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174
Ex
ex
muscle
Deep fibular ner
Anterior tibial ar
F
Fi
and vein
transducer position
Pe
Supe
Chapter 3 · Extremity Veins
Anterior
transducer position
3
terior hallucis muscle and
terior digitorium longus
ve
roneal muscles
ibula
bular artery
tery and vein
rficial fibular nerve
Anterior tibial muscle
Tibia
Great saphenous vein
Saphenous nerve
Deep crural fascia
Posterior tibial artery
and vein, tibial nerve
Sural triceps muscle
Small saphenous vein
Sural nerve
a
. Fig. 3.6 a Cross-sectional anatomy of the lower leg and transducer positions. b Sonoanatomy of the calf veins with the transducer in the pos-
teromedial position. The transverse view shows the posterior tibial artery and vein (left part of image) somewhat posterior to the tibia (T) and the
bular artery and vein posteromedial to the bula (F). Blue indicates ow in the veins, red ow in the artery (with some aliasing resulting from the
low PRF selected to improve sensitivity to slow venous ow). The artery lies within the slightly hypoechoic deep crural fascia and is accompanied
by two veins on the left and right
Posteromedial
major calf veins to rule out muscle vein thrombosis (the same
applies to the deep femoral vein in the thigh). e muscle
veins can be traced in a distal direction from their sites of
entry into the main vein, especially when there is adequate
venous lling with the patient sitting.
e ultrasound examination in thrombophlebitis
serves to determine the extent, in particular the cranial
extent, and involvement of the deep venous system (inow
into deep venous system). is is done by performing compression ultrasound of the great or small saphenous vein in
transverse orientation aer identication of the clinically
inamed segment and using the same criteria as in the diagnostic assessment of thrombosis.
In thrombophlebitis, special attention must be paid to the
sites of entry of the small and great saphenous veins into the
popliteal and common femoral vein, respectively, which are
checked for compressibility in the transverse plane.
In patients examined for thrombosis, compression ultrasound is always performed in transverse orientation, for two
reasons: it makes it easier to identify the vein and follow its
course down the leg and prevents false-negative results during compression. Longitudinally, when pressure is applied, a
noncompressible vein may be displaced and disappear from
the scanning plane, thereby mimicking compressibility.
Posterior
transducer position
b
Function of the proximal valves is evaluated by spectral
Doppler recording in the common and supercial femoral
veins in the recumbent patient during increased abdominal
pressure (Valsalva’s maneuver). Valve incompetence is demonstrated by persistent backward ow to the periphery, indicated by a corresponding color change in the color ow image.
If this test is positive for proximal valve incompetence, it is
progressively extended to the popliteal vein and below- knee
veins to identify the distal end of the incompetent segment.
In patients with competent proximal valves (common
femoral and proximal supercial femoral veins), distal insufciency is identied by the demonstration of persistent ow
reversal (over 1s) in the popliteal vein using spectral Doppler
(. Fig. 3.7) or color ow imaging (in longitudinal orientation) during compression and release with the patient sitting or standing. e best results are achieved with maximum
relaxation of the calf muscles (. Fig.3.7).
Incompetence of the terminal valve of the great saphenous
vein is assessed longitudinally during Valsalva’s maneuver
(. Fig. 3.8). When truncal varicosis is suggested, the great
saphenous vein is followed distally to identify the lowest
point of incompetence through intermittent Valsalva maneuvers (grading according to Hach). In case of suciency of the
proximal segment, the extent of distal varicosis of the great
saphenous vein is determined by intermittent testing along
3.1.2.2 Chronic Venous Insuciency
andVaricosis
In patients with chronic venous insuciency of the deep veins
or varicosis of the supercial veins, the aected venous segments are evaluated for reux using provocative maneuvers
while recording spectral Doppler information in longitudinal
orientation. For identication of valve incompetence of the
deep veins, evaluation is performed at representative sites in
the common femoral, supercial femoral, and popliteal veins.
the vein in the cranial direction (. Fig.3.8b: compression of
the vein with the thumb distal to the transducer) to identify
the proximal and distal points of insuciency (transition
from persistent reux to absent reux upon compression
with subsequent release) in the sitting or standing patient.
is valve function test is also used to diagnose reux in the
small saphenous vein (. Fig.3.9).
To assess valve competence of the perforating veins,
these are rst identied in their typical locations (e.g.,
Prox
compression
Distal
compression
Release
Release
3.1 · Pelvic andLeg Veins
imal
175
Muscle contraction
Fascia Fascia
b
3
Distal
Transducer
Distal C
a
. Fig. 3.7 a Illustration of the proximal and distal valve function test (alternating compression and release) with spectral Doppler measurement
in the popliteal vein. The upper waveform represents the normal ndings obtained when there is proper valve closure (distal compression and
release on the left; proximal compression and release on the right); the lower waveform shows reux due to valve incompetence (C=compression; R=release of compression). In individuals with a competent valve, venous ow with normal respiratory phasicity is followed by augmented
ow toward the heart upon compression of the vein in the calf distal to the sampling site (“KOMP US” in the upper waveform). No ow signal is
recorded upon release of compression (R), consistent with adequate valve closure and absence of reux. Following compression of the muscle
and vein in the thigh, i.e., proximal to the sampling site (“COMP OS” in the upper waveform), there is short reversed ow toward the periphery
until the valve closes. Valve incompetence would be associated with persistent reux. Release of compression in the thigh (“DECOMP OS” in
the upper waveform) results in augmented ow toward the heart. When there is unobstructed venous drainage, the waveform shows a steep
upstroke. The elicited ow increase is less pronounced when a ow obstruction is present between the sampling site and the site of compression
(see. Figs.3.24 and 3.95 (Atlas)). b Venous drainage of the legs. The right drawing shows blood ow and valve function during muscle contraction. The contracting muscle squeezes the surrounding veins, propelling the blood in the draining veins toward the center. Competent valves
prevent reux toward the periphery. The valve function test (compression and release) simulates the role of muscle contraction in venous drainage (muscle pump). c Color ow images and spectral Doppler waveforms obtained in a patient with a duplicated popliteal vein (one competent/
one incompetent branch) nicely illustrate the eect of alternating compression (KOMP) and release of compression (DEKOMP) for identication of
valve incompetence. The popliteal vein closer to the transducer has adequate valve function, seen as absence of reux upon release of compression (“DEKOMP” in the waveform accompanying the two color ow images shown at the bottom). The corresponding color ow image shows no
ow in this popliteal vein, consistent with absence of reux (bottom panel, second color ow image). In the second popliteal vein, there is incompetent postthrombotic valve closure, seen in the waveform (top panel) and the corresponding color ow image with blue-coded ow toward the
periphery in the popliteal vein farther away from the transducer upon release of compression (“DEKOMP” in the waveform). During compression
of the veins in the calf (“KOMP” in the waveforms), both popliteal veins show ow toward the center (red in the rst color ow image in the
bottom panel)
C
VALVE INCOMPETENCE
R
Cockett’s group in the distal medial lower leg, Boyd’s group
in the proximal lower leg, or Dodd’s group in the upper leg)
(. Fig.3.10).
On B-mode images, the perforating veins are identied as
hypoechoic, tubular structures passing through the deep fascia from the supercial to the deep veins. Once identied, the
valve function test is performed as described in . Fig.3.11.
R/prox. C
NORMAL
Ultrasound machine
proximal C
R
R
c
If there is incompetence, (color) duplex with the sample
volume placed in the perforating vein identied by B-mode
imaging will demonstrate reux (retrograde ow from the
deep into the supercial system) during compression of the
calf just proximal to the sample volume. When the valves
function properly, there is no backward ow from the deep
to the supercial veins. Compression of the calf will cause
176
Femoral vein
Great saphenous vein
Small saphenous vein
P
Chapter 3 · Extremity Veins
- Expiration
3
a b c
. Fig. 3.8 a Valve function test in the great saphenous vein. b Transducer position for evaluating valve competence of the distal great saphe-
nous vein. Alternating distal compression of the vein and release during recording of the Doppler spectrum is performed with the left thumb.
c Transverse image of the sonoanatomy of the great saphenous vein (arrow) in the saphenous compartment enclosed by the bright saphenous
fascia anteriorly and the muscle fascia posteriorly. This appearance has been referred to as Cleopatra’s eye and can help the examiner distinguish
the great saphenous vein from branch varices coursing outside this compartment. The great saphenous vein enters the common femoral vein
from anteromedially
- Calf compression
- Inspiration
- Valsalva
- Release of
calf compression
- Compression
proximal
to transducer
. Fig. 3.9 a Valve function
test in the small saphenous vein.
b Transducer position for evaluating valve competence of the
small saphenous vein (see legend
to . Fig.3.8b)
opliteal vein
- Distal calf compression
- Standing on tiptoes
- Thigh compression
- After distal calf
compression
- After standing on
tiptoes
a
stoppage of ow but no reversal. Application of a tourniquet
proximal to the site of evaluation can prevent interference
from ow in insucient supercial veins.
3.1.3 Normal Findings
e leg veins, with their delicate walls and low intraluminal
pressure, are fully compressible when pressure is exerted with
the transducer. When compressed, normal veins become
nearly invisible on ultrasound, or only a hyperechoic reection
indicating the wall but no lumen is seen. e breathing- related
b
intra-abdominal pressure changes lead to respiratory modu-
lation of venous return
with faster ow during expiration
due to lower intra-abdominal pressure (upward movement
of diaphragm) and slower ow during inspiration due to
higher intra-abdominal pressure (downward movement of
diaphragm). is pressure-dependent ow pattern is transmitted through the upper leg veins into the major deep veins
in the distal lower leg and into the major supercial veins
(great and small saphenous veins) in the recumbent patient.
Respiratory phasicity of venous ow may be overridden by
cardiac pulsatility (changes in atrial pressure) in the iliac and
proximal femoral veins, especially in young patients.
Medial view Posterior view
Great
saphenous vein
(gastrocnemius point)
Deep
s
3.1 · Pelvic andLeg Veins
177
3
. Fig. 3.10 Typical locations
of clinically relevant perforating
veins
lower leg vein
Superficial
lower leg vein
- Proximal
calf compression
- Standing on tiptoes
- After calf compression
- After standing on tiptoe
Deep femoral
Dodd’s veins
Hunter’s veins
Boyd’s vein
Sherman’s vein
Cockett’s veins
Small
saphenous
vein
perforators (Hach)
Popliteal perforators
May’s vein
Lateral perforator
erefore, under normal conditions, there should only be
a short reux during Valsalva’s maneuver before valve closure. When the compression-and-release test is performed to
evaluate peripheral valve competence with spectral Doppler
measurement in the popliteal vein, manual compression
at the calf level will result in a rapid increase in blood ow
velocity (unless there is obstruction of venous ow). Like
Valsalva’s maneuver, release of compression should lead to
short reversed ow until the valve closes. e test will allow
more condent assessment and dierentiation of normal and
abnormal function when performed with the patient sitting
and legs dangling (. Fig.3.7).
blood ow:
e pocket-like valves ensure undisturbed ow from the
periphery to the center. Physiologic backward ow induced by
pressure reversal ceases upon closure of the valves (aer a short
reux of 0.3s on average). Valve function tests with manual
compression and release simulate the interplay of the muscle
pump and venous valves in transporting blood back to the heart.
Incompetent
perforator valve
. Fig. 3.11 Valve function test in the perforating veins
Transducer
In summary, the following factors determine venous
5 Vis-a-tergo
5 Variation in intra-abdominal and intrathoracic pressure
(suction pump)
5 Cardiac suction pump (systole, early diastole)
5 Musculovenous pump (requires competent valves):
competent perforating veins prevent blood ow into
supercial veins; competent valves distal to the contracting muscle prevent backward ow (. Fig.3.7b)
3.1.4 Documentation
As with the examination protocol, the documentation of
ndings is dictated by the clinical question to be answered.
3.1.4.1 Deep Vein Thrombosis oftheLeg
e ndings of sonographic valve function tests performed
in patients with deep vein thrombosis (DVT) should be documented without and with compression (ideally split images
showing venous ow without and with compression side
by side). e sites for which these ndings are documented
include the common femoral vein at about the level of the termination of the great saphenous vein, the supercial femoral
vein somewhat distal to the site of entry of the deep femoral
vein, the popliteal vein, and the major veins below the knee
from a posterior approach. e ndings at these representive
sites should be supplemented by images documenting abnormal ndings and a Doppler waveform from the junction of
the common femoral vein and external iliac vein to document unobstructed venous return at the pelvic level.
When the documentation of ndings in patients with
suspected DVT relies on duplex ultrasound, it is generally recommended that this should comprise longitudinal
images with the corresponding waveforms conrming preserved respiratory phasicity of venous return in the common
178
Chapter 3 · Extremity Veins
femoral, supercial femoral, and deep femoral veins near
their terminations and in the popliteal vein.
In addition, if DVT is diagnosed, the abnormal ndings
should be documented (incompressible venous segments) in
transverse images obtained with and without compression or
3
waveforms obtained in longitudinal orientation and showing
absence of ow or an abnormal ow prole. If color duplex
images are stored to document absence of ow, the images must
contain information to the eect that adequate instrument settings including a low PRF and adequate gain were used.
3.1.4.2 Chronic Venous Insuciency
andVaricosis
When ultrasound is performed for varicosis or postthrombotic syndrome, documentation should include longitudinal
B-mode images (optionally supplemented by color duplex
images) with corresponding waveforms from the common,
supercial and deep femoral veins and the popliteal vein.
For the common and supercial femoral veins and for
the great saphenous vein (near its termination), longitudinal
scans with the corresponding Doppler spectra during normal
breathing and Valsalva’s maneuver are required. Terminal
valve function of the popliteal vein and the small saphenous
vein is documented on longitudinal scans with the corresponding Doppler spectra obtained during compression and
release. Color duplex scans alone are inadequate for documenting reux because the duration must be quantied to
dierentiate abnormal reux from the short backward ow
that is normal before valve closure.
3.1.5 Clinical Role ofDuplex Ultrasound
3.1.5.1 Thrombosis andPostthrombotic
Syndrome
3.1.5.1.1 Leg Vein Thrombosis
e incidence of deep vein thrombosis (DVT) of the legs
is 1–2‰ per year and increases with age. Various noninvasive diagnostic tests were developed for the diagnosis of this
common condition, which oen takes an asymptomatic or
unspecic clinical course but has serious early (pulmonary
embolism) and late complications (chronic venous insufciency in about 50% of cases). e tests include plethysmography, thermography, iodine brin test, and Doppler
ultrasonography (Bollinger and Franzeck 1982; Hull etal.
1984; Kakkar 1972; Lepore etal. 1978; Neuerburg-Heusler
and Hennerici 1995; Sandler etal. 1984; Strandness 1977).
e methods are either very time consuming or yield reliable results only in certain venous segments. Continuous wave
(CW) Doppler ultrasound used to be the noninvasive modality
of rst choice in the diagnostic assessment of valvular incompetence of the supercial and deep veins and, as a functional
modality, showed good results at the pelvic and thigh levels
including popliteal artery thrombosis with reported accuracies of up to 90%. However, isolated venous thrombosis below
the knee and central thrombi surrounded by owing blood are
dicult to detect with CW Doppler. A review of 2060 patients
who underwent additional venography yielded a sensitivity of
84% and a specicity of 88% for CW Doppler ultrasound in
demonstrating venous thrombosis (Wheeler 1985).
Combining morphologic information (B-scan) and functional information (spectral Doppler), duplex ultrasound has
gained a central role as a noninvasive modality for venous
diagnosis.
Stasis is an important risk factor for the development of
DVT in addition to a hypercoagulable state and a damaged
vessel wall. us, immobilization plays a crucial role in the
pathogenesis of thrombosis of the deep veins, which primarily arises in the muscle veins in bedridden patients or patients
with cast immobilization of the leg. e risk of thrombosis
without heparin prophylaxis is 10–30% in general surgery
and as high as 54% in hip surgery (Lippert and Pabst 1985).
Venous thrombi are ascending in over 90% of cases and have
an annual incidence of 160/100,000 inhabitants in Germany
with pulmonary embolism occurring in 60/100,000 inhabitants per year. rombosis of the deep pelvic and leg veins is
the source of pulmonary embolism in over 90% of cases. e
importance of isolated venous thrombosis below the knee
should not be underestimated as it may extend cranially and
cause pulmonary embolism, though oen asymptomatic,
in 15–26% of cases (Kroegel 2003). In contrast, iliofemoral
thrombosis has a 56–85% incidence of pulmonary embolism.
e mortality of pulmonary embolism ranges from 0.1% to
5%, depending on the risk group (Polak 1992).
Data on the incidence of paraneoplastic thrombosis
vary with the study population investigated. For thrombosis
without apparent cause such as immobilization, incidences
of 10–34% have been reported in the literature (Silverstein
etal. 1998; Goldberg etal. 1987; Aderka etal. 1986; Monreal
etal. 1989). Recurrent thrombosis without an apparent cause
or thrombophlebitis without varicosis should prompt a
search for an underlying malignancy (Prandoni etal. 1992).
Pareneoplastic venous thrombi tend to be larger at the time
of diagnosis, grow more aggressively, and cause more severe
symptoms (Schulman etal. 2000).
Known risk factors include immobilization, trauma, pregnancy, intake of oral contraceptives, protein-C and protein- S
deciencies, factor V clotting disorder, hyperhomocysteinuria,
and lupus anticoagulant. In addition, an association with atherosclerosis has been proposed (Prandoni et al. 2003) since
inammatory processes play a role in both conditions.
Results on the
leg
are not very consistent. In a study of 1084 lower extremities with acute venous thrombosis, the thrombosis was localized above the knee in 51%, below the knee in 32%, and in
a supercial vein in 17% (Kerr etal. 1990). A venographic
study (Schmitt et al. 1977) of DVT showed concomitant
involvement of the common iliac vein in 16%, external iliac
vein in 33%, common femoral vein in 46%, deep femoral
vein in 45%, supercial femoral vein in 65%, popliteal vein in
66%, anterior tibial vein in 73%, posterior tibial vein in 82%,
and bular vein in 77%.
A study investigating 189 venograms in the early 1990s
(Cogo etal. 1993) identied isolated calf vein thrombosis in
18% of cases. e vast majority of the 82% of patients with
distribution of venous thrombosis in the
3.1 · Pelvic andLeg Veins
179
3
proximal vein thrombosis had popliteal vein involvement,
while only 8% were found to have isolated pelvic vein thrombosis. No case of isolated thrombosis of the supercial femoral vein was reported in this study.
e generous use of diagnostic ultrasound in patients
with clinically suspected DVT can help reduce the incidence
of thrombosis of the pelvic and femoral veins.
e results of a retrospective analysis of DVT distribution
performed by the author in a patient population with 18%
thrombosis prevalence in 2008 conrm that, with generous
use of ultrasound, most patients are identied when thrombosis is still conned to the veins below the knee (indication
for sonography: swelling of the leg or calf pain for which no
other cause was apparent). e analysis included a total of 280
cases of DVT of the legs. Isolated DVT below the knee was
present in 63% of cases (including 8% isolated calf muscle
vein thrombosis), 23% had extension to the popliteal vein and
11% involvement of the femoral and popliteal vein, while only
3% of patients had isolated or concomitant pelvic vein thrombosis. With one exception, isolated pelvic vein thrombosis
extended down to the level of the saphenofemoral junction.
ere was one case of isolated supercial femoral vein thrombosis, which was seen in a patient with duplication of this vein.
In 1.5% of patients, a muscle vein (soleus or gastrocnemius)
was the site of origin of popliteal vein thrombosis, as thrombosis was absent in the other major calf veins. rombosis
of the deep femoral vein with thrombus extension into the
common femoral vein accounted for 0.7% of cases.
e high proportion of isolated calf vein thrombosis in
this population may be attributable to the fact that symptoms indicative of thrombosis following trauma or surgery
of the leg prompted a sonographic examination in all cases,
frequently revealing calf vein thrombosis (in particular of the
bular vein or muscle veins).
Also contributing to this distribution is the policy of early
diagnosis and treatment of DVT of the legs pursued by the
ultrasound laboratory at the author’s institution. is helps
reduce the number of cases with thrombosis of the popliteal and distal supercial femoral veins, which always arise
from ascending calf thrombosis. Our observations therefore
underscore the need for always including the calf veins when
examining patients for vein thrombosis.
Most thrombi arise in the venous sinusoids of the lower
leg muscles or in regions of relatively stagnant blood ow
behind the pocket-like valves of the popliteal and femoral veins (. Figs.3.12a and 3.60 (Atlas)). In the majority of
patients, DVT of the legs develops in the valves of the calf
muscle veins (soleus or gastrocnemius veins) (>50%) or in the
valves of the bular vein. Recirculation in the cusps induces
platelet activation and the release of procoagulant substances, which may lead to the formation of a red thrombus.
It is estimated that 20–30% of such thrombi undergo spontaneous thrombolysis through the simultaneous activation of
the brinolytic system and that approx. 50% of the thrombi
become organized and thus remain clinically asymptomatic.
Approx. 20–30%, however, exhibit appositional growth with
extension into the deep venous system, and from there may
continue to grow cranially. With further growth in the major
deep veins, a thrombus may become free-oating and lead to
pulmonary embolism without causing any severe local clinical symptoms such as swelling or pain. Local clinical symptoms leading to the initiation of diagnostic measures may
thus not occur– unless a thrombus occludes a main vein or
interferes with blood ow by protruding from a muscle or
supercial vein into a major deep vein (see
. Figs.3.61, 3.62,
and 3.63 (all Atlas)).
Depending on ow in the partially thrombosed tributary vein and the ow obstruction caused by the growing
thrombus in the main vein, further growth is ascending or
descending
a
b
. Fig. 3.12 a Turbulent ow and eddy currents in the pocket-like
valves can lead to local stasis with release of procoagulant substances.
b Diagram of a thrombus (left) extending from a tributary (e.g., calf
muscle vein) into the main vein, where it can ascend (center) or
descend (right)
(. Fig. 3.12b). Descending venous thrombosis
180
f
ab
Suprapubic pudendal
Chapter 3 · Extremity Veins
. Fig. 3.13 a Venous
blood ow in thrombotic
femoral vein occlusion
with venous return from
the periphery occurring
primarily through the
3
great saphenous vein
(indicated by arrows).
b Collateral pathways in
descending (isolated)
pelvic vein thrombosis:
suprapubic pudendal and
epigastric collaterals (see
. Figs.3.48 and 3.61
(both Atlas))
Deep
emoral
vein
Iliac vein
Thrombus tail
surrounded
by blood flow
Great saphenous
vein serving
as collateral
Thrombotically
occluded superficial
femoral vein
Epigastric collateral
varices
Thrombotic pelvic
vein (iliac vein)
collateral varices
Great saphenous
vein
Superficial femoral
vein
is less common, and in primary pelvic vein thrombosis,
it is twice as common on the le side. is is attributed to
a pelvic vein spur, a connective tissue structure producing
chronic wall trauma with luminal narrowing, as the vein is
compressed against the spur by the pulsation of the common
iliac artery. e spur is dicult to detect on imaging.
In patients with complete thrombotic occlusion of
the deep leg veins
, blood drains through supercial veins,
chiey the great saphenous vein. e increased blood ow
from the great saphenous vein stops the growth of most
ascending thrombi at the saphenofemoral junction. In the
supercial femoral vein, blood from the deep femoral vein
stops ascending thrombus growth or surrounds a thrombus
extending more proximally (. Fig.3.13a).
In isolated descending pelvic vein thrombosis, the blood
is drained through epigastric collaterals or suprapubic
pudendal veins (. Fig.3.13b). Sonographically, this collateralization is identied by reux in the saphenofemoral junction (see
. Fig.3.45 (Atlas)).
e incidence of early DVT of the legs is much higher
than suspected on clinical grounds due to its fairly asymptomatic course. ere is a risk of serious early (pulmonary
embolism) and late complications (chronic venous insuciency with crural ulceration). For these reasons, diagnostic
tests to detect DVT of the legs should be used liberally
even when patients present with unspecic symptoms. is
is underscored by the fact that ultrasound oers an inexpensive, noninvasive, and accurate diagnostic modality for the
evaluation of these patients and that anticoagulation treatment can eectively reduce the risk of pulmonary embolism
and prevent further thrombus growth.
Ultrasound has the advantage of “illuminating the
blind spots” of venography. In the elderly, stasis due to degenerative ectasia of gastrocnemius and soleus veins is a common source of ascending thrombosis. For technical reasons
(valve function), this form of calf muscle vein thrombosis
and the less common deep femoral vein thrombosis cannot
be identied by venography; these veins are not opacied or
take up the contrast medium only through retrograde ow.
Sonographic data suggest that ascending thrombophlebitis
with thrombus extension from muscle or perforating veins
into the deep venous system is a much more common cause
of DVT than assumed in the past.
e bular vein is a typical source of error in venography, as nonvisualization of this vein may indicate the presence of thrombus, or it may simply be due to limitations of
the method. At the same time, the bular vein is the most
common site of isolated venous thrombosis of the calf with
ascending thrombus growth. In an analysis of 105 cases of
isolated venous thrombosis of the lower leg (without popliteal vein involvement) by our group, the bular vein alone
was aected in 48 instances, the posterior tibial vein in 36,
and both veins in 21. Only one case of anterior tibial vein
thrombosis, attributable to a large traumatic hematoma of
the anterior compartment, was seen. Spontaneous thrombo-
,
sis of the anterior tibial vein is always caused by descending
thrombus growth from the popliteal vein.
So tissue lesions such as abscess, hematoma, or perforated Baker’s cyst cause similar clinical symptoms but usually
have distinct sonographic features allowing them to be differentiated from deep vein thrombosis or to be conrmed by
ultrasound-guided biopsy.
With most venous thromboses starting to develop below
Thrombus Organization and Recanalization
the knee, assessment of the major calf veins and of the muscle
veins in this territory is an integral part of diagnostic sonography in these patients.
z
rombus organization begins on day 3 or 4 with attachment
to the venous wall, and ingrowth of capillaries occurs aer
Edema
3.1 · Pelvic andLeg Veins
181
3
8–12days (Leu 1973). At the end of the rst week, lipoblasts
and brocytes start to induce the formation of collagen brils
that ll the hollow and intercapillary spaces le aer liquefaction and absorption (Rotter 1981). As cellular inltration is
an ongoing process, a thrombus is composed of layers reecting the dierent stages of development. Further organization
is associated with shrinkage of the vein, which can be seen
with ultrasound. Hemolysis with partial degradation of brin
occurs aer days to weeks.
e duration of thrombus organization depends on the
vessel diameter and intraluminal pressure and may additionally be aected by external factors such as application of
compression bandages. Attachment of the thrombus to the
wall by collagen bers will invariably have occurred by day
8–10. rombolytic therapy (e.g., streptokinase) performed
at this time or later will recanalize the vessel but cannot
prevent venous valve destruction in most cases. When surgical thrombectomy is performed at this stage, only central
thrombus portions can be removed, while mural residues
remain and may give rise to the postoperative development
of recurrent thrombi through appositional growth. Residual
thrombotic material near valves induces valve incompetence.
Late sequelae are calcications of the venous wall.
Complete thrombus organization can transform supercial and small veins into strands of brous scar tissue. In
most cases, however, there will be recanalization of the
lumen through the ingrowth of capillaries. e latter dilate
and become merged, thereby re-establishing patency over a
course of several months. However, recanalization is associated with shrinkage and destruction of the valves as well
as brosis and thickening of the wall. e main mechanism
involved in the recanalization of a thrombosed vein is the
high brinolytic potential of the venous wall.
Collateralization and recanalization following acute DVT
lead to the more or less complete reconstitution of venous
drainage. Long segments of an occluded vein are recanalized
in most cases (endogenous thrombolysis). Recanalization is a
highly variable process: it may begin aer 3–4weeks in small
vessels and may take 3–9months in large veins such as the
popliteal and femoral veins. e patency of a deep vein is reestablished 3months aer the onset of thrombosis in about
half of all cases (Killewich etal. 1989).
Venographic studies show that, within 1year, complete
recanalization occurs in up to 35% of all venous thromboses
and partial recanalization in another 55%, with only 10% of
patients showing persistent occlusion. e clinical severity of
the postthrombotic syndrome mainly depends on the degree
of valve incompetence, in particular of the popliteal vein,
while a persisting lumen reduction aer thrombosis has only
a minor eect. Insucient venous return is further compromised by secondary damage (widening with subsequent
valve incompetence) to supercial and perforating veins
resulting from the higher pressure and volume overload due
to collateral ow (secondary varicosis).
Anticoagulation and compression therapy are major
components in the management of thrombosis. e latter serves to limit the extent of progressive dilatation of the
collateral veins induced by the increased outow resistance,
in particular during the rst 3months.
3.1.5.1.2 Chronic Venous Insuciency/
Postthrombotic Syndrome
Chronic venous insuciency (disturbed venous return from
peripheral veins) can have the following causes:
5 Obstruction of deep veins
5 Valve incompetence of deep veins
5 Valve incompetence of supercial veins
5 Valve incompetence of perforating veins
5 Calf muscle pump dysfunction (. Fig.3.14)
e supercial system (varicosis) and deep system (chronic
venous incompetence) may develop secondary changes in
Valve incompetence
Increased venous and
capillary pressure
Increased
permeability
Overload of
lymphatic
vessels
. Fig. 3.14 Diagram of the pathophysiological changes occurring in
chronic venous incompetence. The drawing represents the supercial
venous system on the left and the deep system on the right. When
there is valve dysfunction in a major deep vein, the calf muscle pump
(compression of the veins) fails to propel the blood toward the center
(centripetal), resulting in at least partial reversal of ow toward the
periphery (centrifugal). The ensuing recirculation via incompetent
perforators and dilated varicose supercial veins further contributes
to inecient drainage. The increase in venous and capillary pressure
results in a higher uid inltration and permeability of the damaged
capillary wall. Interstitial edema in turn can lead to an overload of the
lymphatic system, causing lymphatic microangiopathy in severe cases.
Extensive and partially indurated edema in severe chronic venous
insuciency is not due to insucient venous drainage alone but
mainly to secondary lymphatic drainage insuciency (According to
Rieger and Schoop 1998)
182
Normal
AB CD E
III III IV
Chapter 3 · Extremity Veins
response to disease of the respective other system. ese
secondary changes result from the compensatory increase in
pressure and volume and may worsen the state of the already
compromised venous return.
e morphologic features associated with the postthrom-
3
botic syndrome can be demonstrated in part by B-mode
ultrasound but above all by venography. e functional
parameters reecting the severity of reux are reliably determined by duplex ultrasound and play a crucial role in planning treatment (type, extent, and duration of compression
therapy).
Ultrasound also has an important role in documenting
the status of the venous system aer completion of anticoagulant treatment to serve as a baseline in case a patient later
3.1.5.2 Varicosis
Varicosis of the great or small saphenous vein is caused by
valve incompetence. In the primary form this is due to constitutional or external factors. In secondary varicosis, on the
other hand, the valves of the supercial system fail due to
pressure and volume overload resulting from disease (e.g.,
thrombosis) of the deep venous system. Causes of valve
incompetence are:
5 Destruction (postthrombotic)
5 Dilatation with incomplete coaptation
5 Weakness of the venous wall (acquired, congenital)
5 Pressure overload
5 Volume overload (secondary, varicosis)
5 Anomalies
develops symptoms suggesting recurrent thrombosis. Recent
data suggest that patients have an up to 8% risk of recurrence
during the rst months aer the end of anticoagulant treatment and a cumulative 5-year risk of 30%.
Other causes of calf swelling besides acute thrombosis
and chronic venous insuciency include edema of dierent
etiology (cardiac, lymphedema, lipedema). Aer exclusion
of thrombosis and incompetent valves by duplex imaging,
sonography can also provide important clues for dierentiating lymphedema and lipedema. Lymphedema is characterized by the presence of primarily longitudinal, anechoic
cles (due to uid collections) in the thickened subcutaneous
tissue, while in lipedema such cles are absent, and the subcutaneous layer appears rather uniform.
Four grades of varicosis of the great saphenous vein are distinguished according to Hach, depending on the length of
involvement from its termination to its origin (. Fig.3.15).
Grade I is varicosis of the terminal valve, grade II extension to the distal thigh, grade III to the proximal calf, and
grade IV complete incompetence of the vein down to the
ankle.
Primary supercial varicosis can in turn lead to pressure
and volume overload of the deep venous system with sec-
ondary damage
resulting from the formation of pathways of
venous reux. In this situation, the blood draining through
the deep veins reaches a proximal point of insuciency in
the supercial system (typically the terminal valve of the
. Fig. 3.15 Grades of truncal
varicosis of the great saphenous
vein according to Hach: A Normal
blood ow toward the heart in
the great saphenous vein.
B Grade I: incompetent terminal
valve of great saphenous vein,
possibly with concomitant lateral
branch varicosis of accessory
veins. C Grade II: varicosis of great
saphenous vein in upper leg,
possibly with concomitant lateral
branch varicosis. D Grade III:
varicosis of great saphenous vein
extending to proximal lower leg,
possibly with concomitant varicosis of anterior or posterior tributary vein of lower leg. E Grade IV:
varicosis of great saphenous vein
extending down to ankle region
with more or less severe lateral
branch varicosis
F
G
A
ab
3.1 · Pelvic andLeg Veins
183
3
of distal valves (peripheral varicosis, grading according to
D
Hach,
. Fig.3.15).
In incomplete varicosis of the great saphenous vein,
D
C
A
the proximal valves initially tend to be competent, while the
rst dysfunctional valve (i.e., the proximal point of insuf-
ciency
) is more distal. Below this point, the valves of the
great saphenous vein are incompetent. In incomplete vari-
I
cosis, the insucient junction between the supercial and
H
the deep venous system may involve the perforating veins,
a branch of the great saphenous vein, or both. Incompetence
of one or more perforating veins is the most common form.
C
E
In this case, some of the blood entering the supercial system
through the incompetent perforator ows into the distal portion of the great saphenous vein below this junction to then
re-enter the deep system through a distal perforator.
B
B
K
In the second type, a varicose branch is responsible
for reux between the deep venous system and the proximal point of incompetence of the great saphenous vein
(
. Fig.3.16b). In most cases (55%), the incompetent branch
is the lateral accessory saphenous vein (anterior variant);
less commonly it is the medial accessory saphenous vein. In
the posterior variant, the medial accessory saphenous vein
establishes an incompetent venous communication with the
proximal small saphenous vein via the femoropopliteal vein
(Giacomini anastomosis). In this form of incomplete distal
great saphenous vein varicosis, the incompetent Giacomini
. Fig. 3.16 a Diagram of the recirculation pathway in supercial
venous insuciency. Part of the blood draining toward the heart in
the deep venous system (A) ows back to the periphery through an
incompetent terminal valve (D) or through incompetent supercial veins
(great or small saphenous vein; B). The blood is then recirculated from the
supercial to the deep venous system via perforating veins (C), resulting
in volume overload of the deep (A) leg veins (according to Rieger and
Schoop 1998). b Diagram of the dierent forms of incomplete varicosis of
the great saphenous vein (red: lateral branch type, anterior variant; blue:
perforator type; green: lateral branch type, posterior variant). A femoral
vein; B popliteal vein; C competent (intact) proximal portion of the great
saphenous vein; D terminal valve of great saphenous vein; E, F varicose
segments of the great saphenous vein in the distal thigh and lower leg;
G small saphenous vein; H lateral accessory saphenous vein; I Dodd perforator (incompetent); K medial accessory saphenous vein and Giacomini
anastomosis (reux through an incompetent connection between the
small saphenous vein, femoropopliteal vein, medial accessory saphenous
vein, and great saphenous vein). The proximal point of insuciency is the
transition from the competent to the incompetent great saphenous vein
segment (arrows) (see . Figs.3.77 and 3.80 (both Atlas))
anastomosis connects the great and small saphenous veins.
Careful sonographic evaluation of the extent of varicosis with identication of the upper and lower points of
insuciency, secondary involvement of the deep venous
system, and the presence of recirculation pathways is crucial for selecting the most suitable treatment (obliteration,
surgery, compression) (see summary of the components of
a comprehensive sonographic evaluation at the end of this
section and . Table3.6). Surgery is performed to remove
the insucient portion of the aected deep vein between
the upper and lower insuciency points, sparing uninvolved venous segments for later arterial reconstruction.
Incompetent supercial segments and perforating veins
will invariably lead to recurrent varicosis if they are not
removed. is is why precise determination of the distal
point of insuciency and the identication of insucient
perforating veins is crucial for successful surgical management. Duplex ultrasound is the method of choice and gold
great saphenous vein) and then ows back down to the distal point of insuciency (dened as the highest competent
valve or the deepest incompetent valve). At this point, the
blood ows back into the deep system and toward the heart
(. Fig.3.16a). e resulting overload of the perforating and
deep veins induces secondary valve incompetence in these
veins. When the deep vein valves are competent, this condition is referred to as compensated recirculation and when
they become incompetent as decompensated recirculation.
Complete truncal varicosis of the great saphenous vein is
characterized by reux in the saphenofemoral junction (i.e.,
the terminal valve of the great saphenous vein is incompetent). e ensuing pressure buildup causes secondary failure
standard for this indication.
rombophlebitis is a typical complication of varicosis
and is diagnosed by B-mode sonography using the same
criteria as in the assessment of DVT.Since thrombophlebitis oen extends beyond its clinically apparent boundaries,
identication of the proximal thrombus end by imaging is
clinically relevant to rule out involvement of the deep system.
Moreover, further progression of thrombophlebitis into
the deep system must be prevented by high ligation of the
saphenofemoral junction in cases where the disease process
already extends close to the deep veins. Alternatively, transient anticoagulation in combination with local symptomatic
measures can be performed to prevent further progression.