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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5760_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •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

194
Chapter 3 · Extremity Veins
DVT.Evaluation of the calf veins requires little extra time
and is also advocated here although the sonographic examination is less reliable below the knee. Negative ultrasound
DVT (paraneoplasia, immobilization, clotting disorder), the
indication for bilateral examination should be established
generously.
ndings in this territory despite a high pretest likelihood of
disease may be attributable to poor insonation conditions. In
3
such cases, the risk of thromboembolic complications from
proximal propagation of undetected calf vein thrombosis can
be minimized by proceeding according to one of the abovediscussed algorithms (. Fig.3.21), treating inconclusive ndings as if no prior examination of the calf veins took place.
e most practical procedure then is to perform a D-dimer
test or repeat the ultrasound examination aer 1 week.
Another advantage of including the calf veins in the
examination is that ultrasound additionally allows evaluation of so tissue and identication of a ruptured Baker’s cyst
(. Fig. 3.90 (Atlas)), which has a clinical presentation that
is surprisingly similar to that of DVT.Other conditions that
can be identied by ultrasound include hematoma, uid collections in muscle compartments aer trauma, and abscess.
3.1.6.1.3 Pulmonary Embolism
Pulmonary embolism is sometimes incidentally detected
by computed tomography (especially in immobilized ICU
patients), or it may present with severe or very sudden symptoms without any prior signs of DVT.Historically, patients
with pulmonary embolism were examined by bilateral venography to identify the underlying cause; results of studies
from that time indicate that even bilateral venography failed
to detect thrombosis in one third of these patients (Cronan
1993; Smith etal. 1994; Stein etal. 1993). As suspected leg
thrombosis is asymptomatic in these patients, it is unclear
whether compression ultrasound would be helpful in this
setting– given its poor sensitivity in the absence of clinical
symptoms (<60–70%). Anticoagulation treatment of pulmonary embolism will also have a therapeutic eect on pelvic
vein thrombosis, if present. While a large number of sono-
3.1.6.1.2 Additional Examination
oftheAsymptomatic Leg
ere is also disagreement about the need to examine the
asymptomatic leg when deep vein thrombosis (DVT) has
been diagnosed in the other. In the past, when the diagnosis
of thrombosis mainly relied on venography, the invasiveness of the procedure with radiation exposure and contrast
medium administration precluded the additional examination
of the asymptomatic leg. is policy was continued even aer
venography had been replaced by compression ultrasound. e
debate about whether or not to examine the contralateral leg as
well was stoked by conicting evidence regarding the incidence
of thrombosis in the asymptomatic leg (Scheiman etal. 1995;
Strotham et al. 1995). Published incidences range from less
than 1% (Cronan 1996, 1997; Naidich etal. 1996; Sheiman etal.
1995) to more than 20%; however, such high rates are mostly
found in patients with neoplastic thrombus or in fully immobilized patients. Most cases of contralateral disease involve the calf
veins and have a low risk of thromboembolism. Since systemic
anticoagulation is initiated for thrombosis of the symptomatic
leg anyway, any thrombosis present in the contralateral leg
will be simultaneously treated as well. If ultrasound rules out
suspected thrombosis in the symptomatic leg, the likelihood
of nding a thrombus in the other leg is less than 0.5%. ese
patients should then undergo venography because the high
diagnostic accuracy of compression ultrasound in detecting calf
vein thrombosis is limited to symptomatic disease, and when
no symptoms are present, the sensitivity drops to less than 60%.
In summary, while the low incidence of thrombus in
the asymptomatic leg does not seem to justify its routine
examination, the asymptomatic side should be examined in
patients with neoplastic thrombosis and in patients who are
completely immobilized for an extended period of time.
In patients with
careful evaluation of the clinical symptoms is essential to
rule out other more common causes of bilateral disease
(lymphogenic or cardiac). In patients with risk factors for
clinically suspected bilateral DVT,
graphic examinations need to be performed to detect pelvic
or leg thrombosis in a patient population with pulmonary
embolism (although it is the most likely cause of embolism),
the author nevertheless recommends bilateral compression
ultrasound to identify the site of thrombosis in these patients.
Depending on the ndings, additional compression treatment may have to be instituted, one reason being to prevent
the development of postthrombotic syndrome. e detection of a free-oating thrombus by color duplex imaging can
aect the therapeutic regimen despite the controversy about
immobilization in this situation.
e poor performance in detecting DVT aer clinically
suspected pulmonary embolism also shows that ultrasound
or venography of the legs cannot replace
sion of pulmonary embolism
in this setting (Killewich etal.
CT for the exclu-
1993; Sheiman etal. 1999). Contrast- enhanced spiral CT is
the method of choice for ruling out pulmonary embolism.
It is an open question, however, whether a CT scan is also
necessary for conrmation and assessment in patients who
have clinical signs and symptoms of pulmonary embolism
and DVT of the leg and in whom thrombosis has been
conrmed by compression ultrasound and anticoagulation
treatment has been initiated. e necessity depends on the
clinical severity of pulmonary embolism (Rosen etal. 1996;
Goodman and Lipchick 1996).
e risk of inadvertently
when performing compression ultrasound
inducing pulmonary embolism
in patients with
DVT must be taken seriously and implies that compression
must be performed gently at the proximal end of a thrombus, especially when dealing with a free-oating thrombus. Many examiners with a long experience in evaluating
venous thrombosis (Perlin 1992; Schroeder and Bealer 1992)
have probably witnessed the (luckily very rare) occurrence
of pulmonary embolism while performing a compression
ultrasound examination. ere are even some anecdotal
case reports of examinations in which the migration of
thrombotic material from the proximal thrombus end was

3.1 · Pelvic andLeg Veins
195
3
actually documented (. Fig. 3.80 (Atlas)). In all published
reports, the pulmonary embolism induced by compression
ultrasound was asymptomatic. e true prevalence of (small)
pulmonary embolisms following compression ultrasound
is dicult to estimate, even more so as thrombi extending
above the knee are associated with spontaneous, clinically
irrelevant, and asymptomatic pulmonary embolism in >50%
of cases (Cronan 1993).
Chest ultrasound has over 90% accuracy in diagnosing
pulmonary embolism, including small peripheral defects
(Mathis etal. 2005). e detection of peripheral embolism by
the sonographic identication of defects near the pleura has
no prognostic implications for recurrent embolism or death
in clinically asymptomatic patients with deep vein thrombosis; this is why routine chest ultrasound (Egbring and Görg
2007) or other tests for diagnosing pulmonary embolism are
not necessary in this setting.
3.1.6.1.4 Diagnostic Tests Supplementing
Compression Ultrasound
In patients with inconclusive sonographic ndings, the
D-dimer test is of limited value. e test has very low specicity (approx. 50%), and D-dimer levels are also elevated in
patients with other conditions in which coagulation is activated such as surgery, bleeding, sepsis, trauma, pregnancy,
and inammation. e sensitivity of the D-dimer test is very
high (about 95%) in extensive thrombosis, but may be as low
as 65% in isolated calf vein thrombosis (depending on the
assay used), which is also more dicult to detect by ultrasound (Jennersjo etal. 2005).
Venography is still used as the gold standard but also
has poorer performance in the calf, for several reasons:
nonopacication of the bular veins may be due to thrombus or technical limitations, and adequate opacication of
all vein segments of interest fails in about 10–20% of cases.
Evaluation for muscle vein thrombosis is time-consuming or
impossible.
For these reasons, patients in whom the venogram does
not allow adequate evaluation of all relevant vein segments in
the calf should undergo a supplementary ultrasound examination (see
in a duplicated vein may also escape detection by venography
(. Figs.3.57 and 3.58 (both Atlas)).
While studies have demonstrated no advantage of color
duplex ultrasound
nosing acute DVT of the legs, it is helpful in evaluating
recanalization and in identifying thrombus surrounded by
owing blood (. Fig. 3.23) or free-oating thrombus. If a
fresh thrombus is partially surrounded by owing blood,
color duplex imaging will detect ow signals along the vein
wall (between the thrombus and the wall). is is distinct
from early recanalization, which is characterized by ow
conned to the center of the vein or a meandering ow pattern (. Fig.3.23).
e supplementary diagnostic information provided by
color duplex ultrasound in acute DVT of the leg can be summarized as follows:
. Figs.3.55 and 3.56 (both Atlas)). A thrombus
over compression ultrasound in diag-
5 Detection of residual ow near the wall
5 Identication of collaterals
5 Evaluation of veins at the pelvic level
5 Demonstration of recanalization
5 Direct visualization of patent calf veins
At the pelvic level, where it is not always possible to reliably
test compressibility of veins (no abutment, obesity), color
duplex ultrasound can be used instead to evaluate ow: the
absence of ow signals (color ow imaging and spectral
Doppler analysis) indicates pelvic vein thrombosis; conversely, color duplex demonstration of blood ow with normal respiratory phasicity in the Doppler waveform indicates
patency despite incompressibility.
If the main calf veins are dicult to delineate from surrounding muscle tissue by color duplex imaging, the examiner
can try and detect spontaneous or augmented venous ow
along the accompanying arteries. Venous ow is augmented
by compressing the leg below the point of examination.
Collateral circulation will be detectable in patients with
longer-standing thrombosis (dilated veins with spontaneous
ow signals in the deep and supercial compartments). e
presence of collateral pathways is an additional criterion for
dierentiating older and more recent thrombosis and recurrence (see
duplex ultrasound is time-consuming and would prohibit the
liberal use of ultrasound advocated by the author. erefore,
all ultrasound laboratories should implement a standardized
and ecient algorithm for the diagnostic management of
patients with suspected acute DVT.is can be done using
compression ultrasound, which enables examination of both
legs in approx. 10–15min.
sound and (supplementary) color duplex ultrasound in the
diagnostic workup of patients with suspected DVT of the leg
may be summarized as follows:
5 Indications for gray-scale ultrasound/compression ultra-
5 Indications for color duplex ultrasound:
. Figs.3.51 and 3.53 (both Atlas)).
Documentation of the patency of all relevant veins by
In conclusion, the indications for compression ultra-
sound:
5 Evaluation of thrombosis (exclusion, conrmation,
extent, age) with localization and dierentiation
(main veins, muscle veins)
5 rombophlebitis (extent, thrombus protrusion into
major deep vein)
5 Follow-up (spontaneous resolution, thrombolysis,
thrombectomy)
5 Dierential diagnosis: identication of perivascular
structures compressing the vein (Baker’s cyst, so
tissue tumor, hematoma, abscess, wall tumor)
5 Follow-up aer thrombosis (spontaneous or
thrombolysis- induced recanalization)
5 Pelvic vein thrombosis
5 Floating thrombus
5 Chronic venous insuciency/postthrombotic
syndrome (valve incompetence of deep leg veins:
severity of reux, extent, degree of recanalization)

196
Chapter 3 · Extremity Veins
3
. Fig. 3.23a–e Diagnostic role of color duplex imaging in deep vein thrombosis (DVT). a Color duplex imaging does not signicantly improve
diagnostic accuracy compared with compression ultrasound, providing no additional information for ruling out thrombosis (left drawing) or
detecting occlusive thrombosis (right drawing) (see . Fig.3.17). b Color duplex oers advantages in detecting recanalization and estimating
its degree (left drawing) because it depicts spontaneous or augmented ow (e.g., Valsalva maneuver); it also oers advantages in identifying
nonocclusive mural thrombus or free-oating thrombus (right drawing) by detecting ow signals around the thrombus (again, this may require
a provocative maneuver). Settings must be adjusted to depict slow ow (low PRF). c Ultrasound examination performed 6months after an episode of acute DVT of the leg: in the left image (without compression), the shrunken lumen of the femoral vein (<V) is less clearly delineated from
surrounding muscle and connective tissue compared with the lumen of the artery (A). The second image, obtained while applying pressure with
the transducer, shows incomplete compressibility of the vein (see
duplex image (right) reveals the cause of poor compressibility (see b) in this patient: there is only a small recanalized channel with ow coded
in blue in the center of the supercial femoral vein (V). The thin recanalization channel indicates a high residual thrombus burden, which can be
calculated from vein diameters measured with and without compression as follows: residual vein thrombosis (RVT)=3.8mm × 100/5mm=76%
(for more details see . Fig.3.24b). d Longitudinal view (left) and transverse view (right) of thrombus in the popliteal vein (V.POP) partially surrounded by owing blood. All features of acute thrombosis are present: hypoechoic, markedly dilated vein, good demarcation from perivascular
connective tissue, and marginal ow. These features dierentiate this case from older thrombosis with partial recanalization (corresponding
to the rubber phenomenon in venography). e Transverse view (left) and longitudinal view (right) of popliteal vein thrombosis with beginning
recanalization (6weeks after onset): there are ow signals in the center of the lumen (meandering ow and multiple recanalized channels are
also present). The Doppler waveform from this segment reects the ow obstruction due to extensive residual thrombosis: ow is slow and
respiratory phasicity is lost
. Fig.3.19) with a diameter reduction from 5 to 3.8mm (calipers). The color

3.1 · Pelvic andLeg Veins
197
3
. Fig. 3.23 (continued)
5 Varicosis (extent, severity of reux, secondary incom-
petence of main veins; preoperative evaluation:
determination of upper and lower points of insuciency, identication of incompetent perforating veins)
5 Vein mapping prior to bypass surgery (suitability of
saphenous vein for venous bypass graing)
5 Venous aneurysm (size; conguration: spindle-
shaped, saccular, intraluminal thrombosis)
Spectral Waveform Criteria
z
Obstruction of venous return (thrombosis, external compression) leads to increased intravascular pressure distal
to the obstruction, demonstrated by duplex ultrasound as
slower ow (see . Fig.3.24a).
e increased venous ow resistance associated with
occlusion, compression, or persisting postthrombotic
obstruction eliminates the respiratory phasicity of venous
drainage (resulting from changes in intra-abdominal pressure). is loss is reected in the Doppler waveform as a
constant ow velocity in the vein distal to the obstructed
segment and as a reduced ow velocity, which is best appreciated by comparison with the other leg (
following criteria, known from CW Doppler ultrasound,
indicate venous obstruction (. Figs.3.24a, 3.44 (Atlas), 3.46
(Atlas), and 3.49 (Atlas)):
5 Zero ow in the thrombotically occluded vein
5 Decreased ow velocity with reduction or elimination of
respiratory phasicity due to proximal thrombus or com-
pression of the vein by surrounding structures
. Fig.3.24a). e

198
Compression
a
Chapter 3 · Extremity Veins
5 Flow signal not modulated by respiration, possibly of
high frequency, in partially thrombosed or compressed
vessel segments or along thrombus surrounded by owing blood (dierential diagnosis: ow signal from collateral vein not subject to respiratory phasicity)
3
5 Augmented ow (compression and release) abnormally
reduced when thrombosis or ow obstruction is present
distal or proximal to the sampling site
duplex indicate older thrombosis with beginning recanalization. Impaired venous drainage due to thrombus surrounded
by ow or residual thrombus in a recanalized vein with a narrow lumen is identied by the absence of respiratory phasicity in the Doppler waveform (
3.1.6.1.6 Recurrent Thrombosis
. Figs.3.23 and 3.28).
Following completion of treatment aer a rst episode of
deep vein thrombosis (DVT) in an unselected patient population, the risk of recurrence was found to be 13% aer 1year,
3.1.6.1.5 Thrombus Age
Initial hopes of determining thrombus age by means of
sonomorphologic criteria and using this information for
making better treatment decisions (surgery, thrombolysis,
anticoagulation) have been disappointed. What is possible
though is to dierentiate very recent thrombi from much
older ones (. Fig.3.25 and . Table3.4) and dierentiate them
based on increasing inhomogeneity and echogenicity of the
thrombus and shrinkage of the vein diameter (
. Figs. 3.26
and 3.50 (Atlas)). In general, however, there is wide interin-
23% aer 5years, and 30% aer 10years (White 2012). In
another study, 50% of patients had residual thrombosis aer
1 year (Piovella etal. 2002).
Although postthrombotic veins have several characteristic features including persistent occlusion with shrinkage
of aected veins, partial recanalization with irregular and
meandering ow, or residual thrombus with poor dierentiation from perivascular tissue, they cannot always be
dierentiated from acute recurrent DVT with condence.
To improve dierentiation, it is helpful to obtain a detailed
dividual variation in thrombus development, and the criteria
are not reliable enough for therapeutic decision-making.
is holds true especially for the clinically relevant identication of thrombi that are still amenable to recanalization
measures, i.e., thrombi not older than 1 week. Nevertheless,
0
the sonomorphologic criteria can contribute to the therapeutic decision in individual cases. For instance, a homogeneous
thrombus of lower echogenicity in a markedly dilated vein
with good demarcation of the wall and thrombus portions
0
surrounded by owing blood is more likely to respond to
thrombolytic therapy and will undergo rapid recanalization.
Older thrombosis is characterized by progressive narrowing of the venous lumen and a loss of wall conspicuity
(. Fig.3.26a and . Table3.4). e poorer delineation from
0
surrounding muscle tissue and increasing echogenicity of
the thrombus contribute to a lower accuracy of ultrasound in
diagnosing older thrombosis, especially in the calf. Following
the acute stage, early recanalization can also be demonstrated
by color ow imaging. When the recanalized lumen is still
small, sparse and slow venous ow may be depicted aer
augmentation (calf compression, Valsalva’s maneuver) even
Compression
0
Compression
if spontaneous ow is not detectable with the transducer set
to detect slow ow. Both gray-scale ultrasound and color
duplex imaging (with assessment of reux severity) allow
Compression
0
evaluation of venous drainage, which may be compromised
by poor recanalization or postthrombotic changes. e ndings may range from complete recanalization with a normal
sonographic appearance of the venous wall to persistent
thrombotic occlusion with luminal narrowing, residual
thrombi of various size, wall sclerosis, and synechia.
If the sonographic examination shows not only postthrombotic changes but also newly obstructed venous segments (hypoechoic thrombus and dilatation of the vein
compared with the accompanying artery), this is a sign of
recurrent thrombosis (
. Fig.3.26c)– especially if the proxi-
mal thrombus end is surrounded by ow. In contrast, ow
signals in the center of a thrombosed vein depicted by color
. Fig. 3.24 a Diagrams of Doppler waveforms obtained at dierent
sampling sites relative to ow-obstructing venous thrombosis without
and with ow augmentation (manual compression) (see . Fig.3.44
(Atlas)). b, c Quantication of residual thrombus burden after deep vein
thrombosis (DVT). b Calculation of percentage residual vein thrombosis (RVT) (Siragusa etal. 2011). The left drawing illustrates the situation
for a large residual thrombus burden (vein diameter with compression
≥40%; see . Fig.3.23c) and the right drawing the situation for a small
residual thrombus burden (vein diameter with compression <40%).
cCalculation of residual thrombus thickness from the anteroposterior
diameter measured without and with application of pressure with the
transducer (Prandoni etal. 2002 and 2004). Recurrent DVT is dened as
a diameter increase of ≥4mm

3.1 · Pelvic andLeg Veins
199
3
Large residual thrombus burden
Vein diameter with compression ≥40%
Compression
Calculation: RVT =
b
Residual thrombus thickness
Measured as anteroposterior diameter
with compression in transverse orientation
Diameter with compression x 100%
Diameter without compression
Small residual thrombus burden
Vein diameter with compression <40%
Compression
Without compression Compression
Definition of recurrent DVT
Diameter increase ≥ 4 mm
(100% specificity)
c
. Fig. 3.24 (continued)
. Fig. 3.25 a Acute thrombosis of the popliteal vein (V), which is dilated by the thrombus (compare diameter of the accompanying artery (A)).
The wall of the thrombosed vein is sharply demarcated from the surrounding tissue. The thrombus is identied in the gray-scale image as intraluminal hypoechoic, homogeneous material. The right image obtained during compression with the transducer shows that the soft clot is still
somewhat compressible (with a diameter reduction from 11 to 9mm). b Color duplex imaging (transverse view on the left, longitudinal view on
the right) shows no spontaneous or augmented venous blood ow, indicating occlusive thrombosis

200
Chapter 3 · Extremity Veins
. Table 3.4 Sonographic ndings in the diagnostic evaluation of deep vein thrombosis (DVT ) and estimation of thrombus age
Presence of thrombus/thrombus age Ultrasound ndings
Normal vein (no thrombosis) Complete compressibility of vein
Thin wall
3
Acute thrombus (<8days) Incompressibility of vein
Older thrombus (>2–3weeks) Total occlusion:
Postthrombotic lesions Persistent occlusion:
Breathing, Valsalva’s maneuver, and distal compression elicit identical changes in ow
on both sides
No elicitation of retrograde ow in valve function test (indicating adequate valve closure)
Vein diameter at least twice that of accompanying artery
Flow signals near the wall if thrombus is still surrounded by blood or if a free-oating
thrombus is present
Thrombus tending to be homogeneous and hypoechoic
Good delineation of vessel wall, in part with hypoechoic halo
No collaterals detectable by color duplex imaging
– Incompressibility of vein
– Diameter less than twice that of accompanying artery
– No ow signals, thrombus tends to become more hyperechoic and inhomogeneous
– Poor delineation of vessel wall, hyperechoic halo may still be present
Partial occlusion:
– Partial compressibility of vein
– Diameter comparable to that of accompanying artery
– Signs of marginal and central recanalization
– Collaterals begin to form
– Reduced venous lumen (same as or smaller than the diameter of accompanying artery)
– Vessel wall poorly demarcated from surrounding soft tissue
– Fully developed collateral vessels
Partial recanalization:
– Meandering ow pattern in center of vein
– Little or no respiratory phasicity of blood ow
– Short residual occlusions
– Sclerotic thickening and rigidity of vessel wall; incomplete compressibility
Recanalization:
– Flow signal throughout lumen
– Sclerotically altered wall segments alternating with sonographically normal segments
– Identication of incompetent valves using Valsalva’s maneuver or valve function test
(compression and release)
– Variable lumen with widened and narrowed segments
status of residual thrombosis, ideally aer the completion of
anticoagulation treatment, to serve as a new baseline in case
of future recurrence. Criteria of recurrence on compression
ultrasound include incompressibility of a previously normal segment and a marked increase in the thrombus burden
(Piovella etal.2002; Prandoni etal. 2002; Siragusa etal.2011).
Prandoni etal. (2002) reported 99% sensitivity for the diagnosis of recurrent thrombosis in the proximal deep veins.
Still, compression ultrasound may not allow condent
diagnosis of recurrent DVT in 30% of cases (Tan etal. 2010),
and the residual thrombus burden aer a thrombotic event is
at times dicult to dene and to quantify. Moreover, investigators dier in how they dene recurrent DVT or measure
residual thrombus. While some investigators report residual
thrombus thickness as the anteroposterior vein diameter in
mm (Prandoni et al. 2002), others calculate a percentage
thrombus burden from vein diameters measured with and
without compression (Siragusa etal. 2011) (see . Figs.3.23c
and 3.24b). If the sonographic ndings are inconclusive,
the same strategy as in the diagnosis of primary DVT may
be used – either a supplementary D-dimer test and clinical risk assessment according to Wells (see . Fig.3.21) or a
repeat ultrasound examination in conjunction with a repeat
D-dimer test.
Another option to dierentiate older residual DVT from
acute recurrence is magnetic resonance direct thrombus
imaging (MRDTI) (Westerbeek etal. 2008).
3.1.6.2 Chronic Venous Insuciency
While thrombosis can be evaluated by B-mode imaging
alone, Doppler ultrasound is necessary for the hemodynamic
assessment of the severity of poor venous drainage in patients

3.1 · Pelvic andLeg Veins
201
3
. Fig. 3.26 a Older thrombosis (>3months) of the popliteal vein. Transverse views of the vein obtained without compression (left) and with
compression (right). The wall of the thrombosed popliteal vein (V.POP) is blurred and dicult to delineate from surrounding tissue. The vein has
decreased in diameter (and is smaller than the accompanying artery). At this stage (after broblast invasion), the thrombus cannot be compressed
with the transducer (lumen diameter of 3.9 and 3.7mm without and with compression, respectively). b Transverse (left) and longitudinal (right)
color duplex images fail to depict ow in the popliteal vein (V.POP), conrming occlusive thrombosis. The blurred wall and poor delineation from
surrounding tissue are most obvious in the longitudinal image. Red-coded ow indicates the accompanying popliteal artery (A). c Patient with
recurrent mild swelling of the leg 1 year after an episode of deep vein thrombosis (DVT). The color ow images show persistent complete occlusion of the supercial femoral vein (thin vein with poorly dierentiated wall and higher echogenicity in the color ow images (V.F.S, V)). The rst
color ow image additionally shows a fresh appositional thrombus (TH) extending from the old thrombosis into the common femoral vein (V.F.C)
and deep femoral vein (V.P.F). The appositional portion has low echogenicity and is attached to the wall anteriorly with ow posteriorly (blue). It
is well delineated from the wall and causes marked dilatation of the vein. The grays-scale image (leftmost scan) shows a free-oating component
(3cm in length), and the time- motion scan next to it shows the oating thrombus to be highly mobile within the dilated vein (during Valsalva’s
maneuver). There is a risk of pulmonary embolism, and anticoagulation treatment should be resumed promptly. d Older thrombosed veins must
be dierentiated from nerve strands running parallel to vessels, such as the tibial nerve coursing along the popliteal vein (V). A longitudinal image
obtained with a high-resolution probe typically allows identication of the cordlike bundles of nerve bers (arrow), thus distinguishing a nerve
from an old thrombosed vein

202
1
3
4
7
Chapter 3 · Extremity Veins
structures (
. Fig. 3.29a), which are inhomogeneous and
mostly hypoechoic relative to the surrounding connective tissue, prevent full compression. Especially the postthrombotic
femoral vein may be dicult to identify since all that may
remain is a cord-like structure visible on B-scan ultrasound.
3
Acute thrombosis
For this reason, it is helpful to use the accompanying artery
as a landmark. A recanalized femoral vein with incompetent
valves will dilate during Valsalva’s maneuver (. Table3.5 and
. Fig.3.73 (Atlas)).
Hence, B-mode ultrasound alone does not allow reliable
evaluation of the recanalization process as it does not depict
ow in sclerotic segments, and wall sclerosis may preclude
compression of the vein (. Table3.5 and . Fig.3.73 (Atlas)).
e clinical severity of the postthrombotic syndrome
2
. Fig. 3.27 Persistent venous changes following deep vein thrombo-
sis (DVT). 1 Complete recanalization, only valve damage. Normal grayscale and compression ultrasound ndings of the vein. 2 Persistent
occlusive thrombosis. Sonographically, the vein typically has a reduced
lumen (diameter no larger than that of the accompanying artery),
contains material of higher echogenicity, and cannot be compressed.
3 Narrow recanalized lumen. The recanalized vein is often missed by
B-mode or compression ultrasound; color duplex imaging is usually
required to demonstrate ow in the vein (and Valsalva’s maneuver or
compression may be necessary to augment ow). 4 Recanalization
with residual mural thrombus. Visualization of the recanalized vein may
be poor on gray-scale images, and the vein is not fully compressible.
5 Recanalization with persistent wall thickening. In most cases, the patent lumen is sonographically delineated from the thickened wall, and
the vein can be compressed, but full compression is prevented by the
thickened wall. 6 Recanalization with wall sclerosis. Hyperechoic wall,
possibly with focal posterior acoustic shadowing, on B-mode imaging
and incomplete compressibility due to thickened, sclerotic wall. 7 Intraluminal synechia and membranes, which are hyperechoic and slightly
mobile when the vein is compressed. The membranes, typically with
concomitant wall sclerosis, preclude complete compression of the vein
5
6
is chiey inuenced by the degree to which venous return
is compromised, which in turn varies with the degree of
thrombosis and recanalization as well as with the presence
of collateral pathways. Valve incompetence in the main
veins determines the extent of reux, which correlates well
with the extent of the initial thrombosis. Duplex ultrasound
studies demonstrate abnormal reux aer recanalization of
thrombotic deep vein segments in approx. 45–70% of cases
aer 1–3years, while normal ndings with complete recanalization and preserved valve function are seen in 12–30%
patients (Johnson etal. 1995; Markel etal. 1992), and 10–20%
of vessel segments remain completely obstructed (Johnson
etal. 1995).
Venous reux is measured with a Valsalva maneuver to
evaluate proximal valve function and the compression test to
evaluate distal insuciency. e increase in intra-abdominal
pressure induced by the Valsalva maneuver produces a short,
physiologic backward ow with a mean duration of 0.3s
(. Fig.3.29b–e). Reux persisting for over 1s is abnormal.
Studies in patients with stage II or III chronic venous insufciency found sensitivities of 77–91% and specicities of
with chronic venous incompetence. A high-resolution transducer depicts venous wall sclerosis by an increase in echogenicity and thickening of the wall in the presence of a patent
lumen and also identies valves damaged and immobilized
by the sclerotic process. Nevertheless, B-mode imaging
alone is insucient in evaluating the postthrombotic patient
because a recanalized vein will have a normal sonomorphologic appearance in about 30% of cases (
. Fig. 3.27). e
other 70% show wall irregularities and thickening, a strandlike vein with a smaller lumen, or a vein that has become
dilated aer recanalization due to the pressure and volume
overload resulting from incompetent valves (see . Figs.3.69,
3.73, and 3.74 (all Atlas)). If recanalization is delayed, serial
ultrasound will show residual mural thrombi or a thickened
wall, from which residual thrombus cannot be dierentiated.
e aected vein cannot be fully compressed, and color ow
images will depict a narrow lumen with ow signals surrounded by an inhomogeneous area of mixed low and high
echogenicity extending to the perivascular connective tissue
(. Fig.3.28).
Compressibility of the postthrombotic vein increases
with the degree of recanalization, while residual intraluminal
85–100% for reux assessment by duplex ultrasound (Araki
et al. 1993; Neglen and Raju 1992). Moreover, the duplex
ndings correlated better with the clinical stage than did
ascending venography.
Ultrasound with a Valsalva maneuver can be performed
in the recumbent patient, while the
test
has 10% higher diagnostic accuracy when performed
compression-release
with the patient sitting or standing. e vein is compressed
manually distal to the ultrasound probe or in a standardized
manner using a cu for compression. Standardized spectral
Doppler recordings for evaluation of reux in the popliteal
vein are obtained upon sudden deation of a blood pressure cu placed around the calf and inated to 100mmHg.
Sonographic evaluation with use of standardized provocative
maneuvers ensures interindividual comparability in the setting of scientic studies. e compression-release test reproduces the ow variations resulting from contraction-induced
compression of muscle veins (muscle pump).
Because the main veins are also embedded in the muscle,
contraction not only propels blood toward the heart but also
induces ow toward the periphery, which is prevented by
competent valves. In patients with incompetent perforators,

3.1 · Pelvic andLeg Veins
. Fig. 3.28 a Transverse image
shows the artery with red-coded
ow and the femoral vein
posterolaterally (indicated by
calipers). The center of the vein
is recanalized (blue-coded ow)
and surrounded by an inhomogeneous, thickened wall with areas
of high and low echogenicity.
Residual mural thrombus cannot
be dierentiated from the wall,
and the wall is poorly delineated
from surrounding connective
tissue. b The longitudinal color
ow image shows ow in the
center of the recanalized venous
lumen (red, toward transducer)
and extensive residual mural
thrombosis. The low PRF chosen
to depict slow venous ow causes
aliasing in the accompanying
popliteal artery (blue, ow away
from transducer). c Flow reversal
in the vein elicited by Valsalva’s
maneuver (blue, away from
transducer) indicates incompetent valves. In the corresponding waveform (right), the ow
reversal is seen as persistent ow
below the baseline (away from
transducer)
203
3
the muscle pump is also responsible for abnormal reux
from the deep into the supercial veins (. Figs. 3.7b and
3.14). erefore, incompetent valves reduce the eciency of
the muscle pump because venous pressure, which normally
decreases with muscle activity, remains unchanged or drops
only a little. ese complex interactions must be taken into
account when selecting a site for placing the Doppler sample
volume and also in interpreting the ow data obtained.
In severe valve incompetence, as in the postthrombotic syndrome, reux can be induced not only by Valsalva’s
maneuver but also by normal inspiration or deep inspiration
in the horizontal position (. Fig.3.75 (Atlas)). Under normal
conditions, the craniocaudal pressure gradient ensures rapid
valve closure during inspiration and thus prevents reux.
In patients with incompetent valves, the pressure gradient
results in reux persisting until the patient begins to expirate
(reversal of pressure).
Pressure and volume overload occurring distal to post-
thrombotic veins
can lead to secondary damage through
hyperextension of valvular rings in formerly unaected vessel
segments (Killewich etal. 1989). e same pathomechanism
leads to secondary, nonpostthrombotic valve incompetence
of the deep veins in patients with a long history of truncal
varicosity (Trendelenburg private circulation; . Fig.3.30). In
this secondary form, as in primary chronic venous insuciency of the deep leg veins, B-mode images show dilatation
of the aected vein but no wall thickening or inhomogeneous
structures within the lumen. Moreover, the vein can be completely compressed. Under good insonation conditions,
mobility of the valve can be demonstrated, distinguishing
this condition from the postthrombotic syndrome with valve
immobility due to brotic thickening (. Figs.3.29 and 3.43
(Atlas)).
Dierent patterns of reux can be observed, depending
on the underlying mechanism of valve incompetence (Evers
and Wuppermann 1995, 1997). Reux in postthrombotic
valve incompetence sets in immediately with the provocative
maneuver (without signs of valve movement), increases rapidly, peaks during the rst seconds, and then decreases (type
B). Reux will be less severe than expected when overall ow
is reduced due to incomplete recanalization and ow obstruction caused by residual thrombosis (. Fig.3.31). In primary
chronic venous insuciency and primary varicosis, abnormal
reux is slightly delayed compared with physiologic reux,
continuous (see . Fig.3.74 (Atlas)), and slower (type A).
In patients with complete valve failure due to severe
venous dilatation, however, even primary chronic venous
insuciency of the supercial or deep venous system results
in immediate high-frequency reux.
Reux velocity can be used as a semiquantitative measure
of postthrombotic valve damage. It increases during the rst
year and then reaches a plateau. In addition, the velocity and
duration of reux are inuenced by secondary postthrombotic changes caused by pressure and volume overload.
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