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Chapter
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2
Adverse Sequelae and Complications of Venous Hypertension
Figure 2.12 A 52-year-old woman with a 1 to 2 year onset of cutaneous
hyperpigmentation of the anterior tibial and medial malleolar areas. Venous
Doppler examination was diagnostic for an incompetent communicating
vein.
Histologic examination (Fig. 2.15) of the dermis demonstrates a diffuse homogenization of collagen, fragmentation
or absence of elastic fibers, thickening and partial occlusion
of arterioles, and atrophic changes of appendages.
may also be an associated acanthosis and hyperkeratosis of
the epidermis, which rarely results in pseudoepitheliomatous
hyperplasia.
fibrotic, and there may be an associated dermal inflammatory
infiltrate.
3
The lymphatic vessels are usually thickened and
3
Because these changes are those of a nonspecific
dermatitis, the histologic diagnosis of venous dermatitis can
be certain only with clinical correlation.
Other conditions can give the appearance of venous dermatitis and should be ruled out; three cases of myelogenous
leukemia cutis have been reported which appeared to be
venous dermatitis.
142–144
Skin biopsy made the correct diagno-
sis in these cases.
Atrophie blanche
Atrophie blanche is the descriptive name given to the appearance of porcelain-white scars seen on the lower extremities as
a result of infarctive lesions of the skin (Fig. 2.16). This condition was attributed originally to syphilis or tuberculosis in
145
1929.
tion and telangiectasias. Histologically, meandering capillaries are detected at the border of lesions, with their apex
oriented towards the avascular center.
associated varicose veins and signs of venous insufficiency.
However, this descriptive term represents the sequelae of
many disease processes including venous dermatitis, arterio-
34
The white plaques are bordered by hyperpigmenta-
146
The process usually occurs in middle-aged women with
12,141
Figure 2.13 Early venous eczema appearing as a nummular eczema
overlying prominent dilated venules and reticular veins in a 58-year-old
woman.
There
Figure 2.14 Typical appearance of venous dermatitis. The affected area is
erythematous, sharply marginated, and scaly with hyperpigmentation and
excoriations.
Signs
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A
Figure 2.16 Middle-aged woman with venous insufficiency and atrophie
blanche of the medial malleolar area. (Courtesy Kim Butterwick, MD)
B
Figure 2.15 Histologic examination of a patient with longstanding venous
hypertension and overlying venous dermatitis. (See text for description.)
(Hematoxylin–eosin; A, ×50; B, ×200.)
sclerosis, dysproteinemia, diabetes mellitus, hypertension,
systemic lupus erythematosus, scleroderma, juvenile rheumatoid arthritis and idiopathic segmental hyalinizing vasculitis.
Therefore, this physical condition is best thought of as an
intermediate stage between venous dermatitis and varicose
ulceration; the term atrophie blanche is best reserved for the
idiopathic vasculitic condition.
Patients with atrophie blanche have been compared with
patients having severe venous insufficiency but without atrophie blanche. In turn, these have been compared with 10
healthy controls. Laser Doppler perfusion imaging was used,
as were transcutaneous oxygen tension measurements. The
overall results showed that resting blood perfusion was greater
in atrophie blanche areas than in healthy controls, and the
venoarterial response was significantly increased in these atrophie blanche areas. In contrast, there was a decrease in transcutaneous oxygen pressure values in areas of atrophie blanche
lesions and in the skin of patients with chronic venous insufficiency without atrophie blanche. The authors of this study
concluded that basic resting flow in atrophie blanche is higher
compared to that in normal skin and in patients with chronic
venous incompetence, but there is also marked decrease in
flow in response to venous occlusion in these affected areas.
147
In addition to treating venous hypertension, treatment with
antifibrinolytics (i.e. aspirin, dipyridamole); anti-inflammatory
agents (i.e. as dapsone) and pentoxifylline have demonstrated to be helpful especially in patients with idiopathic
148
forms.
Ulceration
Cutaneous ulceration represents the end-stage manifestation
of venous stasis disease. This relationship has been noted for
millennia. Hippocrates was the first to record the associa-
149
tion.
More than 300 years ago, Wiseman
vular incompetence caused by venous thrombosis could result
in a circulatory defect leading to ulceration of the skin.
The prevalence of varicose or post-thrombophlebotic
ulcers has been estimated to be as high as 1% of the United
States population and 2% of the Swedish population
(Fig. 2.17).
in early adulthood, they increase in frequency with age and
peak at approximately 70 years.
males is approximately 3 : 1 after the age of 40, with an equal
incidence before 40 years of age.
3,151–153
Although venous ulcers may have an onset
152–155
154
Seventy-two different causes of leg ulcers have been recognized and grouped into three categories.
90% are of venous etiology,
associated with varicose veins,
ciated with a history of DVT.
3,156,157
40% to 60% of which are
157–159
and 35% to 90% are asso-
3,157–161
Nonvenous causes of leg
ulceration include arterial disease (8%) and ulcers caused by
trauma or those that have bacteriologic, mycotic, hematologic,
neoplastic, neurologic or systemic origins (2%).
The cost of treating leg ulcers in the United States was estimated in 1991 to be between $775 million and $1 billion,
based on the annual cost of ulcer care in Sweden.
150
noted that val-
The ratio of females to
155
Between 75% and
156
162
In
35
Chapter
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2
Adverse Sequelae and Complications of Venous Hypertension
36
Figure 2.17 Chronic venous insufficiency with cutaneous ulceration in a
68-year-old man before treatment.
addition to this cost, there is an estimated loss of 2 million
working days annually in the United States because of leg
163
ulcers.
Therefore, optimizing treatment, or better yet, prevention, is important. Curiously, despite its importance, very
little government funding is allocated towards ulcer treatment.
Patients diagnosed with leg ulcers in the United States spend,
on average, 12.1 days in hospital.
164
Because leg ulcers frequently take much longer to heal with bed rest and ancillary
care, this form of therapy is impractical and not properly
reimbursable.
Color duplex investigation of limbs with reflux and ulceration has shown that distal venous reflux has an important
influence over skin changes and ulceration, and reflux in the
superficial veins appears to be more harmful than that confined to the deep veins even when such deep venous reflux
extends through the length of the limb.
165
Reflux in the local
area near the ulcer also influences ulceration. Local reflux may
be influenced by perforating vein incompetence and outward
flow. Isolated perforating vein outward flow without accompanying superficial reflux or deep reflux is seen in 4% to 6%
of limbs with ulceration.
166
There is much controversy about
the role of surgery in treating such reflux. However, most of
the available data suggest that ablation of superficial venous
reflux and ablation of outward flow through perforating veins
is an appropriate method for the management of patients with
primary venous leg ulceration.
167
Between 20% and 25% of ulcerations have superficial
venous insufficiency, either alone with perforating vein incompetence or as a significant component combined with deep
venous insufficiency.
94,98,99,168,169
In one practice of more than
20,000 lifetime patients, it was estimated that nearly 15% of
patients with major varicose veins developed ulcerations.
Although ulcerations are more common in patients with DVT,
13% of all venous ulcerations are observed in limbs with
superficial venous insufficiency alone.
Cutaneous ulceration usually occurs 10 to 35 years (mean,
24 years) after the onset of varicose veins
assumed to be specifically associated with incompetent calf
perforating veins (see Chapter 9).
170
and is commonly
15,171–173
Dodd and Cockett15
surgically explored 135 limbs with ankle ulceration and found
that the most severe lesions were always associated with an
incompetent perforating vein. Lawrence et al
172
patients with varicosities, both with and without associated
ulceration, using Doppler ultrasound. They found sustained
retrograde flow in incompetent veins in eight of nine ulcer
patients but found it in only one of seven patients with varicose veins without ulceration. However, a recent study using
duplex sonography showed no direct correlation between
incompetent perforators and venous ulceration. Plethysmographic examination indicated that venous hypertension in
superficial veins was the more important factor.
174
One study
of 213 consecutive patients with venous ulceration demonstrated that 90% of patients had sustained ulcer healing (with
a mean follow-up period of 3.4 years) when treated with
saphenous ligation alone, without perforating vein treatment,
even when incompetence of the perforating veins had been
demonstrated.
175
Thus, any operative procedure on varicose
ulcers must correct the underlying abnormal communicating
superficial or perforating veins. Interestingly, no evidence or
history of DVT was reported in up to 24% of patients with
chronic venous leg ulcers;
159,176
therefore, the etiology may be
multifactorial, with the majority of patients having a similar
initiating event: superficial venous hypertension. This may
arise from incompetent perforating veins alone, associated
with an abnormal deep venous system, or with an incompetent superficial venous system.
Stasis ulcerations, unlike most other causes of cutaneous
ulcerations, appear in the gaiter area.
177,178
159,179
The ulcers appear
cyanotic, edematous, and friable. The base is usually covered
with thick granulation tissue that rarely penetrates the deep
fascia. The skin edges are painless, thickened and bleed easily.
Adjacent skin is edematous and inflamed, with associated
dilated venules, eczematous changes and pigmentation.
Calcification of the subcutaneous tissue, often not even adjacent to the ulceration, occurs in a significant number of
patients,
130,181,182
up to 25% in one study (Fig. 2.18).
calcium, acting as a foreign body, may perpetuate the ulceration or actually may be an essential cause of the lesion.
Calcification is probably caused by venous insufficiency and
represents the last stage of the inflammatory response. It
almost always precedes the ulceration.
130
In contrast to venous stasis ulceration, ischemic ulcers
occur most commonly on the anterior and/or lateral leg and
ankle. However, lateral ankle ulcerations may arise from
incompetent small saphenous veins.
184
The base of an ischemic
ulcer is often obscured by a pale yellow, purulent exudate.
Often the borders are poorly epithelialized, with a ‘punchedout’ appearance, and are necrotic with islands of gangrenous
skin. Deep fascia and tendon may be exposed at the base, with
little or no spontaneous granulation tissue.
Leg ulcers can also have multiple causes. Two case reports
of mixed skin ulcers misdiagnosed as pyoderma gangrenosum
and rheumatoid ulcer successfully treated with ultrasoundguided injection of polidocanol microfoam has recently been
reported.
185
Malignant degeneration
A potentially fatal, but fortunately rare, secondary change in
venous ulcers is malignant degeneration (Fig. 2.19). There have
been more than 100 case reports of malignant degeneration
6
of a stasis ulcer in the world literature.
173,186–194
studied
161,180
183
The
Signs
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A
Figure 2.18 A sixty-five-year-old woman with varicose veins, stasis dermatitis, and medial malleolar ulcerations bilaterally. A, Right leg; B, left leg;
C, close-up view of left medial calf demonstrating extensive subcutaneous calcium deposits.
B C
plasia.
201
Chronic scarring from the sequelae of ulceration
mentioned above may obliterate lymphatic channels, leading
to decreased immune surveillance of the scar by immunologically competent cells. This relatively localized immune deficiency provides less protection against cellular mutation,
which allows cellular progression into neoplasia.
202
it seems prudent to perform a biopsy of the base and border
areas of ulcers with these characteristics or of ulcers that persist
for more than 4 months. This is particularly important when
surgically correcting the ulceration with a skin graft. One
patient developed a squamous cell carcinoma following split
skin grafting and, in spite of amputation and radiotherapy,
died from multiple metastasis.
173
Although the appearance of malignant degeneration in a
nonhealing leg ulcer is often characteristic, basal cell carcinoma in the ulcer may either appear as exuberant and trans-
Figure 2.19 Basal cell carcinoma (keratinizing type) arising in an ulcer
in the setting of chronic venous insufficiency in a 77-year-old woman.
The ulceration had been present for at least 6 years. An incompetent
perforating vein was found at the base of the ulceration.
lucent ‘granulation tissue’ or may have no clinical features to
suggest malignancy.
A study of squamous cell carcinomas complicating chronic
venous leg ulcer has revealed some interesting facts. The mean
age at cancer diagnosis was 78.5 years; the median survival
188,191,203
was 1 year. Of these tumors, 11 were well differentiated, 10
moderately differentiated, and 4 were poorly differentiated.
The most common cancers reported are carcinomas (squamous and basal cell) and sarcomas (fibrosarcoma, osteosarcoma and angiosarcoma). Even malignant melanoma has
been reported to occur in chronic venous ulceration.
incidence of malignant degeneration of venous stasis ulcerations is 0.4% to 1%.
before tumor growth is 21 years, with a reported span of 10
to 40 years.
198
193,196-198
The average duration of the ulcer
The onset of malignant change usually appears
195
The
as a rapid growth of exuberant cauliflower-like masses, an
increase in pain, or, in a smaller number of cases, a rapid
extension of the ulcer crater.
198
An increase in induration of
the ulcer borders and surrounding tissue and a failure of the
ulcer to respond to prolonged conservative treatment are also
suspect.
be stimulated by many factors, including chronic dermatitis,
irritation and infection.
199
Transition into a malignant growth is thought to
199,200
Implanted epithelial cells may
produce a chronic foreign-body reaction with subsequent neo-
All patients with poorly differentiated tumors died within 1
year. Metastases were certain in 8 cases.
204
The disease was
lethal in 10 cases, which included all of the poorly differentiated tumors. This suggests that when squamous cell carcinoma in chronic leg ulcers is found, a thorough investigation
must include the degree of differentiation and a definition of
extent of spread. Aggressive treatment is indicated because
poorly differentiated tumors and some moderately differentiated tumors are fatal.
Secondary complications of venous
hypertension–stasis
In addition to the varicose ulcers and dermatologic abnormalities already discussed, external hemorrhage, superficial
thrombophlebitis and DVT are the three most severe and acute
complications of varicose veins.
Therefore
37
Chapter
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2
Adverse Sequelae and Complications of Venous Hypertension
Hemorrhage
Hemorrhage from varicose veins may not be a rare event.
205
Tretbar
sodes of hemorrhagic varicose veins. All but two of his patients
had had varicose veins for more than 20 years. The bleeding
area typically consisted of a mat of ‘blue blebs’, each of 1 to
2 mm in diameter, on the medial ankle. Doppler examination
usually disclosed an underlying incompetent communicating
vein. None of Tretbar’s patients developed serious sequelae
from the bleeding episodes and all were treated successfully
with compression sclerotherapy of the affected veins. However,
bleeding can be profuse and, if unnoticed or improperly
treated, can be fatal.
cose veins from Australia between 1997 and 2000 disclosed
51 deaths where varicose veins were indicated to be the
primary cause of death.
rhage was the cause.
when the skin overlying a varicose vein becomes traumatized
or eroded. Most cases described in the literature occur in
patients with ulcers overlying varices, but profuse bleeding
may also occur from varicosities 1 to 2 mm in diameter (Fig.
2.20)
in England and Wales in 1971.
solitary elderly patients with longstanding varicose veins.
These patients usually live alone and are unable to apply pressure to the bleeding varix or to get help because of physical
disabilities. Rarely, patients may have no history of longstanding varices or overlying ulcers. Hemorrhage in this setting is
usually attributable to the rapid development of venous
hypertension that occurs from DVT.
reported treating 12 patients in 3 years for 18 epi-
15,206–208
A report on the mortality of vari-
209
In one-third of these cases, hemor-
Hemorrhage is usually spontaneous but may also occur
. Twenty-three fatal cases of hemorrhage were reported
206
The patients most at risk are
210
If the varicose vein is under high pressure from venous
insufficiency, as it usually is, the acute hemorrhage may appear
to be arterial in origin. This may result in the inappropriate
application of a tourniquet, which only increases venous
hypertension. If properly recognized, bleeding of venous
origin is easily controlled by raising the affected area above
the level of the heart and applying localized pressure to the
bleeding vein. Leg elevation stops hemorrhage within seconds
to minutes. Sclerotherapy or ligation of the affected vein is
curative but may not prevent further episodes of hemorrhage
from other varices.
Direct pressure over the area of hemorrhage stops the
bleeding, and maintaining that pressure for 5 to 7 days allows
complete healing of the epidermis over the area of the hemor-
211
rhage.
It has been found that a suture of the area of hemorrhage, usually done in a hospital emergency department,
causes venous ulceration. Direct suture, therefore, should be
avoided.
Injection of potentially hemorrhagic veins is mandatory
(Fig. 2.21). In these cases, usual aesthetic concerns do not
apply and it is logical to inject the fragile venules at the very
beginning of the treatment, prior to the necessary reduction
of venous hypertension. Sclerosing injections of bleeding
veins provide an elegant solution to the problem; provided
the sclerosing agent induces a spasm (polidocanol, sodium
tetradecyl sulfate), it stops the hemorrhage and usually prevents a recurrence. The leg should be elevated during injection, and higher than usual concentrations of sclerosing
solution are often required. Foamed sclerosant may also help
stop the bleeding more quickly.
Since the responsibility for skin abrasion and subsequent
hemorrhage lies mostly with patients themselves, advice
should include careful nail trimming and filing, and nocturnal
wear of socks (and maybe even gloves as well). Avoiding
scratching of the skin is also a prerequisite as fewer complications are caused by corticosteroid creams than by ulcers and
hemorrhages caused by scraping.
The ‘shear off’ phenomenon can explain ‘spontaneous’
acute pains of the calf, known in the French literature as ‘whip
pains of the calf’. During a quick movement of the lower limb,
inertia of muscle and fat tissues creates a relative displacement
of the different anatomical layers (Fig. 2.22) responsible for
wrench of communicating or perforating veins, resulting in
pain, hematoma and ecchymosis. This atraumatic lesion is
more common on varicose veins because of the venous wall
remodeling and dysplasia, and because of venous hypertension. Duplex ultrasound shows edema and a small hematoma,
and usually no sign of superficial thrombophlebitis. Local
Figure 2.20 Venulectasia in a 90-year-old man that bled profusely while
the patient was standing. Sclerotherapy caused rapid healing. Figure 2.21 Injection of potentially hemorrhagic veins is mandatory.
38
Deep vein
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Deep
aponeurosis
Saphenous
vein
Saphenous
aponeurosis
Muscle
Figure 2.22 During a quick movement of the lower limb, inertia of muscle
and fat tissues create a relative displacement of the different anatomic layers.
Superficial
tributary
Hematoma
Communicating
vein
Wrench
Perforating
vein
Skin
Subcutaneous
tissue
compression and massage with nonsteroidal anti-inflammatory
cream is the sole treatment.
Superficial thrombophlebitis
Superficial thrombophlebitis (ST) is a painful condition that
fortunately seldom results in serious embolic complications.
In the absence of malignancy, thrombophlebitis of the leg
is almost invariably associated with varicose veins.
Patients with varicose vein ST are younger and have a decreased
incidence of coexistent DVT (9.75% versus 43.75%).
condition results from the development of a clot in a varicose
vein caused by one or more of the following factors: trauma
to the varicosity, stasis of blood flow or occlusion of blood
flow. Fifty percent of cases may occur spontaneously.
evaluation of 51 consecutive patients with venous thrombosis
and varicose veins found 8% with an underlying malignancy,
7% with an antiphospholipid syndrome and a total of 26%
with other systemic illnesses.
216
Therefore it is recommended
that a search for an underlying cause be made.
The great saphenous system is the usual site of ascending
ST. Clinically, one notes a painful, tender, hot erythematous
swelling along the course of the vein, with a variable amount
of perivascular edema. The pain associated with ST is often
severe, probably resulting from inflammation of the dense
network of somatic nerve fibers in the associated subcutaneous tissue.
4
Incidence of ST, irrespective of the presence of varicose
veins, increases with advancing age and inactivity, and with
bed rest as the result of surgery, childbirth or cardiac
disease.
217,218
In patients in whom the incidence of varicose
veins is not stated, ST has been estimated to occur in 0.7% of
women in their fourth decade of life, increasing to 2.6% of
women in the seventh decade.
has been estimated to be 0.4% in the fourth decade, increasing
57
In men, the incidence of ST
57
The actual number of patients
with ST in the United States was estimated in 1973 to be
123,000 yearly. The incidence of ST is substantially higher
when related to the presence of varicose veins.
the lifetime work of one physician with more than 20,000
patients notes an incidence of ST in as many as 20% of patients
with prominent major varicosities.
mated a 50% lifetime incidence of thrombophlebitis in
patients with varicose veins.
219
6
Older papers have esti-
Fegan83 estimates that ST occurs
in approximately 4% of those with varicose veins.
Although the condition is usually treated as a benign com-
plication of varicose veins, the development of DVT, venous
4,212–214
213
The
212,215
An
4
A review of
hypertension and pulmonary emboli may occur in a significant percentage of patients.
of ST in a university hospital disclosed a 10% incidence of
pulmonary emboli with five deaths,
confirmed by others.
emboli may also be related in some cases to a coexistent
4,226,227
DVT.
One study of 44 consecutive patients with ST
212,215,220–224
225
The development of pulmonary
A review of 340 cases
215
and this risk has been
found coexistent DVT in 23%. All of these cases were occult
clinically, with the site of the ST not predictive of DVT.
noninvasive deep venous studies are recommended for all
patients with ST.
Pulmonary emboli and DVT, by definition, were supposed
not to complicate ST unless the thrombus progressed into the
deep venous system, but it has been observed that DVT can
occur in other venous networks. This may happen because of
either progression into a perforating vein or ascending involvement of the common femoral vein at the saphenofemoral
junction (Fig. 2.23) or simply due to the presence of a hypercoagulable state.
ficial or deep venous hypertension develops as a result of
valvular destruction.
into the deep system has been reported to occur in 6%
220
32%
of all cases of ST. In an 11-year retrospective series, 17%
of 133 patients were noted to have extension of the clot into
the deep system.
228
When either of these events occurs, super-
218
Propagation of the thrombotic process
230
Surgical exploration of the saphenofemoral junction, followed by ligation, thrombectomy and limited
vein stripping, has been advocated, particularly if clinical signs
of thrombophlebitis reach the midthigh. We recommend full
anticoagulation. Surgical removal of the thrombosed vein segments and associated varicosities shortens the convalescence
and mitigates recurrences.
form of treatment usually results in extensive scarring. Finally,
229,231,232
Unfortunately, this latter
because DVT may manifest partly in the appearance of ST,
patients should be examined carefully.
Surgical treatment of ST has been dominant when the ST
has affected the GSV and ascended towards the saphenofemoral junction. It is thought that the incidence of DVT is three
times that of normal individuals, and, in the past, with ascending thrombophlebitis of the GSV, an operation under local
anesthesia to ligate and divide the vein was recommended.
However, gradually, anticoagulant treatment has dominated
clinical practice. The advantage, of course, is that the ST is
treated simultaneously by the anticoagulation, compression
and rest. Nonsteroidal anti-inflammatory medications have
been advocated but may have potentially severe side effects.
Since ST is associated with a higher risk of DVT, and since ST
of the GSV when ascending to the junction leads to progression of the clot into the femoral vein, the use of low molecular
weight heparins must be considered – prophylactically for 2
weeks when the clot does not threaten the deep system, but
therapeutic, like for a DVT, when it does.
compression is recommended by most authorities on this
subject.
228
234
External elastic
Deep venous thrombosis
Varicose veins, by virtue of their low blood flow, are considered a high risk factor for DVT.
factors, patients with varicose veins have an incidence of DVT
ninefold that of the normal population.
is thought to occur behind valve cusps, especially when the
valves are incompetent in varicose veins.
the valve cusps then triggers the coagulation cascade and
results in clot propagation.
Stasis of blood flow may cause activation of factors XII,
XI, and IX, which initiates thrombin activity to propagate
thrombus formation through fibrin formation and platelet
aggregation.
238
Stasis may also result in a significant amount
of endothelial sloughing, with exposure of subendothelial collagen and subsequent activation of platelets.
4
Without other predisposing
235
Platelet aggregation
236,237
Thrombosis on
239
An additional
214
Thus,
229
to
233
Signs
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Chapter
Percent of subjects with complaints
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2
Adverse Sequelae and Complications of Venous Hypertension
Common
femoral vein
Deep femoral
vein
Perforating
veins
Great
saphenous
vein
Perforating
veins
A B C
Figure 2.23 Diagrammatic representation of three methods of propagation of superficial thrombophlebitis. A, Thrombophlebitis limited to the superficial
system with blockage by the perforating vein valves and at the saphenofemoral junction. B, Extension of the thrombus into the deep system through
destruction and incompetence of perforating veins. C, Direct extension of the thrombus into the femoral vein at the saphenofemoral junction.
Totten HP: Angiology 16:37, 1965.)
Loosely attached
clot in superficial
femoral vein
Firmly attached
clot in the great
saphenous vein
Extension of
thrombus into
the common
femoral vein
(Redrawn from
reason for the propensity for DVT in patients with chronic
venous insufficiency (which is commonly associated with the
presence of varicose veins) may be related to a faulty fibrinolytic system, correlated with pericapillary deposition of
fibrin.
70% of patients with idiopathic DVT have a decreased tissue
plasminogen activator that probably reflects endothelial dysfunction and a decreased clearance of clotting factors.
erative period.
dence of thrombophlebitis in varicose veins in the postoperative
period, with an incidence estimated at 6% versus the normal
0.5% to 0.7% incidence.
patients less than 60 years of age. With fibrinogen scanning,
DVT occurs in 56% of patients over 60 with varicose veins
versus 41% in patients over 60 without varicose veins. This can
be compared with 56% in patients younger than 60 years with
varicose veins versus 19% in patients less than 60 without
varicose veins.
who are about to undergo surgery, or who are bedridden or
pregnant, should receive thrombosis prophylaxis, such as
wearing a graduated support stocking, to prevent this potentially fatal, albeit rare, complication of varicose veins.
of serious medical problems and are not just of cosmetic
concern. Basle study III
complications of varicose veins – chronic venous insufficiency,
phlebitis and pulmonary embolism – increases with the severity of the varicosity (Fig. 2.24). Even patients with minor telangiectasias and reticular veins in combination demonstrated
a significant increase of these serious medical complications
when compared with patients without these types of veins.
Classification
A classification of varicose veins should be based on anatomic
or subsequent therapeutic considerations. The first anatomic
40
240
This hypothesis has been questioned because up to
240–243
An increased incidence of DVT is also found in the postop-
244–248
This may be related to the increased inci-
249
This is of particular significance in
250
Therefore, all patients with varicose veins
In summary, varicose veins are associated with a number
5
found that the incidence of the major
50
40
30
20
10
No varicosity
N1645
Figure 2.24 Complications according to the type of varicose vein. N
represents the number of persons in the defined group.
L: Peripheral venous disorders: prevalence and socio-medical importance: observations in
4529 apparently healthy persons, Basle Study III, Bern, Switzerland, 1978, Hans Huber.)
classification was proposed by Heyerdale and Stalker
Telangiectasia
or reticular
806
Type of varicosity
Telangiectasia
and reticular
545
Truncal varices
748
(Redrawn from Widmer
251
in
1941 (Table 2.1). This classification is useful in determining
when surgical ligation of the GSV is advantageous before performing sclerotherapy. The list of advantages presented by
Heyerdale and Stalker still holds true today (Box 2.7). The
Basle study
5
classified varicose veins into three groups:
1. Dilated saphenous veins (stem veins)
2. Dilated superficial branches (reticular veins)
3. Dilated venules (hyphenwebs).
Table 2.1 Classification of varicosities of the lower extremities
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Group Varicosities Saphenous System
1 Spider bursts; telangiectatic veins Competent
2 Mild or moderate varicosities Competent
3 Mild, moderate, or marked
varicosities
From Heyerdale WW, Stalker LK: Ann Surg 114:1042, 1941.
Incompetent
Box 2.7
Advantages of ligation of incompetent saphenous vein
• Continuity of the vein is interrupted at the most proximal
point
• Need for cannulization is reduced to a minimum
• Number of local injections necessary for obliteration is
decreased
• Period of treatment is shortened
• Adequate complete thrombosis is obtained with greater ease
• Pulmonary showers are less likely to occur
From Heyerdale WW, Stalker LK: Ann Surg 114:1042, 1941.
Classification
Box 2.8
Vessel classification
Type 1: Telangiectasia, ‘spider veins’
• 0.1–1.0 mm diameter
• Red to cyanotic
Type 1A: Telangiectatic matting
• 0.2 mm diameter
• Red
Type 1B: Communicating telangiectasia
• Type 1 veins in direct communication with varicose veins of
the saphenous system
Type 2: Mixed telangiectatic/varicose veins
• No direct communication with the saphenous system
• 1–6 mm diameter
• Cyanotic to blue
Type 3: Nonsaphenous varicose veins (reticular veins)
• 2–8 mm diameter
• Blue to blue–green
Type 4: Saphenous varicose veins
• Usually over 8 mm in diameter
• Blue to blue–green
Modified from Duffy DM: Small vessel sclerotherapy: an overview. In Callen JP
et al, editors: Advances in dermatology, vol 3, Chicago, 1988, year Book.
Figure 2.25 Duffy type 1 (telangiectasia) on the inner thigh of a 58-year-
old woman.
Figure 2.26 Duffy type 1A (telangiectatic matting) 6 weeks after
sclerotherapy treatment on the lateral calf. Note associated reticular veins,
postsclerotherapy hyperpigmentation and bruising.
252
Duffy
proposed a more complete classification of ‘unwanted
leg veins’. Since one purpose of a classification is to provide a
mechanism for evaluating pathophysiology and treatment, a
modification of the Duffy classification appears useful. It provides comprehensive clinical and therapeutic criteria in an
effort to optimize treatment (Box 2.8 and Figs 2.25 to 2.30).
Varicose veins can be classified into four developmental
stages. The first stage appears as a somewhat dilated blue vein
in association with normal great and small saphenous veins.
This stage usually occurs in teenagers with a family history of
varicose veins. It is asymptomatic.
The second stage appears as a palpable, bulging, moderately dilated vein, usually in association with a larger saphenous vein. Venous Doppler examination is normal; Duplex
scanning may show a dilated but competent saphenofemoral
and/or saphenopopliteal junction. These veins may be symptomatic after prolonged immobilization or standing.
41
Chapter
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2
Figure 2.27 Duffy type 1B (communicating telangiectasia) in a 20-year-old
woman.
Adverse Sequelae and Complications of Venous Hypertension
Figure 2.29 Duffy type 3 (nonsaphenous varicose (reticular) veins) located
over the proximal anterolateral thigh of a 24-year-old woman.
Figure 2.28 Duffy type 2 (mixed telangiectasia and varicose veins with no
direct communication with the saphenous system) in a 54-year-old woman.
There was no evidence (venous Doppler) of incompetence of the
saphenofemoral or saphenopopliteal junctions or of perforating veins.
The third stage represents established varicose vein disease.
The great and/or small saphenous veins are dilated over all or
part of their length. There are associated varicose veins over
the thigh and lower leg, with accompanying venules and
spider veins. The varicose veins themselves may or may not
be incompetent, but gross incompetence is present at the
saphenofemoral and/or saphenopopliteal junctions.
The final, or fourth, stage consists of complications
arising from chronic venous insufficiency and varicose veins.
42
Figure 2.30 Duffy type 4 (saphenous varicose veins). Varicose great
saphenous vein with incompetent valvular function throughout its
length and a grossly incompetent saphenofemoral junction in a 32-year-old
man.
Perforating vein incompetence is present along with cutaneous manifestations of venous stasis disease, including
ulcerations.
The development of varicose vein disease is generally progressive. Six different patterns of GSV varicosity have been
described.
114
These relate to the duration of varicose vein
disease (Fig. 2.31). Certain patients may experience spontaneous stabilization of the disease in the early stages. Treatment
of early-stage disease may prevent the progression and cause
regression of the disease process. A complete understanding
of the anatomy and pathophysiology of the venous system
with regard to varicose veins allows the development of a
rational treatment plan.
Figure 2.31 Patterns of great saphenous vein incompetence in 296 limbs with primary varicose veins. (Modified from Almgren B, Eriksson I: Acta Chir Scand 156:69,
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1990.
© British Journal of Surgery Society Ltd. Reproduced with permission. Permission is granted by John Wiley & Sons Ltd on behalf of the BJSS Ltd.)
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