Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5760_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •Preface to the Third English and Fourth German Edition
- •Preface to the Second English and Third German Edition
- •Preface to the First English Edition
- •Preface to the Second German Edition
- •Preface to the First German Edition
- •Contents
- •1: Fundamental Principles
- •1.1.1.2 Sound Waves
- •1.1.1.3 Generating Ultrasound Waves
- •1.1.1.4.3 Interference
- •1.1.1.5.1 Pulse-Echo Technique
- •1.1.1.5.2 Time Gain Compensation
- •1.1.1.5.3 A-Mode
- •1.1.1.5.4 B-Mode
- •1.1.1.5.5 M-Mode
- •1.1.1.6 Resolution
- •1.1.1.7 Beam Focusing
- •1.1.1.8.2 Linear Arrays
- •1.1.1.8.3 Curved or Convex Arrays
- •1.1.1.8.4 Sector Scanners
- •1.1.1.8.5 Phased Arrays
- •1.1.1.8.6 Mechanical Sector Scanners
- •1.1.1.8.7 Annular Phased Arrays
- •1.1.1.9 Ultrasound Artifacts
- •1.1.1.9.1 Posterior Shadowing
- •1.1.1.9.2 Acoustic Enhancement
- •1.1.1 Gray-Scale Ultrasonography (B-Mode)
- •1.1.1.1 Historical Milestones
- •1.1.1.9.4 Side Lobes
- •1.1.1.9.5 Reverberation Artifact
- •1.1.1.9.6 Geometric Distortion
- •1.1.2.1 Continuous Wave Doppler Ultrasound
- •1.1.2.3 Frequency Processing
- •1.1.2.4 Blood Flow Measurement
- •1.1.3.1 Velocity Mode
- •1.1.3.2 Power Doppler Mode
- •1.1.3.3 B-Flow Mode (Brightness Flow)
- •1.1.3.4 Intravascular Ultrasound
- •1.1.4.2 Mirror Artifact
- •1.1.4.6 Doppler Angle
- •1.1.5 Ultrasound Contrast Agents
- •1.1.5.3.1 Contrast-Enhanced Duplex Ultrasound
- •1.1.5.3.2 Contrast Harmonic Imaging
- •1.1.5.3.3 Stimulated Acoustic Emission Imaging
- •1.1.6.3.1 B-Mode
- •1.1.6.3.2 M-Mode
- •1.1.6.3.3 CW Doppler
- •1.1.6.3.4 PW Doppler
- •1.1.6.3.5 Color Doppler
- •1.1.6.4 Conclusion
- •1.2 Hemodynamic Principles
- •1.2.1 Laminar Flow
- •1.2.2.1 Low-Resistance Flow
- •1.2.2.2 High-Resistance Flow
- •1.2.2.3 Perfusion Regulation
- •1.2.3.1 Poststenotic Parameters
- •1.3 Machine Settings
- •2: Extremity Arteries
- •2.1.1 Vascular Anatomy
- •2.1.1.1 Pelvic Arteries
- •2.1.1.2 Leg Arteries
- •2.1.2.1 Pelvic Arteries
- •2.1.2.2 Leg Arteries
- •2.1.6 Abnormal Findings
- •2.1.6.1 Atherosclerotic Occlusive Disease
- •2.1.6.1.1 Pelvic Arteries
- •2.1.6.1.3 Stenosis Grading
- •2.1.6.1.4 Leg Arteries
- •2.1.6.1.9 Profunda Femoris Artery
- •2.1.6.1.13 Multilevel Obstruction
- •2.1.6.1.14 Arterial Occlusion
- •2.1.6.2 Arterial Embolism
- •2.1.6.3 Aneurysm
- •2.1.6.3.1 True Aneurysm
- •2.1.6.3.2 Pseudoaneurysm
- •2.1.6.4.1 Adventitial Cystic Disease
- •2.1.6.4.2 Popliteal Artery Entrapment Syndrome
- •2.1.6.4.3 Raynaud’s Disease
- •2.1.6.4.5 Buerger’s Disease
- •2.1.6.4.7 Dissection
- •2.1.6.4.8 Arteriovenous Fistulas
- •2.1.7.1 Thromboendarterectomy
- •2.1.7.3 Bypass Graft Surveillance
- •2.2 Arm Arteries
- •2.2.1 Vascular Anatomy
- •2.2.3.1 Atherosclerosis
- •2.2.3.2 Vascular Compression Syndromes
- •2.2.4 Documentation
- •2.2.5 Normal Findings
- •2.2.6.1 Atherosclerosis
- •2.2.6.2 Vascular Compression Syndromes
- •2.2.6.4 Buerger’s Disease
- •2.2.6.5 Raynaud’s Disease
- •2.3 Atlas: Extremity Arteries
- •3.1.2.1.2 Patient Positioning
- •3.1.2.1.3 Examination Technique
- •3: Extremity Veins
- •3.1.1 Vascular Anatomy
- •3.1.2 Examination Protocol
- •3.1.2.1 Thrombosis
- •3.1.2.1.1 Equipment
- •3.1.3 Normal Findings
- •3.1.4 Documentation
- •3.1.5.1.1 Leg Vein Thrombosis
- •3.1.5.2 Varicosis
- •3.1.6.1 Thrombosis
- •3.1.6.1.3 Pulmonary Embolism
- •3.1.6.1.5 Thrombus Age
- •3.1.6.1.6 Recurrent Thrombosis
- •3.1.6.3 Varicosis
- •3.1.6.3.1 Treatment Options
- •3.1.6.4 Varicophlebitis
- •3.1.7 Rare Venous Disorders
- •3.1.7.1 Venous Aneurysm
- •3.1.7.1.1 Sonographic Workup
- •3.1.7.3 Venous Compression
- •3.1.7.4 Venous Adventitial Cystic Disease
- •3.1.8 Vein Mapping
- •3.1.9.1 Deep Vein Thrombosis
- •3.1.9.1.1 Ultrasound Versus Venography
- •3.1.9.3 Varicosis
- •3.2.1 Vascular Anatomy
- •3.2.3 Normal Findings
- •3.2.4 Documentation
- •3.2.5 Clinical Role
- •3.3 Atlas: Extremity Veins
- •4: Arteriovenous Fistulas
- •4.1.1 Background
- •4.2.2 Hemodialysis AV Fistula
- •4.5 Documentation
- •4.7 Hemodialysis Access Complications
- •4.7.1 Hemodialysis Access Stenosis
- •4.7.1.3 Proximal Feeding Artery Stenosis
- •4.7.2.1 Peripheral Ischemia
- •4.7.2.2 Hemodialysis Access Aneurysm
- •4.7.2.3 Inadequate or Excessive Fistula Flow
- •4.7.2.4 Arm Swelling
- •4.8.1 Therapeutic Decision-Making
- •4.8.2 Surveillance Programs?
- •4.9 Atlas: Arteriovenous Fistulas
- •5: Extracranial Cerebral Arteries
- •5.1.1 Carotid Arteries
- •5.1.2 Vertebral Arteries
- •5.2.1 Carotid Arteries
- •5.2.2 Vertebral Arteries
- •5.3 Documentation
- •5.4 Normal Findings
- •5.4.1 Carotid Arteries
- •5.4.2 Vertebral Arteries
- •5.5.1 Carotid Arteries
- •5.5.1.1 Stenosis Grading
- •5.5.1.2 Plaque Morphology
- •5.5.2 Vertebral Arteries
- •5.6.1 Carotid Arteries
- •5.6.1.1.1 Intima-Media Thickness
- •5.6.1.1.2 Plaque Features
- •5.6.1.1.4 Plaque Thickness
- •5.6.1.1.5 Plaque Morphology: Plaque Surface
- •5.6.1.3 Occlusion
- •5.6.1.3.1 Persistent Primitive Hypoglossal Artery
- •5.6.1.4 Postoperative Follow-Up
- •5.6.1.4.1 Carotid Endarterectomy (CEA)
- •5.6.1.4.2 Carotid Artery Stenting (CAS)
- •5.6.1.4.5 Stent Dislocation
- •5.6.2 Vertebral Arteries
- •5.6.2.1 Stenosis
- •5.6.2.2 Occlusion
- •5.6.2.3 Dissection
- •5.6.2.4 Subclavian Steal Syndrome
- •5.8.1 Dissection
- •5.8.2 Vasculitis
- •5.8.3 Fibromuscular Dysplasia
- •5.8.4 Aneurysm
- •5.8.5 Arteriovenous Fistula
- •5.8.6 Idiopathic Carotidynia
- •5.8.7 Vasospasm
- •5.10 Atlas: Extracranial Cerebral Arteries
- •6.1.1 Vascular Anatomy
- •6.1.1.1 Aorta
- •6.1.1.2 Visceral Arteries
- •6.1.1.3 Renal Arteries
- •6.1.2.1 Aorta
- •6.1.2.2 Visceral Arteries
- •6.1.2.3 Renal Arteries
- •6.1.2.3.1 Ultrasound Technique
- •6.1.3 Normal Findings
- •6.1.3.1 Aorta
- •6.1.3.2 Visceral Arteries
- •6.1.3.3 Renal Arteries
- •6.1.5.1 Aorta
- •6.1.5.1.1 Abdominal Aortic Aneurysm
- •6.1.5.2 Visceral Arteries
- •6.1.5.3 Renal Arteries
- •6.1.6.1 Renal Arteries
- •6.1.6.1.2 Therapy-Oriented Stenosis Grading
- •6.1.6.1.3 Contrast-Enhanced Ultrasound (CEUS)
- •6.1.6.1.5 Diagnostic Algorithm
- •6.1.6.1.6 Renal Artery Occlusion
- •6.1.6.1.7 Transplant Kidney
- •6.1.6.2 Visceral Arteries
- •6.1.6.2.1 Celiac Trunk
- •6.1.6.2.2 Visceral Artery Aneurysm
- •6.1.6.2.3 Dissection
- •6.1.6.2.4 Superior Mesenteric Artery
- •6.1.6.2.5 Acute Mesenteric Artery Occlusion
- •6.1.6.3 Aorta
- •6.1.6.3.2 Abdominal Aortic Aneurysm
- •6.1.6.3.6 Aortic Dissection
- •6.2.1 Vascular Anatomy
- •6.2.1.1 Vena Cava
- •6.2.1.2 Renal Veins
- •6.2.2 Examination Technique
- •6.2.2.1 Vena Cava
- •6.2.2.2 Renal Veins
- •6.2.3.1 Renal Veins
- •6.2.3.2 Portal Venous System
- •6.2.4 Normal Findings
- •6.2.4.2 Portal Venous System
- •6.2.5 Documentation
- •6.2.6.1 Vena Cava
- •6.2.6.1.1 Membranous Vena Cava Obstruction
- •6.2.6.2 Renal Veins
- •6.2.6.3.1 Splenic Vein Thrombosis
- •6.2.6.4.1 Portal Vein Thrombosis
- •6.2.6.4.2 Portal Hypertension
- •6.2.6.4.3 Hepatic Veins

204
Chapter 3 · Extremity Veins
3
. Fig. 3.29 a Intraluminal synechia (. Fig.3.73 (Atlas)) seen as hyperechoic reections from the lumen. Such strands obstruct ow and can cause
severe valve incompetence by adhering to valve cusps. b A time-motion scan obtained with the ultrasound beam through the valve leaets allows good
evaluation of valve motion: the leaets (VK) are open and close to the wall during expiration (E), and they are closed during inspiration (I) as a result of the
increased intra-abdominal pressure, preventing reux of the venous blood (closed leaets seen in the center of the lumen). c Imaging during Valsalva’s
maneuver demonstrates adequate valve closure (VK) in the supercial femoral vein (V.FEM.S), indicated by a short ow reversal (ow toward the periphery) just before valve closure and by cessation of reversed ow upon complete closure. d Postthrombotic damage, with sclerotic xation of the valve leaflets to the wall, results in failure of the valve (VK) to close and is indicated by persistent reux (ow away from transducer, toward the periphery) during
Valsalva’s maneuver. e In this patient, the corresponding time-motion scan shows failure of the damaged valve (VK) to close because of postthrombotic
adhesion to the wall and sclerotic rigidity (compare normal valve closure in b)
3.1.6.3 Varicosis
e variability of venous reux patterns makes it necessary
to establish the following data to identify candidates for varicose surgery and to select the most suitable approach and
extent of the operation (see 7 Sect. 3.1.5.2):
5 Terminal competence/incompetence of the great and
small saphenous veins
5 Proximal and distal points of insuciency in patients
with major vein insuciency (to spare adequate vein
segments for future bypass procedures)

ab c
3.1 · Pelvic andLeg Veins
. Table 3.5 Ultrasound ndings in patients with the
postthrombotic syndrome (see . Figs.3.23 and 3.27)
Ultrasound technique Sonographic criteria and ndings
205
3
B-mode imaging
(normal in 30–40% of
patients)
Color duplex imaging Degree of recanalization
Narrowing of vessel lumen
Blurred wall structure
Thickened wall
Wall sclerosis, intramural calcications
Intraluminal connective tissue
strands, synechia
Echogenic vessel lumen
Not fully compressible
Incompetence of major veins
Better visualization of wall sclerosis
and of postthrombotic wall lesions
Identication of collaterals
Incompetence of supercial veins
(secondary)
Perforator incompetence
5 Identication of incompetent perforators (to minimize
risk of recurrence) and status of the deep venous system
(Wong etal. 2003)
5 Exclusion of secondary, postthrombotic varicosis (pres-
ence of residual thrombi obstructing ow?)
5 Exclusion of arterial obstruction (risk of disturbed post-
operative wound healing)
Valve function of supercial veins is evaluated in the same
way as in the deep venous system, namely by spectal Doppler
imaging during provocative maneuvers. While ow reversal
is also seen in color ow images, only spectral Doppler permits accurate measurement of reux duration. Clinically, it
is important to identify the proximal extent of venous insufciency (. Fig. 3.16a). In complete varicosis of the great
saphenous vein, the proximal point is identied by repeated
Doppler sampling during Valsalva’s maneuver beginning at
the saphenofemoral junction. e vein is then followed down
the leg, repeating this test until the distal point of insuciency is identied (transition from reux to normal ow).
is point determines the grade of great saphenous vein
varicosis
according to Hach (. Figs.3.15, 3.16, and 3.32). In
Hach grades I to III, varicose side branches oen enter the
vein at the level of the distal point of insuciency.
A short reux (<0.3s) before valve closure is normal in
the main veins, while reux with backward ow persisting
for >0.5s is abnormal according to the criteria of the Union
Internationale de Phlébologie (UIP). Investigators meanwhile may advocate dierent cuto values for dierent vein
. Fig. 3.30a–c Development of chronic venous insuciency with
valvular incompetence of the deep veins secondary to truncal varicosity of the great saphenous vein. a Physiologic blood ow direction
in deep and supercial veins (red arrows). Perforating veins drain
the blood from the supercial to the deep venous system. b Truncal
varicosis of the great saphenous vein is associated with retrograde
ow through perforators back into the supercial venous system. This
hypercirculation (Trendelenburg private circulation) is compensated
as long as the valves of the deep veins remain competent, but it leads
to dilatation of supercial side branches and perforators as well as
volume overload of the deep veins. c Hypercirculation eventually
becomes decompensated as a result of volume overload, leading to
dilatation and subsequent valve failure of the deep veins. This valve
failure in turn leads to pressure-induced dilatation and secondary
valve incompetence of further perforating veins (Cockett’s, Boyd’s, and
Dodd’s perforating veins). Finally, the muscle pump becomes ineective, resulting in full-blown drainage insuciency
segments, with some regarding reux durations of up to 1s
as normal (Coleridge-Smith etal. 2006).
Clinically apparent varicose changes of the great saphenous
vein are oen restricted to the lower leg. Nevertheless, duplex
imaging frequently also reveals incompetence above the knee,
where dilatation of the great saphenous vein is less pronounced
due to the lower intravascular pressure. A study by our group
including 103 patients with great saphenous vein varicosis
demonstrated involvement of the saphenofemoral junction
in 66% of the patients with clinically normal ndings of the

206
Great saphenous vein
distal
b
distal
Chapter 3 · Extremity Veins
3
. Fig. 3.31 Patient with postthrombotic syndrome and extensive residual thrombus following an episode of acute three-level thrombosis. The
residual thrombus leaves only a narrow patent channel, resulting in ow obstruction with slower ow in the popliteal vein. In the valve function
test with manual compression and release of the calf, this is reected in a reduced blood ow velocity during compression (left color ow image
with red-coded ow) and less marked reux (in terms of duration and magnitude) upon release of compression (blue-coded ow in right image)
than expected in severe valve incompetence
segments can be spared in case they are required for future
bypass gra procedures.
Four main types of incomplete truncal varicosis are dis-
tinguished:
5 In incomplete varicosis of the perforator type with an
intact saphenofemoral junction, distal incompetence of
the great saphenous vein originates from an insucient
a
. Fig. 3.32 Valve incompetence of major supercial veins. Left draw-
ing: distal point of insuciency (a) with pressure-induced dilatation of
a side branch or perforating vein (varicose degeneration) joining the
main vein at this level. Normal vein segment with functioning valves
distal to this point. Right drawing: proximal point of insuciency (b).
Normal vein with competent valves proximal to the point of insuciency and valve incompetence distal to it
perforating vein, e.g., a Dodd vein in the upper leg (see
. Fig.3.80 (Atlas)).
5 In incomplete varicosis of the lateral branch type with
proximal competence, the distal great saphenous vein
varicosis is maintained by varicosis in a side branch, e.g.,
an insucient lateral accessory vein in the thigh (see
. Fig.3.77 (Atlas)).
5 In the posterior type, venous incompetence involves
the small saphenous vein and femoropopliteal vein,
from where it extends to the great saphenous vein via an
accessory branch of the latter (Giacomini anastomosis)
(see . Figs.3.16b and 3.65 (Atlas)).
5 Distal varicose lateral branches such as veins com-
municating between the great and small saphenous veins
can maintain secondary varicose changes of the distal
saphenous vein.
if clinical signs of varicosis are only apparent below the knee.
In patients who have undergone stripping of the great
saphenous vein, a remaining stump can be identied with
Valsalva’s maneuver, but several years aer surgery, it cannot
always be reliably dierentiated from neoreux or neovascularization (Turton etal. 1999).
In incomplete great saphenous vein varicosis, only the
distal valves are incompetent while the terminal and preterminal valves are intact. It is important, especially in incomplete great saphenous vein varicosis, to identify the upper
and lower points of insuciency so that competent vein
thigh. erefore, evaluation of the junction is mandatory even
Preoperative identication of the upper point of insuciency in distal varicosis by duplex imaging is important to
ensure complete surgical removal of the incompetent vein
segments, thereby preventing recurrence and sparing competent venous segments for possible later bypass procedures.
e dilated varicose segments are identied in the standing
patient, followed to the point of insuciency, and marked
on the skin. Surgeons will benet most from real-time sonographic evaluation of venous morphology and function if
they perform the examination themselves.
In incomplete distal great saphenous insufficiency, the
Valsalva test yields no valid results because the proximal

3.1 · Pelvic andLeg Veins
207
3
valves still function properly. Instead, thecompressionand- release test is performed with the patient standing. The incompetent great saphenous vein depicted by
B-mode ultrasound is followed upward to identify the
proximal point of insufficiency for tailoring the surgical
procedure. Divisions into arch veins can thus be identified by duplex imaging as well and evaluated for incompetent valves. The ultrasound examination thus enables
accurate identification of all incompetent venous segments prior to surgery.
e examination should include the perforating veins,
which can be identied in their typical locations (Cockett’s,
Boyd’s, and Dodd’s perforators). Perforator competence
is evaluated by duplex ultrasound using the compressionand- release test in the standing patient. Evaluation may be
easier when a tourniquet is applied to stop blood ow in the
supercial veins. Identication of incompetent perforators is
important in order to eliminate them as potential sources of
recurrent varicosis (
Perforator incompetence is suggested by reux from the
deep into the supercial veins in the compression-and- release
test (. Fig.3.11). Incompetent perforating veins arising from
the great saphenous vein below the knee are identied by
B-mode imaging as slightly tortuous, tubular structures
coursing to the posterior tibial vein territory in the transfascial compartment (see . Fig.3.79 (Atlas)). Competent perforating veins are usually so small that they will not be detected
unless a thorough search is done with a high- resolution
transducer and the patient in the standing position.
In a comparative study, 95.5% of a total of 252 incompetent perforating veins diagnosed by color duplex ultrasound
were conrmed intraoperatively. In comparison, venography
identied only 65% of these incompetent perforating veins
(Stiegler etal. 1994). e accuracy of palpation alone is 49%
and that of CW Doppler 75%.
e ultrasound examination for incompetence of the
small saphenous vein
standing. If the deep veins are still competent, however, insufciency can only be evaluated by using the compression- andrelease test and not the Valsalva maneuver, unless there is
simultaneous valve incompetence of the femoral and popliteal veins (
able saphenopopliteal junction, spectral Doppler is obtained
while performing the compression test using the other hand
or a cu to compress the vein distal to the transducer. e
course of the small saphenous vein is then traced downward with repeated compression to identify the distal point
of insuciency. Valve incompetence is suggested by dilatation– primarily in the popliteal fossa– and a tortuous course
resulting from elongation of the vein.
the preoperative workup to rule out secondary postthrombotic major vein insuciency. e latter is a contraindication to surgery because interruption of collateral pathways
(involving the great saphenous vein) would result in further
deterioration in patients with existing postthrombotic ow
obstruction due to occlusive residual thrombi.
. Fig.3.33). Aer identication of the highly vari-
It is very important to include the deep venous system in
. Figs.3.10 and 3.33).
is also performed with the patient
3.1.6.3.1 Treatment Options
During endovenous interventions, such as radiofrequency
ablation or intravascular laser therapy, ultrasound is used to
monitor correct positioning of intraluminal probes. In foam
sclerotherapy, ultrasound allows real-time monitoring of the
spread of the sclerosant, and foam migration into the deep
venous system can be prevented by compressing the terminal
portion of the vein being treated.
In endovenous radiofrequency ablation, the introducer
sheath is advanced from a distal access using ultrasound guidance and placed in the great saphenous vein just below the
site of entry of the supercial epigastric vein (see . Fig.3.82
(Atlas)) to prevent occlusion of this vein during treatment.
Ultrasound enables good visualization of the supercial
epigastric vein in this area as it extends cranially from the
saphenofemoral junction. e saphenous side branches arising more distally, in particular the lateral and medial accessory veins, will be obliterated by the thermal energy applied
during radiofrequency ablation. e intervention is performed under tumescent anesthesia, which is applied under
sonographic guidance and serves to compress the target vein,
thereby ensuring a good energy transfer to the vein wall, and
also to protect the surrounding structures from heat damage.
Tumescent anesthesia is performed by injecting tumescent uid (modied Klein’s solution) around the vein once the
catheter is in place. is is done under ultrasound guidance
and serves to create a circumferential uid layer of 4–5mm
around the vein and compress it (target diameter for the great
saphenous vein: 4–6 mm) (see . Fig. 3.82 (Atlas)). ese
conditions have been shown to ensure nearly pain-free endovascular laser treatment. Although the tumescent solution
spreads within the saphenous compartment, it is necessary to
inject the uid along the course of the vein every few centimeters, starting proximally and using ultrasound for guidance.
Duplex ultrasound has an important role in identifying contraindications to endovenous ablation treatment
(laser or radiofrequency) or conditions requiring a modi-
ed approach
5 Chronic or acute phlebitis, which may hinder advance-
ment of the ablation probe (see
(both Atlas))
5 Anatomic variants that preclude passage of the abla-
tion probe. The catheter used in the Venefit proce-
dure (formerly known as VNUS ClosureFast) has
a lumen allowing ultrasound-guided insertion of a
guidewire via a distal introducer sheath for advance-
ment of the radiofrequency probe to the sapheno-
femoral junction.
5 Identication of varicose veins that are too close to the
skin surface (to prevent skin burns, the distance should
be at least 1cm following injection of Klein’s solution)
5 Aneurysmal dilatation of the great saphenous vein
(>2.5cm).
Sonographic evaluation aer endovenous laser or radiofrequency ablation of the saphenous vein aims at ruling out
thermal damage and thrombosis of the common femoral
:
. Figs.3.65 and 3.80

208
Chapter 3 · Extremity Veins
. Fig. 3.33 a Valve incompe-
tence of a Boyd perforator in
the calf. The valve function test
reveals normal ow from the
supercial to the deep venous
system (leftmost image, blue-
3
coded ow) and ow reversal
upon release of compression
(rightmost image, red-coded
ow) (F=fascia, V.S=great
saphenous vein). The Doppler
waveform shows persistent reux
from the deep into the supercial
system (ow above the baseline,
toward the transducer). b The
Doppler waveform from the
saphenopopliteal junction (sample volume as indicated in the
longitudinal view obtained with
the transducer in the popliteal
fossa). There is ow toward the
heart during manual compression
of the calf (away from transducer,
below the baseline) and persistent retrograde ow upon release
(above the baseline), indicating
severe valve incompetence
vein or popliteal vein. Successful closure of the varicose vein
is seen as thickening and thrombosis without ow (see
. Fig.3.83 (Atlas)).
Approx. 3 days aer treatment, all patients should
undergo a duplex ultrasound evaluation for thrombosis and
thermal damage and signs of thrombus growth in the common femoral vein and popliteal vein (Lawrence etal. 2010).
e so-called CHIVA technique is an alternative strategy that aims at hemodynamic correction by interruption
of recirculation pressure loops, while sparing the saphenous
veins for venous drainage. Sites of recirculation from the
deep system into the supercial veins are identied by duplex
imaging and marked for open surgical ligation. Outcome is
evaluated by duplex ultrasound to ensure that all recirculation routes have been eliminated and that ow in all patent
veins is from the supercial into the deep system.
Recurrent varicosis is the occurrence of varicosis at a
new site or in a varicose vein segment previously treated by
sclerotherapy or endovenous ablation. Recurrent varicosis in
the strict sense cannot occur aer varicose vein resection or
crossectomy with great saphenous vein stripping. In this situation, varicosis can recur if the residual saphenous stump is
too long and veins terminating proximally connect to this
stump or to a saphenous branch. us, when a patient presents with suspected recurrence, the rst diagnostic step is to
evaluate the saphenofemoral junction using duplex imaging.
Valsalva’s maneuver is performed to identify any incompetent
lateral branches entering the residual great saphenous vein and
connecting to a more distal supercial vein and to determine
whether a persisting lateral or medial accessory branch is present that has undergone varicose degeneration (. Table3.6).
A limitation of duplex ultrasound is that it does not
always allow reliable dierentiation of a residual saphenous vein trunk from neoreux or neovascularization (see
. Fig.3.84 (Atlas)).
3.1.6.4 Varicophlebitis
Varicophlebitis is dened as thrombotic inammation of a
varicose supercial vein
and is a typical complication of varicosis. rombophlebitis is an inammation of a previously
healthy vein and typically occurs as a paraneoplastic complication. e clinical relevance of varicophlebitis has long been
underestimated. Its most serious complication is thrombus
extension into the deep venous system
, typically through
the junction of the great saphenous vein (. Fig.3.34) or small
saphenous vein and less commonly through perforators.
e risk of progression of supercial thrombophlebitis into the deep venous system is 16% with 70% of cases
accounted for by thrombus extension via the saphenofemoral junction and 20% by progression through perforators
(Chengelis etal. 1996).
e possible complications of deep vein thrombosis and a
relatively high risk of pulmonary embolism (caused by freeoating components; Bergquist 1986) have led to adoption of

3.1 · Pelvic andLeg Veins
209
3
. Table 3.6 Pretherapeutic ultrasound examination in
varicosis: relevant diagnostic information to be obtained for
adequately planning the therapeutic strategy
Duplex ultrasound
ndings
Incompetent great
saphenous vein/
saphenofemoral
junction vs. peripheral/
lateral branch varicosis
Secondary varicosis
with (postthrombotic)
incompetence of the
deep leg veins
Upper and lower points
of incompetence in
incomplete saphenous
vein varicosis
Incompetent perforating veins
Postthrombotic
syndrome with partial
or complete occlusion
by residual old
thrombus
Exclusion of PAOD/
arterial occlusion (using
time-ecient protocol)
Therapeutic relevance
Stripping/ligation/endovenous
intervention
Compression treatment, surgery in
exceptional cases only; ulcer:
perforator dissection, division of
fascia
Sparing of relevant competent vein
segments for possible later bypass
graft operations
Ligation of incompetent perforators
identied by ultrasound for
prevention of recurrent varicosis
Contraindication to varicose surgery
(impaired venous drainage would
deteriorate further)
Prevention of disturbed postoperative wound healing
. Table 3.7 Classication of varicophlebitis and recom-
mended treatment based on extent dened by compression
ultrasound
Extent of phlebitis Recommended treatment
Varicophlebitis of a lateral
branch or of the great
saphenous vein below the knee
Varicophlebitis of the great
saphenous vein in the thigh but
far below the saphenofemoral
junction or ascending small
saphenous vein thrombosis
with extension above the level
of the May perforator
Thrombophlebitis ascending to
the junction or close to the
junction (proximal 5–10cm) of
the great or small saphenous
vein
Thrombus extends beyond the
saphenofemoral or saphenopopliteal junction with DVT of
variable severity
Varicophlebitis with secondary
DVT resulting from thrombus
extension through an
incompetent perforator (“collar
stud thrombosis”)
Local anti-inammatory
treatment, antiinammatory medication,
possibly short-term
anticoagulation
2–4weeks of anticoagulation with low-dose heparin
Crossectomy, severing of the
great saphenous vein or small
saphenous vein; anticoagulation treatment alone in
exceptional cases only
Anticoagulation with
low-molecular-weight heparin
and overlapping change to
phenprocoumon (6months)
Anticoagulation with
low-molecular-weight
heparin and overlapping
change to phenprocoumon
(6months)
. Fig. 3.34 Longitudinal and transverse images of thrombophlebitis
of the great saphenous vein (V.S.M) with thrombus (TH) adhering to
the wall and extending 1.5cm into the common femoral vein (V.F)
a more aggressive therapeutic strategy in patients with supercial varicophlebitis extending close to the saphenous junction.
e foremost aim in the management of varicophlebitis is to
prevent deep vein thrombosis (DVT) and the attendant risk
of embolic complications, which is why a therapy- oriented
classication system appears reasonable (. Table3.7).
e need to perform ultrasound in all patients with clinically
manifest disease arises from the fact that patients with clinical
signs of calf varicophlebitis (classic signs of inammation such
as redness or pain, tumor) oen have disease extending above
the knee even when the thigh appears normal. Ultrasound is
performed to dene the proximal extent of thrombophlebitis
as a basis for planning treatment. A study reports propagation
into the deep venous system in 10–25% of cases (Utho etal.
2010), causing symptomatic and asymptomatic pulmonary
embolism in 4% and 33% of cases, respectively.
In the Prospective Observational Supercial rombophlebitis (POST) study (Quéré etal. 2012), a complete sonographic exploration of the deep venous system in more than
800 patients with proven thrombophlebitis revealed DVT in
nearly a quarter of the study population. In this subset, DVT
was contiguous with supercial vein thrombosis in 42% of
patients and noncontiguous in another 42%. Five patients
had isolated contralateral DVT.
erefore, the workup of these patients should always
include
venous system
compression ultrasound evaluation of the deep
with special attention to possible extension of
thrombosis through incompetent perforators. Concomitant
DVT of the calf is seen in up to 20% of patients and is especially
common in patients with paraneoplastic thrombophlebitis.

210
Chapter 3 · Extremity Veins
3.1.7 Rare Venous Disorders
complications have occurred, while no consistent strategy has emerged for the management of incidental venous
3.1.7.1 Venous Aneurysm
For a long time, the term aneurysm was only used to refer to
local widening of arteries, while the venous counterpart was
3
described as ectasia or aneurysmal dilatation. Venous aneurysm is now commonly used to designate a marked, localized
sacculated or spindle-shaped dilatation of a venous segment
(at least 2.5–3 times the normal luminal diameter). Data on
the incidence of venous aneurysms are scarce, and most case
reports do not mention a size threshold.
Histologically, a venous aneurysm is a true aneurysm
with a wall consisting of all venous layers but with thinning of
the muscle layer. Medial sclerosis may occasionally be present. e etiology is unknown, but various mechanisms have
been proposed including embryonal defects, excessive local
pressure in narrow anatomic spaces, and trauma (Fischer
etal. 1996; Smets etal. 1997; Aldridge and Comerota 1993).
Venous aneurysms are very rare (120 case reports or case
series in the literature) and mainly occur in the legs, in particular the popliteal vein. Aneurysms of leg veins account
aneurysms, especially when they are fusiform. Deep vein
aneurysms have been discovered incidentally by ultrasound
in nearly all body regions, including the neck veins (see
. Fig. 3.100 (Atlas)), the arm veins, and the splenoportal
system, but rarely cause thromboembolic complications.
romboembolism is most common in aneurysm of the
popliteal vein, the most commonly aected leg vein. Both the
popliteal artery and vein are subject to shear and mechanical
stress during knee movement, which promotes the detachment of thrombotic material from popliteal aneurysms.
Experimental investigations in models have shown that
quasilaminar ow is predominant in fusiform aneurysms
while turbulent ow with ow separations occurs in saccular aneurysms (Brunner etal. 1997; Haaverstad etal. 1995).
Stasis in dead water zones in an aneurysm can give rise to
thrombus formation (see . Figs. 3.35 and 3.85a (Atlas)).
Only anecdotal cases of pulmonary embolism caused by
venous aneurysms have been reported (Biesseaux etal. 1994;
Seino etal. 1994).
for approx. 65% of all venous aneurysms, 17% occur in neck
veins, and 14% in the arms (overview in Ritter 1993). Leg
aneurysms mainly aect the major deep veins but may also
occur in the supercial compartment, where they have to be
dierentiated from varicosis and regional or diuse phlebectasia, which, when occurring in the calf veins, may take the
form of long tubular ectasias (see . Fig.3.89 (Atlas)).
Most venous aneurysms remain undetected unless there
is thrombus formation or pulmonary embolism secondary to
local thrombosis and patients undergo workup to identify the
underlying cause of embolism. Other complications are due
to compression of surrounding structures, typically manifesting as abnormal sensations, and very rarely rupture and hemorrhage. e popliteal vein is the most common site of venous
aneurysm in the leg, and mechanical factors are considered
major contributing factors to aneurysm formation at this site.
Some venous aneurysms present with calf swelling or are
detected incidentally in patients scheduled for treatment of
varicosities.
As with arterial aneurysms,
fusiform or spindle-shaped
(. Fig. 3.35) and saccular aneurysms are distinguished.
Sonographically, an isolated venous aneurysm must be differentiated from ectatic dilatation, which involves longer segments. While some investigators dene venous aneurysm as
a permanent and irreversible localized dilation of a deep vein
to two times (McDevitt etal. 1993) or three times its normal
diameter (Maleti etal. 1997), many case reports give no size
denition. When the supercial venous system is aected,
an isolated aneurysm must be distinguished from varicose
lesions and thromboembolic complications from thrombophlebitis. Only two cases of thromboembolism of supercial venous aneurysm have been reported in the literature
(Gillespie etal. 1997; Siani etal. 2010).
ere is agreement in the literature that a saccular
venous aneurysm should be resected when thromboembolic
3.1.7.1.1 Sonographic Workup
Duplex ultrasound is the method of rst choice for the diagnostic workup of thromboembolism. Allowing assessment
of overall aneurysm size including thrombosed portions,
duplex ultrasound, and in particular color duplex, is superior to venography, which is limited because it is an indirect,
luminographic technique. e exibility of ultrasound permits evaluation of aneurysm shape in dierent planes and
dierentiation of spindle-shaped from saccular venous aneurysms (see . Figs.3.85, 3.86, 3.87, and 3.88 (all Atlas)). True
aneurysms of the popliteal vein and other veins must be distinguished from terminally dilated small veins at their sites of
entry into larger veins. Here again, ultrasound is superior to
all other imaging modalities. However, very careful evaluation in dierent planes is necessary, particularly of the terminal small saphenous vein and terminations of muscle veins.
Distal vein compression to augment ow may be necessary
for adequate evaluation. e incidence of spindle-shaped
venous aneurysms depends on the size threshold used. When
dened as a persistent focal dilatation of at least twice the
normal vein diameter, venous aneurysm is not an uncommon incidental nding but is relevant only when its diameter
is 2.5 to 3 times that of the normal vein. Many large venous
aneurysms (>3 times the normal diameter) appear saccular.
Two factors – aneurysm shape and intra-aneurysmal
thrombosis– are crucial for
therapeutic management. In
the supercial popliteal vein, both can be accurately characterized by color ow imaging and compression ultrasound.
Blood ow in a nonthrombosed aneurysm can be assessed
by gray-scale or color duplex ultrasound in transverse orientation but preferably in longuditinal orientation. At times,
spontaneous contrast (known as the cigarette smoke sign)
may be present, indicating very slow ow (. Fig. 3.35a).
Consistent with the above-mentioned experimental model

3.1 · Pelvic andLeg Veins
211
3
. Fig. 3.35 a Large saccular aneurysm (26mm) of the popliteal vein in transverse and longitudinal orientation (leftmost and rightmost images).
The appearance in transverse orientation suggests a thrombosed aneurysm cavity (no ow signals due to stasis). The second image (obtained
with calf compression (WADENKOMP) to augment ow) still shows no ow in the area of stasis (S). While the absence of ow, even with augmentation, is consistent with partial thrombosis, thrombus is ruled out by complete compressibility of this segment when pressure is applied with
the transducer (KOMP, third image). b Contrast-enhanced ultrasound (CEUS) provides no additional diagnostic information in this situation. The
contrast-enhanced color duplex image (right) suggests absence of ow (even with gentle calf compression) in the area of stagnant blood (S)
within the saccular popliteal vein aneurysm (V) already identied by conventional ultrasound. In the CEUS image (left) and the corresponding
B-mode image (center section) obtained with a reduced mechanical index (MI), microbubbles are absent from the area of stagnant blood (S)
and only distribute in areas of owing blood (indicated by “KM. in V.A”) above the popliteal artery (A). While the CEUS ndings are also consistent
with a partially thrombosed aneurysm, this is ruled out by complete compressibility (see a). However, severe stasis of blood as in this aneurysm is
associated with a high risk of thrombus formation. c Spindle-shaped aneurysm of the popliteal vein (transverse views on the left and longitudinal
views on the right) with an abrupt increase in diameter from 7mm to 20mm (in transverse view) just below the saphenopopliteal junction. Complete compressibility reliably rules out thrombus in the aneurysmally dilated segment of the popliteal vein (second transverse view, V.POP>). The
Doppler waveform shows no reux in the compression-and-release test (KOMP/DEKOMP), consistent with competent valves proximal and distal to
the aneurysm

212
Chapter 3 · Extremity Veins
studies (Brunner and Hauser 1997), ultrasound can show that
quasilaminar ow is predominant in spindle-shaped venous
aneurysms, while saccular aneurysms are characterized by
turbulent ow and ow separations. Intra-aneurysmal deadwater zones promote thrombus formation. Color duplex
3
ultrasound does not allow reliable dierentiation of stagnant blood in deadwater zones from areas of thrombosis.
Compression ultrasound is required to reliably dierentiate
stagnant blood from thrombosis in a venous aneurysm.
Stagnant blood in a venous aneurysm also needs to be
dierentiated from slow ow. is is most reliably done during compression and release applying gentle pressure at the
calf level to augment ow. A supplementary option to dierentiate stagnant blood and slow ow is contrast-enhanced
ultrasound
(CEUS) (Schäberle 2014). During the venous
phase of microbubble inow, CEUS can impressively reveal
areas of turbulent ow and stagnant blood (absence of ow
signals) in a saccular venous aneurysm (. Fig.3.35).
the aneurysmal wall segment with vein gra interposition or
closure by direct suture. However, the question when to treat
needs to be reconsidered in view of the fact that more venous
aneurysms, oen spindle-shaped and typically involving the
popliteal vein, are detected incidentally through the wider
use of ultrasound in patients with suspected thrombosis.
Since local aneurysmal dilatation of a single vein segment
does not cause calf swelling (and duplex ultrasound allows
adequate evaluation of valve function proximally and distally), the only
risk of thromboembolic complications
justication for surgical elimination is the
. To prevent surgical
overtreatment in this preventive situation, a risk stratication
strategy based on ultrasound ndings is warranted. Contrastenhanced ultrasound (CEUS) is useful in identifying areas of
prethrombotic stasis of blood (. Fig.3.35).
In a follow-up study of the analysis already discussed above
(Schäberle 2001, 2014), the author’s group found no thrombotic components in any of the 13 spindle-shaped aneurysms
(>2.5-fold normal vein diameter), and no patient had clinical
3.1.7.1.2 Prevalence ofVenous Aneurysms
inUltrasound Studies
e frequency of venous aneurysms in unselected populations is not known, and there are no data on the proportion of
symptomatic to asymptomatic venous aneurysms. Two large
ultrasound studies of patients presenting with dierent venous
symptoms (mostly workup of varicosis) found a prevalence
of asymptomatic aneurysms of the deep leg veins of 0.1% in
3500 patients (Franco etal. 1997) and 0.2% in 3880 patients
(Labropoulos et al. 1996). One study reports a surprisingly
high prevalence of 1.5% (all body regions) with two thirds
accounted for by aneurysms of the deep leg veins (Gillespie
etal. 1997). An analysis conducted by our group identied four
saccular and four spindle-shaped aneurysms of the popliteal
vein (focal diameter increase to at least 2.5 times the normal
vein diameter) in 11,500 ultrasound examinations of the deep
leg veins performed for suspected thrombosis and varicose
workup, corresponding to a prevalence of 0.07% (Schäberle
and Eisele 2001). Two of the saccular aneurysms were partially
thrombosed and were diagnosed in patients with pulmonary
embolism. e other two saccular aneurysms were incidental
ndings, one of them in a patient with concomitant DVT of
the calf. us, the prevalence of saccular venous aneurysms
requiring treatment was 0.035% in this population (half of
them with thrombus and thromboembolic complications).
e higher prevalence in patients undergoing ultrasound
workup prior to varicose surgery suggests an association of
venous aneurysms with degeneration of the supercial venous
system. is in turn points to wall degeneration as a possible
underlying mechanism, which is conrmed by histologic studies (Sigg etal. 2003; Lev etal. 1952; Friedmann etal. 1990).
signs of prior episodes of pulmonary embolism. Assessment
of blood ow in these aneurysms by color duplex ultrasound
or CEUS revealed mostly laminar ow and no regional stasis
of blood. ese patients were managed by surveillance (the
former policy of anticoagulation treatment was abandoned at
the author’s institution), and no thromboembolic complications were observed. e eight sonographically detected saccular aneurysms of the popliteal vein included one aneurysm
in a patient with complete thrombosis of the popliteal vein and
major calf veins. Two of the patients had partially thrombosed
aneurysms and pulmonary embolism. Five of the aneurysms
were detected incidentally (in patients with swelling). All saccular aneurysms in this series were resected because ow analysis
revealed vortexing with areas of stagnant blood or thrombus.
While investigators agree that saccular venous aneurysms
should be resected (Gabrielli etal. 2010, 2011; Sessa etal. 2000;
Coman etal. 2000; Uematsu etal. 1999; Gosselin etal. 1997;
Labropoulos etal. 1996), there is disagreement regarding the
management of spindle-shaped venous aneurysms. Most investigators advocate a conservative strategy along the lines outlined
above (Labropoulos etal. 1996; Rubin etal. 1995; Gobin etal.
1997; Sessa etal. 2000). Others recommend surgical resection
also for spindle-shaped aneurysms (Tumko etal. 2013; Gabrielli
etal. 2012). Anticoagulation treatment is another controversial
issue in the management of venous aneurysms.
One case of paradoxical embolism has been described
(Manthey etal. 1994). Most venous aneurysms are incidentally
detected in patients undergoing ultrasound to rule out DVT of
the leg. e patients typically report pain and swelling.
In venography, ow phenomena caused by contrast
medium in muscle veins entering the popliteal vein in the
popliteal fossa and in the small saphenous vein may mimic
3.1.7.1.3 Therapeutic Relevance of Sonographically
Detected Venous Aneurysms
Resection is indicated for sonographically detected saccular aneurysm
complications. e preferred technique is tangential resection with lateral plication of the venous wall or resection of
regardless of thrombosis or thromboembolic
thrombus, impairing the identication of thrombus and
evaluation of its extent in popliteal vein aneurysm.
Ultrasound ndings, on the other hand, provide the basis
for a dierentiated approach to the treatment of the rare
popliteal vein aneurysms (incidence of 0.07% of all patients
examined for suspected DVT of the leg in our study).

3.1 · Pelvic andLeg Veins
213
3
Intraoperative ndings and follow-up results conrm the
validity of duplex ultrasound, which is the method of rst
choice in venous aneurysm.
In summary, a conservative strategy is justied if ultra-
sound demonstrates a saccular aneurysm
to 3 times the diameter of the vein proximal and distal to it.
For larger spindle-shaped aneurysms, surgical resection may
be contemplated, especially if CEUS or color duplex ultrasound with ow augmentation demonstrates stagnant blood
within the aneurysm. Conversely, a saccular aneurysm
should be resected when its size exceeds twice the normal
vein diameter (Gabrielli etal. 2012). e need for surgical
repair of these aneurysms is also underscored by reported
embolic complication rates of 24–32% for (saccular) venous
aneurysms (Sessa etal. 2000).
3.1.7.2 Tumors oftheVein Wall
Unilateral venous stasis or disturbed drainage with leg edema
of unclear origin can point to a benign or malignant tumor
of the vein wall. Such tumors can give rise to appositional
thrombus growth as wall compression or inltration progresses. Ultrasound (possibly supplemented by MRI or CT)
allows direct demonstration of the tumor as a circumscribed
wall thickening, dierentiating it from venous thrombosis
and thus providing the basis for establishing the indication
for surgical resection. Benign tumors of the vein wall include
papillary endothelial hyperplasia, hemangioma, leiomyoma,
and broma. Malignant tumors are angiosarcoma, leiomyosarcoma, and malignant hemangioendothelioma (
and . Fig.3.97 (Atlas)).
Benign wall tumors are more clearly demarcated sonographically compared with malignant tumors, which tend
to inltrate perivascular connective tissue (Reix etal. 1998;
Kutzner and Schneider-Stock 2010). Malignant tumors arising from vein walls in the lower extremity are rare and can be
dicult to dierentiate from thrombus with both gray-scale
and compression ultrasound as well as with other imaging
modalities. Misdiagnosis is a common problem, especially in
patients with secondary, tumor-induced thrombosis of the
peripheral veins, and can lead to initiation of antithrombotic
treatment. In a small series of 7 malignant venous tumors,
the mean duration from initial symptoms to diagnosis was
7months (up to 2years) (Reix etal. 1998).
Histologically,
walls
are divided into two groups: malignant leiomyosarcomas and the less common hemangioendotheliomas. e
latter usually have a better prognosis aer complete surgical resection as they have a lower tendency to metastasize
(Enzinger and Weiss 1993; Sebenik etal. 2005). More commonly than other tumors, leiomyosarcomas arise from larger
veins (van Gulik etal. 1991; Gonzales et al. 1965; Dzsinich
etal. 1993; Kutzner and Schneider-Stock 2010). A review of
a so tissue tumor registry identied 90 epithelioid hemangioendotheliomas of the venous system (Enzinger and Weiss
1995; Sebenik 2005) but only a few case reports of epithelioid hemangioendotheliomas in larger veins exist (Reix etal.
1998; Weiss and Enzinger 1982; Harris etal. 1989; Schröder
malignant tumors arising from the vein
no larger than 2
. Fig.3.36
etal. 2001; Charette etal. 2001). ey typically develop in the
smaller veins of so tissues (Fischer etal. 1982; Kutzner and
Schneider-Stock 2010) or parenchymal organs such as the
liver, less commonly in major veins (Ferretti etal. 1998; Lau
etal. 1998; Delin etal. 1990; Schröder etal. 2001).
Epithelioid hemangioendothelioma can show circum-
scribed or invasive growth and usually arises from a small
vein, rarely from an artery (Traverse etal. 1999) or a thickwalled vein (Charette etal. 2001; Enzinger and Weiss 1995;
Kutzner and Schneider-Stock 2010). e tumor tends to grow
transmurally without destroying the vessel wall (Kutzner and
Schneider-Stock 2010), causing dilatation and obliteration.
Although these tumors are rare, they may be encountered
in vascular ultrasound examinations of patients with suspected
thrombosis of the legs (see dierential diagnostic features in
the legend of . Fig.3.36). With its high resolution, ultrasound
is superior to other imaging modalities, and venography may
even lead to the misdiagnosis of thrombus because it merely
shows a defect in opacication without providing clues to the
underlying cause (Schröder etal. 2001; Reix etal. 1998).
Vessel wall tumors must be dierentiated from paravascular tumors such as neurogenic tumors, which tend to be
spindle-shaped and grow along vessels (
3.1.7.3 Venous Compression
e venous wall has only a thin muscle layer and is therefore
easily compressed by lymphoma (predominantly in the true
pelvis and groin), perivascular tumors, hematoma, abscess,
and arterial aneurysm (primarily aecting the popliteal
artery), causing ow obstruction and clinical signs of thrombosis (. Fig.3.37b). With its ability to visualize both the vein
itself and the surrounding structures (see . Figs. 2.87, 2.92,
3.49, and 3.93 (Atlas)), ultrasound will either demonstrate
the cause of disturbed drainage directly or provide clues
guiding further, more specic diagnostic procedures such as
ultrasound-guided aspiration or biopsy.
In rare cases, popliteal entrapment syndrome involves
both the artery and the vein, for instance in individuals with
an ectopic popliteal muscle or pronounced hypertrophy of
the heads of the gastrocnemius muscle. In such cases, outow obstruction can be elicited by active plantar exion (see
. Fig.3.98 (Atlas) and 2.31).
Only augmented ow elicited by distal compression may
be detectable when a vein is compressed by an external structure. Normal respiratory phasicity is lost distal to the ow
obstruction. When there is ow in a small residual lumen,
spectral Doppler depicts a high-frequency ow signal resembling a stenosis signal (see . Fig.3.95 (Atlas)).
3.1.7.4 Venous Adventitial Cystic Disease
Venous adventitial cystic disease is very rare, occurring 80–50
times less commonly than its arterial counterpart. As in the
arteries, the lesions are histologically true ganglia (in terms
of cyst contents and wall composition) in the adventitial layer
of the diseased vein. e cysts have been attributed to ectopic
synovial cells and compromise the venous lumen (Paty 1992;
Schraverus 1997; Chakfe 1997; Hach-Wunderle 2003).
. Fig.3.37a).
Соседние файлы в папке Библиотека им академика М.И. Перельмана
