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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

334
Chapter 5 · Extracranial Cerebral Arteries
5
. Fig. 5.30 a Recanalization after internal carotid artery (ICA) occlusion (thin patent lumen with slow, pulsatile ow). The external carotid artery
(ECA) takes a more supercial course. b When insonation conditions are poor and acoustic shadowing from calcied plaques prevents thorough
evaluation, ECA occlusion may be mistaken for ICA occlusion. To avoid this error, it is important to follow the occluded artery cranially: in the
example, the distal portion of the occluded ECA is relled by a collateral (ECA KOL). When the ICA is occluded, distal relling only occurs in individuals with a persistent primitive hypoglossal artery (PPHA). Another pitfall to be borne in mind is that the postocclusive ECA waveform becomes
more like that from the ICA (internalization; b). In this situation, the temporal tap maneuver can help conrm the identity of the ECA (.
Fig.5.6)
reported incidence is 0.027–0.26% (Yilmaz et al. 1995).
Autopsy data suggest that patients with a PPHA typically
have other variants of vascular anatomy (Vasovic etal. 2008).
A common association is a hypoplastic or aplastic vertebral
artery with the main supply to the posterior circulation coming from the ICA via the PPHA (Elhammady et al. 2007).
is is why patients with high-grade carotid stenosis may
show disturbed perfusion of the posterior circulation
(Kanazawa etal. 2008; Yuasa etal. 2005). In very rare cases of
total or subtotal ICA occlusion, a PPHA supplies blood to the
distal ICA (. Fig.5.31). In 2007, Ehammady etal. published
what they claimed to be the rst report of a PPHA with retrograde ow in a patient with high-grade proximal ICA stenosis. Much earlier, however, in 1992, Widmann and Sumpio
reported a patient with ow in the distal ICA and absence of
ow proximally, which was initially misdiagnosed as pseudoocclusion. Intraoperatively, they found proximal ICA occlusion and distal relling via a PPHA.Published data on the
frequency of PPHAs (incidentally) detected during carotid
artery ultrasound examinations are not available. In a retrospective analysis of 6300 patients who underwent carotid
duplex ultrasound for suspected carotid stenosis or other
indications, the author identied PPHA in 0.08% of cases.
More than half of the PPHAs (0.05%) showed retrograde ow
because they functioned as collaterals in proximal ICA occlusion. It is expected that, with awareness of this collateral pathway, more PPHAs will be identied by color duplex ultrasound
in the future (Schäberle 2013). However, the sonographic
detectability of PPHA strongly depends on the insonation
conditions and is impaired in severe atherosclerosis with calcied plaques. erefore, the frequency is likely to vary with
the composition of the patient population investigated.
A PPHA with normal ow typically has a thin caliber
(. Fig. 5.31d, e) and is more dicult to detect and dierentiate from ECA branches than a dilated PPHA recruited
as a collateral in high-grade ICA stenosis or occlusion
(. Fig.5.64b–d (Atlas)).
Sonoanatomically, a PPHA arises from the ICA slightly
cranial to the bulb and runs to the skull base dorsomedial to
the ICA.It courses through the hypoglossal canal to join the
vertebrobasilar system, where aneurysmal dilatation may
occur.
In addition, there may be compression of the hypoglossal
nerve, and iatrogenic injury of the PPHA during carotid endarterectomy (CEA), like high-grade carotid stenosis, can
cause disturbed perfusion of the posterior circulation in
patients with a hypoplastic vertebral artery.
5.6.1.4 Postoperative Follow-Up
5.6.1.4.1 Carotid Endarterectomy (CEA)
ree operative techniques are available for carotid endarterectomy (CEA) in patients with carotid artery stenosis
(. Fig.5.32).
In patients with a wide carotid bulb, CEA can be performed with direct closure of the arteriotomy. A possible
complication of this procedure is the inadvertent creation of
a relative stenosis compared with the distal ICA lumen by
pulling the vessel wall too tight.
is complication can be prevented by interposing a
synthetic or venous patch
aer CEA to compensate for the
relative narrowing that may be created by primary closure.
Too wide a patch, on the other hand, will lead to ectasia or
even aneurysm with development of turbulent ow.
In eversion CEA, the ICA is transected at its origin, and
the outer layer over the stenosing plaque-intima cylinder is
everted and dissected along the vessel until the intima
appears fairly normal again. At this point the cylinder is transected, and the outer wall layer is re-inserted into the common carotid artery (CCA).

de
5.6 · Ultrasound Criteria, Measurement Parameters, andDiagnostic Role
a
335
5
b
. Fig. 5.31 Persistent primitive hypoglossal artery (PPHA) a Patient with atrial brillation and absolute arrhythmia and sonomorpholic ndings
pointing to embolic internal carotid artery (ICA) occlusion. Sonographic evaluation shows a normal common carotid artery (CCA) and bifurcation, while no ow is detectable in the ICA just distal to the bifurcation. The distal extracranial ICA segment has monphasic ow and normal ICA
pulsatility (PSV of 90cm/s). The patient subsequently underwent angiography. The rst angiogram conrms ICA occlusion with distal relling via
a PPHA, which ensures adequate blood ow in the aected ICA territory. In this situation, the contralateral ICA or posterior cerebral circulation
is not required to provide compensatory blood ow to the brain. The second angiogram shows the late phase of relling of the distal ICA via the
PPHA. b Dilated PPHA with retrograde ow (red, toward transducer, A.P) with a PSV of 125cm/s (the occluded segment of the ICA is seen in the
right half of the image). c The patent distal ICA has a normal-diameter lumen and a ow volume similar to an unobstructed ICA (PSV of 95cm/s
and normal pulsatility). These ndings conrm good perfusion via the dilated PPHA.Delayed systolic upslope (acceleration time), compared with
the unaected contralateral side, is the only sign of postocclusive ow in the waveform from the distal ICA.Based on these ultrasound ndings,
surgery is unnecessary or even harmful. In addition, duplex ultrasound identied a compensatory increase in blood ow in the vertebral artery
(PSV of 110cm/s; not shown). d, e Normal ICA with PPHA.The example illustrates the incidendal detection of a PPHA, seen as a thin artery arising from the unobstruced extracranial ICA (d, with ICA waveform). The ow direction is orthograde (blue), as in the ICA (e, with PPHA waveform).
Normally, the ICA does not give o extracranial branches. Color reversal (from red to blue) is due to a change in ow direction relative to the
transducer (curved array)
c

336
Chapter 5 · Extracranial Cerebral Arteries
. Fig. 5.32a–d Surgical and
interventional restoration of
patency in internal carotid artery
(ICA) stenosis. a Carotid endarterectomy (CEA) with direct closure.
b CEA with patch angioplasty.
c Eversion CEA. d Percutaneous
transluminal angioplasty (PTA)
with carotid artery stenting (CAS)
5
Each CEA technique alters postoperative carotid bulb
anatomy in a specic way: while CEA with patch insertion
leads to an unphysiologically wide carotid bulb, the other two
CEA techniques reduce bulb width to the normal ICA diameter. As a result of the loss of normal bulb anatomy, the correlations that exist in the native ICA no longer apply, and the
two methods of carotid stenosis grading (local versus distal)
yield the same results. e PSV ratio (intrastenotic to prestenotic PSV in the ICA) therefore oen allows reliable grading
of recurrent stenosis aer CEA (which tends to involve the
segment distal to the bifurcation or the distal end of the segment operated on). However, in the follow-up of patients
aer CEA with patch insertion, the hemodynamic eects of
the caliber variation at the distal patch end must be taken
into account in interpreting the sonographic ndings.
Moreover, each CEA technique is prone to specic com-
plications
that must be carefully ruled out by postoperative
ultrasonography. e complications of the primary closure
technique, apart from relative narrowing as an early complication, include an intimal step or an intimal ap. Elongation
of the ICA can lead to kinking with development of a stenosis
unless the excessive segment is resected.
Patch angioplasty is susceptible to thrombotic deposits,
but these may resolve, even aer days, following treatment
with heparin and platelet aggregation inhibitors (see
. Fig.5.78 (Atlas)). However, such thrombotic deposits can
also induce transient ischemic attacks (TIAs) or early occlusion. Aneurysmal dilatation due to excessive correction gives
rise to turbulent ow. Suture aneurysms primarily occur in
association with infection and aer insertion of a synthetic
patch. At the junction of the patch with the distal ICA, detachment of the intima can lead to the same complications as
direct closure. Use of a venous patch can give rise to the formation of a true aneurysm due to the physiologically weaker
venous wall. Over time, patients may develop recurrent stenosis. Hence, in the follow-up examination, special attention
must be paid to intimal hyperplasia in the suture area.
Suture line complications are rare in eversion CEA, while
step formation at the transition to the native intima is somewhat more common (. Table5.14).
. Table 5.14 Sonographic evaluation for postoperative
complications after carotid endarterectomy (CEA)
CEA
technique
CEA with
direct closure
CEA with
patch
angioplasty
Eversion CEA Retraction of suture line,
Evaluation of operative
site
Relative stenosis,
recurrent or residual
stenosis
Thrombotic deposits in
the patch area without/
with hemodynamically
signicant stenosis,
suture aneurysm,
ectasia, infection,
recurrent stenosis
suture aneurysm,
recurrent stenosis
Evaluation of distal
ICA
Intimal step,
intimal ap, intimal
dissection, kinking,
intimal hyperplasia
Intimal step,
intimal ap, intimal
dissection, kinking,
intimal hyperplasia
Intimal ap, intimal
step, intimal
dissection, intimal
hyperplasia
e specic complications of the dierent CEA techniques must be borne in mind when performing the mandatory postoperative duplex scan. Postoperative sonography is
impaired by scattering through edema, which may aect
both B-mode and spectral Doppler imaging. e use of a
lower-frequency transducer (5 or even 3.5 MHz) yields
B-mode images with a poorer resolution but oen facilitates
both the identication of the target artery within the edematous tissue and spectral Doppler measurement for exclusion
of early occlusion, residual stenosis, or thrombotic deposits.
e development of recurrent stenosis has been investigated in numerous studies with postoperative follow-up by
duplex ultrasound (. Fig.5.33). However, the studies do not
address the problem of the diagnostic accuracy of ultrasound
in detecting the above-described early complications under
the poorer postoperative insonation conditions (. Figs.5.78
and 5.79 (Atlas)). Clinical experience indicates that patients
with transient ischemic attacks (TIAs) aer CEA with patch

5.6 · Ultrasound Criteria, Measurement Parameters, andDiagnostic Role
. Fig. 5.33 Moderate recurrent
carotid stenosis in transverse and
longitudinal orientation (caused
by a ap-like, oating structure,
indicated by arrow in the 2
longitudinal views) after carotid
endarterectomy (CEA) with patch
angioplasty (seen in the near
wall). The PSV is 180cm/s
337
5
closure oen have thrombotic deposits on the synthetic
patch, even if no hemodynamic eect is apparent in the Doppler waveform. e deposits may completely resolve within
days to weeks under heparin and antiplatelet therapy. No
studies have investigated these complications in terms of
their possible impact on patch selection. Color duplex ultrasound allows dierentiation of intimal dissection and intimal
aps, which are oen seen as hyperechoic oating structures
in the bloodstream.
e ow pattern in a suture aneurysm is the same as in a
pseudoaneurysm. To-and-fro ow can be demonstrated by
color duplex or spectral Doppler (see 7 Sect. 2.1.6.3 and
. Figs.5.70 and 5.71 (both Atlas)).
If semiclosed endarterectomy of the external carotid
artery (ECA) is performed, intimal aps or dissection may
give rise to stenosis or occlusion. ey rarely have functional
or clinical signicance but must be considered in the dierential diagnosis when examining the ICA.
e intimal step at the proximal end of the operated on
segment in the CCA is oen highly conspicuous in the
B-mode image but has no clinical or functional relevance as
the step attens out in the direction of the owing blood.
Recurrent stenosis within the rst 12months of surgery
is due to neointimal proliferation (unless the operation has
been technically inadequate). Recurrence seen aer 2years is
attributable to the progression of atherosclerosis. Based on
the follow-up data from more than 160 studies including
over 62,000 patients, the average restenosis rate is 6% (range,
0–50%) (Kallmayer etal. 2014). Plaque echogenicity (mean
GSM) is lower than in primary ICA stenosis (
. Fig.5.35e)
without this indicating a higher stroke risk (Pavela et al.
2014). e incidence of symptomatic recurrent carotid stenosis is 2% with the recurrence rate being markedly higher
aer CEA with direct closure than aer patch angioplasty
(12% versus 5%). Overall, approx. 20% of all stenoses seen
aer CEA are accounted for by residual stenoses, 50% develop
within 2years, and 30% occur later. Long-term follow-up of
380 patients for 16years revealed restenosis rates of 5.8%,
9.9%, 13.9%, and 23.4% aer 1, 3, 5, and 10years, respectively; however, only 2.1% of patients were found to have
high-grade recurrent stenosis (> 80%) (Mattos et al. 1993;
Roth etal. 1999). In the follow-up aer CEA, sonographic
evaluation of the unoperated side with identication of progressive atherosclerosis appears to be more relevant than
imaging of the side where CEA was performed. It has been
proposed that routine duplex surveillance in the rst
6months is not required when an intraoperative completion
study has conrmed the technical adequacy of the repair
(Pross etal. 2001;
. Fig.5.34). However, experience seems to
indicate that it is common to detect thrombotic deposits in
patients with postoperative TIAs despite normal intraoperative ndings, especially when a synthetic patch has been
used. Such deposits respond well to heparin treatment (follow- up within 4 weeks is recommended).
5.6.1.4.2 Carotid Artery Stenting (CAS)
Following percutaneous transluminal angioplasty (PTA)
with carotid artery stenting (CAS), ultrasound depicts the
stent as a mesh-like structure. A diagnostic Doppler waveform is dicult to obtain from the stented carotid segment
during the rst days, presumably because the stent is not yet
incorporated. Aer this initial period, the scanning conditions are the same as before stent placement. Stents are also
prone to thrombotic deposits, which may cause stenosis but
will recede aer initiation of treatment with heparin and
platelet antiaggregators. e distal stent end is especially
prone to recurrent stenosis (. Figs. 5.35, 5.82 (Atlas), and
5.83 (Atlas)).
Scientic evidence suggests that higher blood ow velocity cutos are needed for postinterventional surveillance of
patients aer CAS (Stanziale etal. 2005). Loss of compliance
of the arterial wall
aer stent insertion results in higher normal velocities; thus, it has been proposed that a PSV of up to
150 or 180cm/s should be considered normal in a stented
carotid artery segment (Chahwan etal. 2007; Lal etal. 2004).
5.6.1.4.3 Scientic Discrepancies Regarding
Restenosis Grading After CAS
Several studies investigating restenosis aer carotid artery
stenting (CAS) proposed peak systolic velocity (PSV) thresholds of 150–240cm/s for >50% stenosis and 300–450cm/s
for >70% (to 80%) stenosis (Alexander etal. 2007; AbuRahma
etal. 2008; Lal etal. 2008; Stanziale etal. 2005; Kwon etal.
2007; Zhou etal. 2008; Chi etal. 2007). Most of these studies
assessed stenosis severity using North American Symptomatic Carotid Endarterectomy Trial (NASCET) methodology.
When European Carotid Surgery Trial (ECST) methodology
is used, the PSV cutos for identifying equivalent degrees of

338
Chapter 5 · Extracranial Cerebral Arteries
. Fig. 5.34 Diagnostic
algorithm for the follow-up of
patients after carotid endarterectomy (CEA) based on NASCET
grading of restenosis. CAS carotid
artery stenting, TEA thromboendarterectomy
Duplex follow-up after
surgical repair
within one week of surgery
and at 6 months
<30% restenosis
30–69% restenosis 70–99% restenosis Occlusion
5
Follow-up at
12-month intervals
(& contralateral
carotid!)
Follow-up at
6-month intervals
Early restenosis
(<2 years): intimal
hyperplasia
Focal Diffuse
Angiography with
CAS
Follow-up only of
contralateral carotid
Late restenosis
(>2 years):
atherosclerosis
Angiography
Reoperation:
TEA & patch,
graft interposition
stenosis should be approx. one third lower because a given
PSV indicates a higher-grade local stenosis (ECST) compared with the distal degree (NASCET). e second issue to
be considered is that dierent velocity criteria apply when
grading in-stent restenosis compared with restenosis in a
nonstented carotid artery. Two studies investigating carotid
restenosis proposed cutos of 180 and 200cm/s for >50%
restenosis (NASCET criteria) in unstented carotid arteries
versus 220 and 240 cm/s for in-stent restenosis (Lal et al.
2008; Chi etal. 2007). According to these studies, the cuto
for in-stent restenosis is only approx. 10–20% higher than for
restenosis in native carotid arteries.
e need for modied velocity criteria in stented carotid
arteries was also conrmed by AbuRahma etal. (2008), who
conducted a ROC analysis to determine cutos for dierent
degrees of in-stent carotid restenosis. In this study, a PSV
threshold of 154cm/s for >30% stenosis (by NASCET criteria) showed 99% sensitivity and 89% specicity. e optimal
PSV cuto for >50% stenosis was 224cm/s, which had 99%
sensitivity, 90% specicity, 99% positive predictive value,
90% negative predictive value, and 98% overall accuracy.
e ideal cuto for >80% stenosis was 325cm/s with 100%
sensitivity, 99% specicity, and 99% accuracy. e diagnostic
accuracy of absolute PSV was compared with end-diastolic
velocity (EDV) and also with the ratio of PSV in the stented
ICA to the PSV in the CCA.is comparison showed that
PSV provided the most reliable criterion for sonographic
stenosis grading in 144 patients in whom the results were
compared with angiography. Nineteen of the patients had
>50% in-stent restenosis. Large PSV ranges were found for
dierent categories of stenosis (dened by angiography,
NASCET criteria): range of 142–256cm/s with a mean PSV
of 178/s for 30–50% stenosis (n=38); 201–408cm/s with a
mean PSV of 278cm/s for 50–80% stenosis (n= 11); and
58–613cm/s with a mean of 403cm/s for 80–99% stenosis
(n=8).
A minor limitation of published ultrasound studies of
carotid in-stent restenosis is the small number of cases investigated. Although some study populations include more than
100 patients with duplex ultrasound aer CAS (
. Table5.15),
ROC analysis was usually performed in subsets of 10–20
patients who underwent angiography because they had restenosis of at least 50% and were candidates for possible reintervention.

ab
cd
5.6 · Ultrasound Criteria, Measurement Parameters, andDiagnostic Role
339
5
Moreover, most studies use CT angiography (or magnetic
resonance imaging) as the method of reference for color
duplex imaging rather than the gold standard of angiography
in two or three planes, neglecting the inherent methodological limitations of CT angiography, especially in the carotid
bifurcation. is introduces an additional inaccuracy into
the ROC analysis of sonographic velocity thresholds. Most
investigators use catheter-based angiography only in patients
undergoing repeat PTA for higher-grade stenosis; as a result,
the gold standard is available only for these cases.
In the discussion of velocity thresholds for quantifying
carotid in-stent restenosis compared with restenosis of nonstented arteries, it was initially overlooked that the approximately one third higher cutos proposed in studies using
NASCET methodology could not simply be converted to
ICA
1
3
ECA
2
6
equivalent cutos for in-stent restenosis grading using ECST
methodology. Instead, it turned out that PSV cutos for diagnosing in-stent restenosis based on ECST methodology
should only be slightly higher than cutos for nonstented
arteries (see
. Table 5.9). Higher blood ow velocities in
stented carotid segments may be attributable to several factors. One is rigidity of the stented arterial wall, which results
in higher PSV within the stent; however, it has also been
shown that pulsatility varies with the stent device used. At
the same time, it is hard to believe that the dierence in rigidity between a stented segment and an atherosclerotic, calcied ICA with higher-grade stenosis is so large as to explain a
30% dierence in PSV or to justify a 30% higher PSV cuto
for in-stent restenosis. e lumen reduction by the stent does
not explain this dierence either.
4
5
CCA
. Fig. 5.35 a Common sites of early and late complications and progressive atherosclerosis after carotid endarterectomy (CEA): 1 intimal ap;
2recurrent stenosis due to plaque; 3 neointimal proliferation with recurrent stenosis; 4 postoperative external carotid artery (ECA) occlusion;
5 damage from clamping, step, plaque progression at proximal end of CEA; 6 suture aneurysm. b Early and late complications after carotid artery
stenting (CAS): neointimal hyperplasia; recurrent plaque with stenosis; ECA stenosis, when ICA stent crosses the ECA origin. (For stent dislocation,
see . Fig.5.85 (Atlas)). c Moderate recurrent stensosis caused by intimal ap (arrow) seen at follow-up 1week after CEA (PSV of 150cm/s).
d Recurrent stenosis caused by neointimal proliferation 8months after CEA. e Recurrent stenosis caused by plaque (P) due to progressive atherosclerosis is often identied by echolucency without this indicating an increased risk of embolism (images obtained 6years after CEA). The Doppler
waveform conrms high-grade recurrent stenosis with a PSV of 350cm/c. f Suture aneurysm. This patient presented with local swelling due to a
large hematoma after CEA.The ultrasound examination reveals to-and-fro ow (with systolic (s) inow and diastolic outow (d) in the waveform
from the site of suture line rupture identied by color duplex ultrasound. A suture line rupture should always alert the examiner to the possibility
of infection as an underlying cause

340
Chapter 5 · Extracranial Cerebral Arteries
¬Patch®
¬Patch®
5
e
f
. Fig. 5.35 (continued)
. Table 5.15 Dzsound criteria for in-stent restenosis after carotid artery stenting (CAS)
Author, year No. PSV (cm/s) ICA/CCA ratio
> 50% > 70% > 80% > 50% > 70% > 80%
AbuRahma 2008 144/19 224 325 3.4 4.5
Lal 2008 189/29 220 340 2.7 4.1
Stanziale 2005 118/19 225 350 2.5 4.75
Peterson 2005 170
Chi 2007 13 240 450 2.45 4.3
Wei Zhou 2008 237/22 300 4
Kwon 2007 200 2.5
No.: total number of patients with CAS examined with duplex ultrasound/number of patients who underwent angiography or CT angiography
CCA common carotid artery, ICA internal carotid artery, PSV peak systolic velocity
5.6.1.4.4 Stenosis Grading Based onthe
Continuity Equation
As recurrent stenosis at the proximal stent end (i.e., the
junction between the common carotid artery (CCA) and the
stent) is less common than in-stent restenosis or stenosis at
the distal stent end (. Fig.5.37b), abrupt doubling of peak
systolic velocity (PSV)
ment– which is well established for diagnosing stenosis in
peripheral arteries– can be used for the diagnosis of hemodynamically relevant in-stent restenosis (50% stenosis) in
the carotid system as well (. Figs.5.36, 5.37, and 5.38). When
the increase in intrastenotic PSV is determined using the
in a continuous Doppler measure-

5.6 · Ultrasound Criteria, Measurement Parameters, andDiagnostic Role
341
. Fig. 5.36 Patient with restenosis after carotid artery stenting (CAS). Continuous spectral Doppler imaging revealed a focal increase in peak
systolic velocity (PSV) in the stent from 100cm/s in the prestenotic segment to 210cm/s in the stenosis. For this measurement, the spectral
Doppler waveform was recorded by moving the transducer along the artery in a cranial direction in order to continuously shift the sample volume from the prestenotic to the intrastenotic segment of the stent, while maintaining a constant Doppler angle (the segment along which the
Doppler tracing was recorded is indicated by >>…<< in the B-mode image). The pre- and intrastenotic PSVs give a PSV ratio of 2, consistent
with 50% in-stent restenosis. Restenosis in this case is not caused by stent dislocation but by the rigidity of the snugly tting stent: elastic recoil
of the short, stenotic, brace-like plaque at the origin of the ICA (identied by hyperechogenicity) results in conical tapering of the stent. The
example illustrates how PSV increases as the cross-sectional area decreases along the tapering stent. Although the stent is patent, increasing
ow resistance in the narrowing portion of the stent causes hemodynamically relevant stenosis. This type of stenosis is more dicult to identify
by angiography
5
PSV ratio, this velocity should be related to PSV just
upstream of the in-stent restenosis rather than to PSV in the
common CCA.However, in some studies (AbuRahma etal.
2008; Lal et al. 2008; Stanziale et al. 2005; Peterson etal.
2005; Chi et al. 2007), investigators determined the CCA/
ICA PSV ratio for diagnosing ICA in-stent restenosis, proposing cuto ratios of 2.5–3.4 for >50% stenosis and 4–4.5
for >70% or >80% stenosis. While calculation of the intrastenotic PSV increase in relation to the PSV in the CCA
accounts for systemic eects on PSV as well as compensatory ow increases in patients with contralateral stenoocclusive ICA lesions, in-stent restenosis grading using the
CCA/ICA PSV ratio is subject to the same pitfalls as in the
native arteries: PSV in the CCA varies with the volume ow
rate in the external carotid artery (ECA), which increases
when the ECA is recruited as a collateral. is problem can
be avoided by measuring the prestenotic PSV for calculation
of the velocity ratio in the proximal ICA, which is oen possible, as in-stent restenosis in the carotid territory tends to
occur upstream of the origin of the ECA. Using the PSV
from the proximal ICA is more reliable because it is not
inuenced by other factors such as hemodynamic eects of
branching arteries, diameter variations, or dierences in
vessel wall rigidity. Ideally, the prestenotic PSV for calculation of the velocity ratio should be measured within the stent
to eliminate possible eects of the stent on vessel lumen
width or wall rigidity. Use of the PSV ratio also avoids the
well-established problems that arise from the wide variation
in absolute PSVs measured for a given angiographic degree
of stenosis and the fact that this parameter is aected by a
variety of other factors (AbuRahma etal. 2008). In a compilation and analysis of an as yet small number of patients, the
author identied nine patients with higher- grade carotid instent restenosis, classied as >75% stenosis based on the
continuity equation and a cuto ratio of intra- to prestenotic
PSV in the ICA of >4. Absolute intrastenotic PSV in these
nine patients ranged from 230–455cm/s (
. Figs.5.36, 5.37,
and 5.38 and . Figs. 5.81, 5.82, and 5.83 (Atlas)). All nine
cases were conrmed by subsequent angiography. Stenosis
grading using this PSV ratio is dierent from both ESCT and
NASCET methodology (local versus distal carotid stenosis
grading) but is methodologically closer to the latter. Dierences in diameter between the carotid bulb and the distal
ICA are eliminated when a stent is in place. In this articial
situation of a relatively constant ICA diameter, it follows
from the continuity equation that a PSV ratio of 2 or doubling of PSV indicates 50% cross-sectional area reduction,
while a ratio of 4 corresponds to 75% area reduction in the
stent. A 75% cross-sectional area reduction corresponds to
50% diameter reduction when caused by circumferential stenosis. Conversely, 50% diameter reduction caused by an
eccentric plaque results in a smaller cross-sectional area
reduction, and therefore the resulting stenosis has a less
severe hemodynamic eect and causes a smaller increase in
PSV (
. Fig. 5.27). While causing less severe stenosis, an
eccentric plaque is thicker and exposed to greater shear
stress, which increases the risk of embolism (. Fig.5.15a).
is risk must be taken into consideration as well when
assessing the therapeutic relevance of carotid in-stent
restenosis.

342
Chapter 5 · Extracranial Cerebral Arteries
5
a
ICA
Intrastenotic PSV
Prestenotic PSV
ECA
Stent
b
. Fig. 5.37 a High-grade carotid in-stent restenosis at the distal stent end with an intrastenotic-to-prestenotic PSV ratio of >4 (calculated
from intrastenotic PSV of 414cm/s and prestenotic PSV of 97.6cm/s– the latter measured in the stent just distal to the ECA origin). The site of
PSV increase is identied by moving the transducer cranially while obtaining a continuous spectral tracing at a constant Doppler angle (curvedarray transducer, tilted to achieve good Doppler angle, 54° in the example) (see .
restenosis with a PSV ratio>4 but with an absolute intrastenotic PSV of only 268cm/s). The angiogram (right) shows high-grade ICA in-stent
restenosis (projection plane). b Diagram illustrating the author’s approach to grading carotid in-stent restenosis based on the continuity equation
(see . Fig. 1.44 and 7 Sect. 1.2.3). This approach avoids the confusion regarding distal versus local stenosis grading (NASCET versus ECST) and
exploits the fact that a stented carotid artery segment has a fairly constant diameter and that most in-stent restenoses occur within the stent farther away from the ECA origin or even at the distal stent end. The drawing shows the sites where prestenotic and intrastenotic PSV for calculation
of the PSV ratio should be measured. This is the most accurate method for grading in-stent restenosis of the ICA (see . Figs.5.81, 5.82, and 5.83
(all Atlas))
CCA
PSV ratio for grading in-stent
ICA stenosis
In-stent restenosis
Fig.5.83b (Atlas) for another example of high-grade in-stent
B-ow ultrasound (see . Fig.5.86 (Atlas)) and contrast-
enhanced ultrasound (CEUS) (Clevert et al. 2011) (see
7 Sect. 5.6.1.1.8) allow very accurate morphologic grading of
carotid in-stent stenosis. e diagnostic performance is comparable to angiography, while B-ow imaging aords higher
spatial resolution.
5.6.1.4.5 Stent Dislocation
While ultrasound provides no valid diagnostic information
in patients with dislocation of an aortic stent, it is well suited
to evaluate patients with suspected dislocation of an ICA
stent. In the carotid territory, duplex ultrasound with a highfrequency transducer provides highly resolved information

5.6 · Ultrasound Criteria, Measurement Parameters, andDiagnostic Role
. Fig. 5.38a, b Illustration
of stenosis grading in a native
common carotid artery (CCA) and
stented CCA using the continuity
equation. Study-based velocity
cutos have not been dened for
grading CCA stenosis. a In this
patient, >75% stenosis is diagnosed based on a peak systolic
velocity (PSV) ratio>4 (calculated
from PSVs of 264 and 61cm/s).
b Following stent implantation,
the patient developed in-stent
restenosis due to elastic recoil of
the plaque; restenosis is classied
as moderate based on a PSV ratio
of 2.7 (PSVs: 158/58cm/s) (see
. Figs.5.36 and 5.37 for how
to obtain a continuous spectral
Doppler tracing for PSV measurement along the stented arterial
segment). The angiogram conrms in-stent restenosis (arrow)
of the CCA
343
5
on blood ow within the stent or between the stent and the
wall of the native artery (see . Fig.5.85 (Atlas)). e ndings
can be corroborated by contrast-enhanced ultrasound
(CEUS), and the time-motion mode provides additional
information on pressure-related stent movement within the
arterial lumen. A diameter mismatch between the artery and
an uncoated stent can result in blood ow between the stent
and the native arterial wall. Here, ultrasound is superior to
angiography because, following opacication, the thin bloodstream outside the stent lumen is dicult to dierentiate
from ow within the lumen.
Straightening of an elongated and tortuous ICA by a rigid
stent can lead to kinking distally. Color duplex imaging
allows identication of kinks and associated stenosis as well
as any (postural) reduction in cerebral perfusion, which may
occur in patients with bilateral carotid stents.
5.6.2 Vertebral Arteries
5.6.2.1 Stenosis
e origin of the vertebral artery may be dicult to evaluate
by color duplex imaging when a kink or loop is present. Aris-
ing at a right angle from the subclavian artery, the vertebral
artery exhibits disturbed ow at its origin, which must not be
mistaken for stenosis. e curved course at the origin may
lead to Doppler angle uncertainty and an unreliable ow
velocity calculation for stenosis grading.
Virtually all atherosclerotic stenoses of the vertebral
artery occur at its origin. Since there is wide variation in peak
systolic velocities and in the ow volume of the vertebral arteries and there may be marked dierences in caliber between the
two vertebral arteries (hyperplasia, hypoplasia), no absolute
cuto value (as for the carotid arteries) can be dened to discriminate between low-grade and hemodynamically signicant stenosis (. Figs.5.39 and 5.40). erefore, indirect criteria
such as turbulent ow at the origin or markedly reduced pulsatility compared with the contralateral artery can be considered but should be interpreted with caution. Vertebral artery
stenosis is suggested when PSV at the origin is at least 50%
higher than in more distal segments. Grading of stenosis at the
vertebral artery origin is dicult for several reasons:
5 Absolute PSV cuto: unreliable due to interindividual
variation and variable perfusion
5 Comparison with contralateral side: precluded due to
variability or possible hypoplasia
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