialized countries, an improvement of their understanding
can lead to a better primary prevention of the disease. Finally,
progression of varicose veins is far from being fully understood, although therapeutic interventions targeted at secondary or tertiary prevention are widely advocated to patients all
over the world. Follow-up studies exploring the natural history
of varicose veins will be of great benefit and importance.
62,301
An autopsy study of the
However, one study of 31 normal
300
64
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C H A P T E R
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Pathophysiology of Telangiectasias
4
The term telangiectasia was first coined in 1807 by Von Graf
to describe a superficial vessel of the skin visible to the human
1
eye.
These vessels measure 0.1 to 1 mm in diameter and
represent an expanded venule, capillary or arteriole. Telangiectasias that originate from arterioles on the arterial side
of a capillary loop tend to be small and bright red and do not
protrude above the skin surface. Telangiectasias that originate
from venules on the venous side of a capillary loop are blue,
wider, and often protrude above the skin surface. Sometimes,
telangiectasias, especially those arising at the capillary loop,
are red at first but with time become blue, probably due
to increasing hydrostatic pressure and backflow from
deep veins.
2,3
Classification
Redisch and Pelzer4 classified telangiectasias into four types
based upon clinical appearance (Fig. 4.1):
1. Sinus or simple (linear)
2. Arborizing
3. Spider or star
4. Punctiform (papular).
Papular telangiectasias are frequently present in patients
with collagen vascular disease. Spider telangiectasias are red
and arise from a central filling vessel of arteriolar origin. Red
linear telangiectasias occur on the face (especially the nose)
or legs. Blue linear or anastomosing telangiectasias are found
most often on the legs.
Raymond-Martimbeau and Dupuis
classification based on the relationship between telangiectasias and superficial as well as deep veins. Using duplex ultrasound, they evaluated 525 consecutive patients with 884
zones of telangiectasia without underlying saphenous or perforator vein incompetence. They found that 8.8% of the telangiectasias joined the deep venous system, 12.6% joined the
superficial venous system, 71.2% were directly connected to
reticular veins and 7.4% had no obvious connection. This is
in contradistinction to the reports of very high incidence of
arterial venous anastomoses for leg telangiectasias.
The actual etiology of telangiectasias may be identical to
that of varicose veins.
Martimbeau and Dupuis suggest that valvular damage occurs
with subsequent venous hypertension that is transmitted to
epidermal vessels, which then elongate and dilate. Our
research has implicated a leukocyte–endothelial interaction
that relates intercellular adhesion molecule-1 and monocytes
to adherence and migration of cells.
damage is produced by monocytes in the interstitial tissue.
Thus, pharmacologic treatment of telangiectasias may be possible in the future.
This Chapter discusses the pathophysiology and anatomy
of telangiectasias occurring on the lower extremities.
6
However, the findings of Raymond-
3
have proposed another
5
7
Valve and vein wall
Patterns
Two common patterns of telangiectasias on the legs of women,
besides red or blue streaks, are the parallel linear pattern,
usually found on the medial thigh (Fig. 4.2), and the arborizing or radiating cartwheel pattern, seen most often on the
lateral thigh (Fig. 4.3).
seem to run in families and may form anastomosing complexes as large as 15 cm in diameter. The arborizing type on
the lateral thigh usually appears with ‘feeding’ reticular veins
(see Fig. 1.11). These complexes have been termed venous
stars, sunburst venous blemishes and spider leg veins by
various authors.
9
These two subsets of telangiectasias
Pathogenesis
The pathogenesis of each type of telangiectasia is somewhat
different. Multiple factors may play a role in the development
of new blood vessels or the dilation of existing blood vessels
(see Chapters 2 and 8). Acquired telangiectasias probably
result from the release or activation of vasoactive substances,
such as hormones and other chemicals. Conditions associated
with increased or activated vasoactive substances include
anoxia, infection and certain physical factors that results in
capillary or venular neogenesis.
development of telangiectasia is the medial thigh. This has
been thought to be, in part, a result of pressure exerted by
crossing the legs. A report on tissue atrophy in a woman with
associated telangiectasia at the site of pressure where her legs
crossed suggests that intermittent pressure results in subcutaneous tissue loss or atrophy.
edge, no formal studies on tissue pressure have been
performed. Box 4.1, an extension of observations made by
13
Shelley
etiologies associated with telangiectasias arising on the lower
extremities.
as well as Anderson and Smith,14 lists the major
4,10,11
One common area for the
12
Unfortunately, to our knowl-
Incidence
The incidence of varicose and telangiectatic leg veins in the
general population is presented in Chapter 2. The relationship
between varicose veins and spider leg veins (telangiectasias)
is profound. The anatomy and pathophysiology of telangiectasia is presented in Chapters 1 and 3. Telangiectasias increase
in incidence with advancing age.
valence of telangiectasias is 3.8%, with 26% occurring on
8
the legs.
seeking treatment of unwanted spider leg veins. Duffy,
nonrandomized survey of his patients, reported a 90% family
history of varicose or telangiectatic leg veins. Patients included
16
Two surveys have detailed the characteristics of patients
15
Among neonates, the pre-
17
in a
Chapter
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4
Pathophysiology of Telangiectasias
A B
C D
Figure 4.1 Four types of telangiectasias. A, Simple. B, Arborized. C, Spider.
D, Papular.
(Adapted from Reddish W, Peltzer RH: Am Heart J 37:106, 1949.)
Figure 4.3 Common appearance of cartwheel or radiating telangiectasia
pattern on the lateral thigh of a 42-year-old woman. Note the feeding blue
reticular vein at the distal aspect of the telangiectatic pattern.
Figure 4.2 Typical appearance of telangiectasia located at the medial thigh
in a 54-year-old woman. Note the feeding reticular vein proximal to the
telangiectasia.
three sets of identical twins with similar appearing leg telangiectasias. Sadick,
18
in a nonrandomized survey of 100
patients seeking treatment, found a 43% family history of
varicose or telangiectatic leg veins. Both surveys found that
one third of the patients first noted the development of these
veins during pregnancy. Among this subset of patients, veins
became most severe after the third pregnancy.
17
Between 20%
and 30% of patients developed these veins before pregnancy,
and 18% of women noted the onset of the veins while taking
oral contraceptives. Both authors concluded that the development of leg telangiectasia is probably a partially sex-linked,
autosomal dominant condition with incomplete penetrance
and variable expressivity.
72
Pathophysiology
Multiple conditions – inherited, acquired, as well as iatrogenic
– are involved in telangiectasia formation.
Genetic/congenital factors
Numerous genetic or congenital conditions (listed in Box 4.1)
display cutaneous telangiectasia. The pathogenesis for the
development of telangiectasia in these syndromes is unknown.
Genetic syndromes associated with leg telangiectasias include
nevus flammeus (alone or as a component of Klippel–
Trénaunay syndrome (KTS)), nevus araneus, angioma serpiginosum, Bockenheimer’s syndrome (diffuse genuine
phlebectasia), congenital neuroangiopathies (especially
Maffucci’s syndrome), congenital poikiloderma, essential progressive or generalized telangiectasia, cutis marmorata telangiectatica congenita, and diffuse neonatal hemangiomatosis.
Nevus flammeus
Nevi flammei (port-wine stains) affect 0.3% to 1% of the
population,
as men.
incidence
been described.
on any part of the body. They most commonly occur on the
face but may cover large areas of the body, including an entire
arm, leg, or trunk (Fig. 4.4). Lesions often overlay the distribution of peripheral nerves. Nevi flammei are usually macular
and vary in color depending upon the extent and depth of
vascular involvement. Lesions become progressively nodular
and darker with time and may ulcerate and bleed from minor
trauma.
Histologic examination shows a collection of thin-walled
capillary and cavernous vessels arranged loosely throughout
the superficial and deep dermis (Fig. 4.5). These vessels represent dilations of postcapillary venules within the superficial
19,20
with women being twice as likely to be affected
21,22
Cases are usually sporadic, but a 10% familial
21
and an autosomal dominant inheritance have
23–26
Lesions occur in various shapes and sizes
Box 4.1
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Causes of cutaneous telangiectasia of the lower extremities
Genetic/congenital factors
Vascular nevi
• Nevus flammeus
• Klippel–Trénaunay syndrome
• Nevus araneus
• Angioma serpiginosum
• Bockenheimer’s syndrome
Congenital neuroangiopathies
• Maffucci’s syndrome
• Congenital poikiloderma (Rothmund–Thomson syndrome)
Essential progressive telangiectasia
Cutis marmorata telangiectatica congenita
Diffuse neonatal hemangiomatosis
Acquired disease with a secondary cutaneous component
Collagen vascular diseases
• Lupus erythematosus
• Dermatomyositis
• Progressive systemic sclerosis
• Cryoglobulinemia
Other
• Telangiectasia macularis eruptiva perstans (mastocytosis)
• Human immunodeficiency virus (HTLV-III)
Component of a primary cutaneous disease
Varicose veins
Keratosis lichenoides chronica
Other acquired/primary cutaneous diseases
• Necrobiosis lipoidica diabeticorum
• Capillaritis (purpura annularis telangiectodes)
• Malignant atrophic papulosis (Degos’ disease)
Hormonal factors
Pregnancy
Estrogen therapy
Topical corticosteroid preparations
Physical factors
Actinic neovascularization and/or vascular dilation
Trauma
• Contusion
• Surgical incision/laceration
Infection
• Generalized essential telangiectasia
• Progressive ascending telangiectasia
• Human immunodeficiency virus (HTLV-III)
Radiodermatitis
Erythema ab igne (heat/infrared radiation)
(Modified from Goldman MP, Bennett RG: J Am Acad Dermatol 17:167, 1987.)
Figure 4.4 Nevus flammeus in a 68-year-old man without any associated
soft tissue abnormalities. Note that the lesion extends down the posterior
thigh.
Figure 4.5 Histologic section of a nevus flammeus taken from the
forehead of a 66-year-old man immediately after treatment with the argon
laser. Note the location of the enlarged blood vessels within the middle and
deep dermis. Because this lesion has just been treated, the overlying
epidermis demonstrates thermal changes, and the vessels are thrombosed.
(Hematoxylin–eosin, ×80)
(Courtesy Richard Fitzpatrick, M.D.)
Pathophysiology
dermis, with a mean depth of 0.46 mm.27 In infancy, histopathologic changes of cutaneous vasculature are minimal.
With advancing age, however, these lesions usually undergo
progressive ectasia and erythrocyte stasis.
cavernous hemangiomas arising from arteriovenous malformations may occur within the lesions.
evidence of other vascular malformations or neovasculariza-
27
tion.
Further, some lesions on the legs may be associated
with prominent telangiectasias and reticular varicose veins
(Fig. 4.6).
27
Although rare,
28
There may also be
A nevus flammeus can also be a component of a larger
congenital vascular disease; the most common that involves
the leg being KTS.
Klippel–Trénaunay syndrome
With KTS (Fig. 4.7), the cutaneous vascular abnormality is
associated with underlying varicose and telangiectatic veins
with or without significant abnormalities of the deep and
73
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