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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

c
ab
Chapter 5 · Extracranial Cerebral Arteries
374
a
b
5
. Fig. 5.73a–c (Atlas) Dissection of CCA.
In De Bakey type I aortic dissection, the dissection extends into the common carotid artery (CCA).
a The B-mode image depicts the dissection in longitudinal and transverse planes as an intraluminal ap oscillating during the cardiac cycle.
b Color ow imaging dierentiates the true lumen of the CCA (CCA W.L) with antegrade ow toward the brain from the false lumen (F.L) (V.J, jugu-
lar vein).
c The ow direction demonstrated in the false lumen depends on the placement of the sample volume relative to the re-entry site. Forward ow
is demonstrated if the re-entry is distal to the sample volume and to-and-fro ow, as in the example, if it is proximal. The image shows ow in the
true lumen displayed in blue (toward the periphery, away from transducer) and aliasing, while there is to-and-fro ow in the false lumen (here
displayed in red, toward transducer)
. Fig. 5.74a, b (Atlas) Posttraumatic ICA dissection.
a Long posttraumatic dissection of the internal carotid artery (ICA) extending from the bifurcation to the base of the skull with thrombosis of the
false lumen. Unlike atherosclerotic changes, thrombotic dissection is characterized by a homogeneous and hypoechoic sonomorphologic appearance. The thrombosed false lumen is long and tortuous and partly attaches to the vessel wall. Occasionally, as in this example, the entry site can
be identied by the depiction of pulsatile ow signals in the color duplex mode (right image).
b The blood ow velocity measured by spectral Doppler indicates that the luminal narrowing due to the dissection does not yet cause highergrade stenosis (PSV of 120cm/s)

ab
5.10 · Atlas: Extracranial Cerebral Arteries
375
. Fig. 5.75a, b (Atlas) Posttraumatic ICA dissection with patent true and false lumen.
a Posttraumatic ICA dissection extending from the carotid bulb to the skull base. The longitudinal image on the right (inverted display) shows
the true lumen coded in red and the false lumen coded in blue. The transverse image (left) shows 50% diameter reduction of the true lumen and
partial thrombosis (hypoechoic portion) of the false lumen (coded in blue) (V=internal jugular vein; ECA=external carotid artery).
b Following the course of the ICA cranially in transverse orientation reveals that the false lumen extends to the skull base. The image shows the
proximal ICA on the left and its distal portion on the right. The true lumen is coded in red (inverted display)
5
. Fig. 5.76 (Atlas) Takayasu’s arteritis.
Concentric wall thickening is pathognomonic of arteritis. Takayasu’s arteritis predominantly aects the subclavian artery and common carotid
artery (CCA). The example shows the CCA in the power Doppler mode. The transverse image (leftmost section) demonstrates concentric diameter
reduction (>50%), which involves a long vessel segment. The transverse image in the middle and the longitudinal image on the right obtained
after 2weeks of cortisone treatment show slightly reduced but persistent concentric wall thickening of the CCA
. Fig. 5.77 (Atlas) Temporal
arteritis.
Transverse (left) and longitudinal
(right) images of the temporal
artery showing luminal narrowing
(size reduction from 3 to 1mm;
calipers) due to inammatory
concentric wall thickening

376
Chapter 5 · Extracranial Cerebral Arteries
. Fig. 5.78 (Atlas) Postoperative follow-up after carotid endarter-
ectomy (CEA).
Postoperatively, there may be luminal narrowing due to thrombotic
deposits, in particular when a synthetic patch has been interposed.
Thrombotic deposits protruding far into the lumen and causing hemodynamically relevant narrowing are a source of embolism. The patch
itself is seen as a bright line (wall near transducer) with a hypoechoic
deposit on the luminal side (T)
5
a
b
. Fig. 5.79a, b (Atlas) Carotid endarterectomy with patch closure.
a Early postoperative sonomorphologic appearance of the vessel wall after carotid endarterectomy (CEA) with patch angioplasty (Dacron patch).
The image on the left depicts the transition from the patch (P) to the native internal carotid artery (ICA) with the sample volume for Doppler
measurement. The corresponding Doppler waveform indicates normal ow velocities. The image on the right shows the proximal end of CEA and
the patch (P) with a step in the far wall at the transition (indicated by double arrowheads). The caliber mismatch is unproblematic, causing no ow
obstruction because the larger diameter is downstream. Intima–media thickness (IMT) in the common carotid artery (CCA) is increased to 1.1mm
(calipers).
b At 6-month follow-up after CEA with patch closure, there is evidence of early neointimal formation at the transition from the patched segment
to the distal ICA.There is good evaluation of this segment (P) using gray-scale imaging, which shows no hemodynamiclly relevant luminal narrowing (PSV of 90cm/s)

5.10 · Atlas: Extracranial Cerebral Arteries
. Fig. 5.80a–e (Atlas) Recur-
rent stenosis after carotid endarterectomy (CEA)
a Postoperative B-mode image
(left) after carotid endarterectomy (eversion) shows an intimal
ap within the lumen (to the right
of the “ICA” label) with aliasing
in the color duplex mode (color
spillover obscuring the ap). The
peak systolic velocity (PSV) of
250cm/s indicates >70% stenosis
(by ECST criteria; see . Fig.5.9b
and . Table5.9).
b Thrombosis progressed due to
thrombotic deposits and neointimal proliferation within a few
weeks (PSV >300cm/s with very
turbulent ow in the stenotic
segment).
c Angiogram conrming highgrade stenosis after CEA due
to intimal ap and thrombotic
deposits.
Anastomotic stenosis after
bypass procedure between subclavian artery and ICA for CCA
occlusion.
d Doppler waveform from the
internal carotid artery (ica) distal
to the bypass graft anastomosis
shows typical signs of poststenotic ow (delayed systolic
rise and slightly reduced PSV of
70cm/s).
e These ndings are attributable
to proximal stenosis at the site of
anastomosis of the bypass graft
(bp) with the subclavian artery
(a.subcl). There is aliasing in the
color duplex image, and Doppler
interrogation demonstrates >70%
stenosis (PSV of 350cm/s). The
B-mode image (left) reveals a ap
(arrow). This ap is obscured by
color spillover in the color duplex
mode and was not adequately
seen in the angiogram (not
shown)
377
5
a
b
c
d
e

378
ab
Chapter 5 · Extracranial Cerebral Arteries
5
. Fig. 5.81a, b (Atlas) Change in pulsatility after carotid artery stenting (CAS).
a Changes in the Doppler waveform after carotid artery stenting (CAS). A long segment of the internal carotid artery (ICA) exhibits an increased
peak systolic velocity (PSV) of 153cm/s and slightly increased pulsatility without evidence of stenosis (3.8mm stent diameter). The PSV measured
in the stented segment would indicate 40% NASCET stenosis and 50–60% ECST stenosis in the native ICA.Here, the higher PSV and greater pulsatility are due to the smaller lumen and rigidity of the stented segment, respectively.
b Angiogram without signs of residual or recurrent stenosis in the stented ICA.The patent lumen within the stent is smaller than that of the native
artery
a
. Fig. 5.82a, b (Atlas) ICA in-stent restenosis– neointimal proliferation.
Examination of the internal carotid artery (ICA) after stenting shows long-stretched narrowing of the stented lumen due to neointimal proliferation. The morphologic appearance suggests 50% lumen reduction
a. The peak systolic velocity (PSV) measured in this segment is 143cm/s (which is similar to the PSV measured in the nonstenotic stented ICA, see
b
. Fig.5.81a). However, a PSV ratio of 2 is calculated from this PSV and the PSV of 58cm/s measured in the proximal stented segment (bulb)
b. A ratio of 2 corresponds to approx. 50% stenosis according to the continuity equation. The PSV ratio allows reliable grading of in-stent restenosis because the stent creates a straight channel of uniform caliber, and there a no hemodynamic eects of arteries arising from the stented segment. This example illustrates that the PSV ratio is a more reliable parameter than absolute intrastenotic PSV for grading carotid in-stent restenosis

a b
5.10 · Atlas: Extracranial Cerebral Arteries
a
379
5
b
. Fig. 5.83a, b (Atlas) Grading of in-stent restenosis– PSV ratio.
a In-stent restenosis of the internal carotid artery (ICA) can be identied and graded sonographically by obtaining a continuous spectral Doppler
tracing of the stented arterial segment. Because a stented segment has a rather constant diameter, determination of the peak systolic velocity
(PSV) ratio in the stented portion allows reliable identication and grading of in-stent restenosis. In the case presented, the Doppler tracing shows
a focal increase in PSV from 67.1 to 138cm/s in the stented segment, indicating >50% stenosis. Conversely, the absolute intrastenotic PSV of
138cm/s is still below the PSV cuto for hemodynamically relevant in-stent restenosis identied by ROC curve analysis. The Doppler waveform
shown was obtained by continuous spectral Doppler recording from the proximal to the distal stented ICA segment (indicated by “>> <<” in the
color duplex image). The left portion of the waveform reects the hemodynamic situation upstream of the stenosis, while the right portion shows
the abrupt increase in PSV at the site of in-stent stenosis. The corresponding angiogram shows in-stent restenosis at the distal stent end (arrow).
b High-grade in-stent restenois 1.5cm upstream of the origin of the external carotid artery with a PSV ratio of 5 (calculated from an intrastenotic
PSV of 268cm/s and a prestenotic PSV of 44cm/s). The abrupt increase in PSV was identied by continuous spectral Doppler recording moving
the tilted transducer (at an angle of 52°) along the artery in a cranial direction. The angiogram shows 80% ICA in-stent restenosis (projection
plane)
. Fig. 5.84a, b (Atlas) High-grade in-stent restenosis after carotid artery stenting (CAS).
a High-grade in-stent restenosis 2years after carotid artery stenting (CAS). Mixed echogenic and echolucent plaque with an intrastenotic peak
systolic velocity (PSV) of almost 4m/s.
b Angiogram: High-grade in-stent restenosis of the ICA, conrming the ultrasound ndings presented in a

380
d
Chapter 5 · Extracranial Cerebral Arteries
5
a
b
. Fig. 5.85a–d (Atlas) Stent dislocation.
a Longitudinal image (left) and time-motion image (right) showing dislocated stent (ST) in the internal carotid artery (ICA). There appears to be
a lumen with blood ow between the stent and the vessel wall, as indicated by ow signals. Note that the stent is subject to pulsatility eects (in
the time–motion display), showing paradoxical stent motion as the stent is compressed by the owing blood and pressure in the false lumen (X)
during systole (S).
b The Doppler waveform from the false lumen between the stent and the arterial wall demonstrates ow along the stent toward the head with a
peak systolic velocity (PSV) of 60cm/s.
c The stent lumen is not compromised (PSV of 90cm/s).
d The patient initially refused a repeat intervention and the stent became even more dislodged with an increase in the size of the lumen between
the stent and the arterial wall. In the gray-scale image (leftmost image), a long segment of the stent including its end is seen to be detached
from the arterial wall closer to the transducer, while it tightly adheres to the opposite wall. The color ow image and spectral Doppler show ow
between the detached stent and the native arterial wall. The time-motion mode (which displays movement of structures over time) shows pulsatile movement of the detached stent, resulting in a variable distance between the stent and the native arterial wall of 5mm (D3) during systole
and 4.2mm in late diastole (D4). The Doppler waveform shows more pulsatile ow in the lumen between the stent and the native arterial wall
than within the stent
c

5.10 · Atlas: Extracranial Cerebral Arteries
381
5
a
d
b c
e
f
. Fig. 5.86a–f (Atlas) Alternative ultrasound techniques: B-ow mode, 3D ultrasound.
a B-mode ow imaging analyzes the amplitude signal of the reecting particles in the interval between two pulses. The movement of reecting
particles is encoded in terms of ow direction, velocity, and number. A narrowed vessel segment is depicted with higher signal intensity as a result
of the larger number of reecting particles and faster ow due to the reduced cross-sectional area. In addition to hemodynamic parameters, the
B-ow mode also provides morphologic images with high resolution of plaques and the vessel wall, enabling good dierentiation of the plaque
surface and surface irregularities (ulceration) from the patent lumen. The image presented shows plaque on the near and far walls of the carotid
bulb. The luminal narrowing resulting from these plaques is indicated by the higher signal intensity of the perfused lumen in this segment.
b Advantages of B-ow imaging are its little angle dependence and the good morphologic discrimination between vessel wall and patent lumen.
Its major drawback is its susceptibility to artifacts induced by the highly pulsatile wall motion that occurs in the presence of high-grade stenosis
caused by plaque. Like all ultrasound techniques, the B-ow mode is impaired by signal scattering and acoustic shadowing due to calcied structures. This is why B-ow imaging has not replaced the hemodynamic spectral Doppler technique in detecting and characterizing vascular pathology. The example illustrates how the B-ow image is degraded by acoustic shadowing from calcied plaque. The higher signal in the vessel lumen
indicates the stenotic jet. Still, spectral Doppler interrogation continues to be the most reliable method for quantifying high-grade stenosis.
c Three- dimensional displays can provide a good overview of vascular anatomy and relationships in the presence of atypical variants or elongation. At its current state of development, however, this technique contributes little to stenosis grading and evaluation of plaque morphology (see
e). Due to artifacts caused by vessel pulsation and atherosclerotic plaques, 3D displays have no advantage over 2D displays in answering relevant
angiologic and vascular surgical questions. The example depicts the CCA on the right with the superior thyroid artery above and the ICA (bottom)
and ECA (top) on the left.
d–f B-ow imaging for evaluation of in-stent restenosis (Images d–f courtesy of M.Jung, from Schäberle 2011).
d Color duplex with spectral Doppler analysis (top left) and power Doppler mode (top right) shows normal ndings after carotid artery stenting
(CAS). The B-ow mode (bottom left) and B-ow with speckle reduction imaging (SRI) (bottom right) conrm that there is no relevant luminal narrowing but the images do not depict wall deposits or neointimal proliferation within the stent.
e High-grade ICA stenosis before (top) and after (bottom) CAS.B-ow imaging (top right) is superior in visualizing the plaque surface and ulcer
compared with the color duplex mode (top left: 3D reconstruction). The images after CAS were obtained using the B-ow mode (bottom left) and
the B-ow mode with SRI (bottom right); the B-ow mode is comparable to contrast-enhanced ultrasound (CEUS) in terms of stent delineation
and allows morphologic stenosis grading.
f Color duplex image, B-ow image, and CT angiogram of high-grade ICA in-stent restenosis. Like all ultrasound techniques, B-ow imaging is
degraded by artifacts such as acoustic shadowing, which limits morphologic stenosis grading using this technique

ab
ef
Chapter 5 · Extracranial Cerebral Arteries
382
5
c
. Fig. 5.87a–g (Atlas) Vertebral artery.
a Origin of the vertebral artery from the subclavian artery interrogated with the transducer in the supraclavicular position. The ow prole is similar
to that of the internal carotid artery (ICA). The identity of the vertebral artery is conrmed by transmission of the oscillations elicited by tapping the
mastoid area (as illustrated in the waveform shown).
b Care must also be taken not to confuse the thyrocervical trunk (T.TC) with the vertebral artery (A.VERT). It supplies the thyroid and therefore has
a similar waveform and comes more easily into view, in particular when the insonation conditions are poor, because its origin from the subclavian
artery is closer to the transducer than the origin of the vertebral artery.
c Vertebral artery coded in red between two transverse processes (WK). The vein (V) is depicted closer to the transducer with ow in blue.
d Spectral Doppler imaging of the vertebral artery by interrogation of the atlas loop (transducer placed below the mastoid and directed toward the
contralateral eye) stems from the era of CW Doppler ultrasound and has become less important with the advent of duplex ultrasound. However, this
approach is useful to sample the vertebral artery Doppler spectrum during functional testing performed to diagnose postural compression of the
vertebral artery by a vertebral body. In this setting, evaluation of the atlas loop enables follow-up of postocclusive waveform changes in a fairly xed
position during movements of the neck. As with CW Doppler, changes in ow direction are reected in the Doppler waveform. In the example, there
is ow toward the transducer in the proximal portion of the atlas loop. In the distal atlas loop, ow is away from the transducer.
Hypoplastic vertebral artery.
e Hypoplastic vertebral artery with a diameter of 1.6mm and reduced ow velocity, in particular during diastole (PSV of <40cm/s and EDV of
<5cm/s). A compensatory increase in ow is measured in the contralateral vertebral artery (PSV of 90cm/s and diameter of 4mm; not shown).
f, g Vertebral artery hypoplasia.
f Hypoplastic vertebral artery (A.VERT) with a diameter of 1.9mm depicted at the origin from the subclavian artery (A.S).
g The contralateral vertebral artery, also shown at the origin from the subclavian artery (A.S), is hyperplastic (diameter of 4.7mm). The Doppler wave-
form from the hypoplastic vertebral artery shows more pulsatile ow. Individuals with a very hypoplastic vertebral artery have an increased risk of
brain stem infarction. Moreover, as in the patient shown, certain rotational movements of the head can cause transient brain stem syndrome resulting from intermittent compression of the contralateral hyperplastic artery on its course through the foramina. This can cause reproducible episodes
of vertigo with certain head positions, which will disappear after a few seconds when the head is returned to its normal position
d

cd
5.10 · Atlas: Extracranial Cerebral Arteries
g
. Fig. 5.87 (continued)
383
5
a
. Fig. 5.88a–d (Atlas) Vertebral artery origin stenosis.
a Color duplex imaging shows aliasing due to turbulence at the origin of the vertebral artery (coursing leftward in the display) from the subclavian
artery (A.SUBCL). At the origin, color coding is absent from the lumen due to plaque with acoustic shadowing. The spectral waveform documents
the stenosis with a peak systolic velocity (PSV) of 320cm/s and an end-diastolic velocity (EDV) of 80cm/s. The vertebral artery is distinguished
from the thyrocervical trunk, which has a similar ow prole, by the transmission of the oscillations from rhythmical tapping of the distal vertebral
artery below the mastoid (indicated by arrows in the waveform).
b Angiogram: Stenosis (arrowhead) at origin of vertebral artery.
Grading of vertebral artery stenosis.
c Grading of vertebral artery stenosis based on absolute PSV cutos (as used for grading ICA stenosis) is unreliable due to the wide normal PSV
variation in the vertebral arteries. In the case presented, there is borderline stenosis with a PSV of 150cm/s. This case also illustrates the diculties
in achieving adequate Doppler angle correction in the arched course of the vertebral artery. The ratio of intrastenotic to poststenotic PSV allows
reliable grading of mild to moderate stenosis but not of high-grade stenosis.
d A rather high poststenotic PSV of 60cm/s with a slightly delayed systolic rise is measured in the V2 segment, and the resulting PSV ratio indicates approx. 60% stenosis
b
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