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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

2.1 · Pelvic andLeg Arteries
. Table 2.8 Sonographic dierentiation of vascular abnormalities in B-mode imaging
73
2
Diagnostic information
provided by B-mode
imaging
Circumscribed wall thickening (intima), low/high
echogenicity, acoustic
shadowing?
Concentric wall thickening of
long segment (.
Dilated appearance
(.
Fig.2.27)
Anechoic cystic wall lesions
Fig.2.29)
(.
Abnormal arterial course,
possibly with external
compression (.
Vascular lumen not anechoic Embolic or thrombotic
Intraluminal echogenic
structures, ap-like
Fig.2.33)
Fig.2.31)
Suggested diagnosis Measurement performed with
Atherosclerotic plaque Stenosis grading: waveform
Arteritis Measurement of wall thickness
Aneurysm, dilated angiopathy Measurement of aneurysm
Adventitial cystic disease Degree of stenosis, which may
Vascular compression syndrome,
stenosis or occlusion? (entrapment syndrome)
occlusion, artifact, inadequate
machine settings (consider
clinical presentation: symptoms
of critical ischemia?)
Dissection Color duplex to conrm
duplex imaging (optimized
settings)
(adjust PRF and gain settings)
and length of involved segment,
stenosis grading, occlusion?
(higher-frequeny transducer)
diameter, intravascular
thrombus?
vary with cyst size (repeat
examination)
Functional assessment:
increasing stenosis (or even
occlusion) with increasing
plantar exion/vascular
compression by muscle
Color duplex to determine
length of occlusion (very low
PRF, higher gain)
diagnosis by identication of
true and false lumen
Further diagnostic testing to
resolve inconclusive duplex
ndings (if therapeutically
relevant)
CEUS, MRA, IA DSA (depending
on treatment options contemplated)
Inammatory parameters, ESR,
MRA
Color duplex, CT, IA DSA if
surgery is indicated (periphery)
CT, MRA
CT for documentation of
abnormal arterial course
Angiography, MRA
Angiography, CTA
CEUS contrast-enhanced ultrasound, CT computed tomography, CTA computed tomography angiography, ESR erythrocyte sedimentation
rate, IA DSA intra-arterial digital subtraction angiography, MRA magnetic resonance angiography, PRF pulse repetition frequency
Medial sclerosis in diabetics is characterized by diuse
calcication of the middle layer of the arterial wall. e calcications produce irregular and inhomogeneous wall thickening with scattering and acoustic shadowing, impairing
both B-mode and color ow imaging.
In the limb arteries, the high peripheral resistance
gives rise to pulsatile, nearly laminar ow. e normal
Doppler waveform is triphasic with a narrow bandwidth
and a clear systolic window. A triphasic waveform is characterized by a steep systolic rise and subsequent decrease,
followed by a short early diastolic reux and forward ow,
with the magnitude and duration depending on the vascular territory supplied. Physiologic changes in the laminar
ow prole can occur at vessel origins and in curved segments.
An obstruction caused by stenosis or external compression leads to ow acceleration in proportion to the cross-
sectional area reduction (see . Fig. 1.44) and ow becomes
turbulent (see . Fig. 1.46). A slight increase in ow velocity can already be observed with 30–50% luminal narrowing, but a relevant drop in peripheral arterial blood
pressure (ABI) is unlikely at rest. Low-grade stenosis
(<50%) has only little eect on the ow prole. With
increasing luminal narrowing, however, ow becomes less
pulsatile with turbulence and eddy currents downstream
of the stenosis. A reduction of the cross-sectional area
exceeding 75% (>50% diameter reduction) is associated
with a marked intrastenotic increase in PSV of more than
100% compared with the prestenotic arterial segment
(Jäger etal. 1985; Moneta etal. 1992). Flow becomes less
and less pulsatile, ultimately resulting in a monophasic
waveform
(. Fig. 2.14), which characterizes blood ow
both within and downstream of a high-grade stenosis
(Cossman etal. 1989; Polak etal. 1991; Kohler 1990).

74
Super
f
ar
P
ar
a
Chapter 2 · Extremity Arteries
Common
2
femoral
artery
ficial
emoral
tery
opliteal
tery
1.0
1.0
0.4
1.0
0.4
0.4
A
B
C
D
bA
bC
. Fig. 2.14 a Diagram of Doppler waveform changes induced by supercial femoral artery stenosis at dierent levels of the lower extremity
arterial tree. bA Nearly normal triphasic waveform from common femoral artery (far upstream of the stenosis). bB Prestenotic waveform from
proximal supercial femoral artery with slightly reduced peak systolic velocity (PSV) and reduced or absent early diastolic dip but steep systolic
upstroke. bC Monophasic ow prole with more than doubling of intrastenotic PSV compared to prestenotic PSV. bD Monophasic poststenotic
waveform from popliteal artery with delayed systolic upstroke and low PSV (damped waveform)
bB
bD

2.1 · Pelvic andLeg Arteries
75
2
e changes depicted by (color) duplex ultrasound at the
site of stenosis are known as direct stenosis criteria and the
poststenotic changes in the ow prole as indirect stenosis
criteria. For the leg arteries, the stenosis criteria are as follows:
5 Direct stenosis criteria:
5 Absolute intrastenotic PSV>180cm/s
5 Focal increase in PSV, expressed as intrastenotic-to-
prestenotic PSV ratio
Ȥ PSV ratio>2 indicates >50% stenosis (diameter
reduction)
Ȥ PSV ratio>4 indicates >75% stenosis (diameter
reduction)
5 Perivascular vibration
5 Indirect stenosis criteria:
5 Flow prole:
Ȥ Damping (triphasic/monophasic)
Ȥ Delayed systolic rise
Note, though, that the indirect criterion of monophasic ow
merely indicates a change from high-resistance to lowresistance ow due to peripheral vasodilation. Several (physiologic and pathologic) factors can alter the normal
waveform
5 Physiologic:
5 Pathologic:
Duplex ultrasound using the direct stenosis criteria has
83–99% accuracy in identifying hemodynamically signicant stenosis and occlusion of the aortoiliac and femoropopliteal arteries compared with angiography (. Tables 2.7 and
2.20). In a study of 125 patients with stage II-IV peripheral
arterial occlusive disease (PAOD) presenting with typical
symptoms, conducted by the author’s group (1998), (color)
duplex ultrasound detected hemodynamically relevant
steno-occlusive lesions with 96% sensitivity, 98% specicity,
and 97% accuracy compared with angiopgraphy. In this
study population, 31 percent of the patients had femoropopliteal steno-occlusive disease, 12% pelvic level involvement,
18% lesions in the arteries below the knee, and 39% had multilevel disease.
associated with mild to moderate stenosis is displayed in
brighter shades of red or blue (primarily within the stenosis
jet) or suggested by color aliasing (when a low PRF is used).
With increasing stenosis severity, retrograde ow components associated with eddy currents and ow separations are
depicted as color changes. High-grade stenosis with turbulent ow is characterized by a mosaic of colors and aliasing.
:
5 Muscle activity
5 Fever
5 Hypercirculation
5 Downstream infection
5 Vasodilation in response to upstream occlusion
In color duplex imaging, the subtle ow acceleration
triphasic
Color duplex imaging performed with adequate settings thus
enables rapid localization of a stenosis and semiquantitative
estimation of its severity.
Precise stenosis quantication, however, requires spectral
Doppler analysis, which is highly sensitive in depicting the
hemodynamic changes occurring in the prestenotic, intrastenotic, and poststenotic arterial segments (
Proximal to a high-grade stenosis, ow may become less
pulsatile due to changes in peripheral resistance. In the spectral display, however, the steep systolic rise remains
unchanged (in contrast to a postocclusive waveform). e
closer the sample volume is placed to a high-grade stenosis or
occlusion, the less the prestenotic waveform is aected by
collateral ow. When no hemodynamically signicant collaterals arise between the sample volume and the ow
obstruction, there may be very pronounced pulsatility or
even to-and-fro ow (thump pattern; see . Fig. 1.46).
Flow acceleration increases with the degree of stenosis (as
predicted by the continuity equation), eventually resulting in
loss of the triphasic ow prole. Depending on the degree of
stenosis, the poststenotic Doppler waveform will show a
decreased PSV, a delayed upstroke, and reduced pulsatility or
even monophasic ow (
becomes turbulent. In larger arteries such as the iliac and
femoral arteries, high-grade stenosis may also be suggested
by the so-called confetti phenomenon outside the blood vessel (due to tissue vibration) or by high-frequency Doppler
signals, the so-called seagull’s cry.
e loss of pulsatility distal to a high-grade stenosis
(. Fig.2.14) or occlusion is due to a decrease in peripheral
resistance (widening of collateral vessels, reduced arteriolar
tone) and a pressure gradient across the stenosis. e pressure dierence between the heart and the periphery is no
longer equalized during a single cardiac cycle and there may
be ow throughout diastole.
Calcied plaque with acoustic shadowing may preclude
direct color duplex evaluation of a stenotic segment. In this
situation, the examiner should compare prestenotic and
poststenotic Doppler waveforms (. Table2.10). If there is no
change in PSV or the character of the waveforms between the
prestenotic and poststenotic sampling sites, the plaque does
not cause hemodynamically relevant luminal narrowing (see
. Fig.2.64 (Atlas)).
2.1.6.1.5 Stenosis Grading: Ultrasound
. Table 2.9). In addition, ow
. Table2.9).
Versus Angiography
Most studies comparing duplex or color duplex ultrasound
and angiography in patients with PAOD show good agreement between the two modalities with sensitivities and specicities of 85% to 99% (. Table 2.7). More recent studies
report values of over 90%, but earlier studies describe surprisingly good results for conventional duplex ultrasound as
well: as early as 1986 Jäger etal. found 96% sensitivity and

76
Chapter 2 · Extremity Arteries
. Table 2.9 Grading of peripheral artery stenosis (. Figs. 1.46, 2.14, 2.20, and 2.21). The degree is dened as the percentage reduction
in vascular cross-sectional area. The criteria are not fully applicable in branching vessels. There are no strict boundaries between the
dierent degrees of stenosis as the hemodynamic eects of a stenosis depend on a complex interaction of dierent factors (modied
2
according to Wolf and Fobbe 1993; Cossman etal. 1989; Polak etal. 1991)
Stenosis degree (Color) duplex
(intrastenotic)
(Color) duplex (just
distal to stenosis)
Waveform far distal to
stenosis
Waveform proximal
to stenosis
PSV ratio
a
No stenosis Triphasic waveform
(PSV <150cm/s)
20–50%
Low-grade
stenosis
51–75%
Moderate
stenosis
76–95%
High-grade
stenosis
>95%
Subtotal
occlusion
Occlusion No ow signal
Increase in PSV
(150–200cm/s)
Further increase in PSV
(200–350cm/s)
Slight reduction in
pulsatility
Very pronounced
increase in PSV
(>350cm/s)
Reduction in pulsatility
Monophasic
Marked increase in PSV
(> 4m/s) and
end-diastolic velocity
(depending on
collateralization)
Monophasic
detectable
Clear spectral window
Markedly pulsatile
ow
Steep systolic upslope
Only mild turbulence
Moderate spectral
broadening may occur
Eddy currents
Possibly slight
turbulence
Partial lling-in of
systolic window
Considerable
turbulence
Complete lling-in of
systolic window
Monophasic ow
Pronounced turbulence
Completely lled-in
systolic window
Monophasic
Very reduced ow in
distal segment
Marked damping of
waveform
Monophasic
Unchanged Unchanged <1.5
Same as prestenotic Normal 1.5–2
Slightly reduced
pulsatility
Longer systolic
acceleration time
Reduced pulsatility
Flattened systolic peak
Considerably reduced
pulsatility
Monophasic
Very at systolic peak
Monophasic
Normal 2–4
Amplitude normal or
slightly reduced (compared to other side)
Pulsatility may be
reduced upstream of
collateral origins
Reduced amplitude
Prestenotic pulsatility
increased directly
before stenosis but
reduced upstream of
collateral origins
Low amplitude
Thump pattern
immediately before
occlusion: increased
pulsatility, small
complex with large
negative component
Decreased pulsatility
upstream of collateral
origins
>4
>4
a
PSV ratio: intrastenotic peak systolic velocity divided by prestenotic peak systolic velocity
81% specicity for the demonstration of abnormal changes
. Table 2.10 Duplex ultrasound of the peripheral arteries–
intrinsic limitations of the method
Technique
Limitations
in the pelvic and leg arteries by duplex ultrasound compared
with angiography. It is noteworthy that the sensitivity is the
same and the specicity higher compared with the agreement between two radiologists interpreting the same angiograms (97% sensitivity, 68% specicity).
B-mode Calcied plaque: posterior acoustic shadowing
Edema: scattering
Doppler Calcied plaque: posterior acoustic shadowing
Maximum ow velocity detectable: limited by PRF
While many investigators conclude that duplex ultrasound is a valid method for the detection and grading of signicant (femoropopliteal) stenosis (>50%), it is noteworthy
that they use either absolute peak systolic velocity (PSV) or
the PSV ratio (intrastenotic PSV divided by prestenotic PSV)

2.1 · Pelvic andLeg Arteries
77
2
with dierent cuto velocities for dening 50% or 70% stenosis (. Fig.2.21).
An examiner using absolute PSV rather than the PSV
ratio
for grading stenosis must be aware that the intrastenotic PSV reects not only the degree of stenosis but also the
eects of various other factors:
5 Systolic blood pressure
5 Poststenotic PSV (varies with magnitude of collateraliza-
tion)
5 Vessel wall elasticity (medial sclerosis– higher pulsatility)
5 Sympathetic tone, outow restistance, peripheral
vasodilatation
5 Collateral function:
5 Artery in which PSV is measured functions as a
collateral: PSV↑
5 Artery in which PSV is measured is bridged by a
collateral: PSV↓
Because the eects of these inuencing factors, particularly
those of collateralization (
mate, the PSV ratio allows more reliable stenosis grading (see
7 Sect. 1.2.3) than absolute intrastenotic PSV (Ranke et al.
1992) (. Fig.2.18). e PSV ratio, in turn, is a measure of the
PSV increase at the site of stenosis relative to the normal prestenotic segment and therefore cannot be used at sites of bifurcation, where the hemodynamic situation in the prestenotic
segment is dierent and hemodynamic eects of ow in the
other branching vessel are dicult to estimate. A case in point
is the femoral artery bifurcation: in a patient with highergrade stenosis at the origin of the supercial femoral artery,
the PSV ratio calculated with use of the PSV in the common
femoral artery as the prestenotic value will not yield consistent
results. is is because blood ow velocity in the common
femoral artery is aected by blood ow in the profunda femoris artery, which in turn increases with the extent to which the
latter functions as a collateral to bridge the obstructed supercial femoral artery. erefore, absolute PVS appears to be a
better velocity criterion for grading stenosis at this site.
Most authors investigating absolute velocity parameters
for stenosis grading in the femoral bifurcation used
curve analysis to dene PSV cutos
profunda femoris artery, for instance, a PSV threshold of
180cm/s was found to accurately identify hemodynamically
relevant stenosis (>50% stenosis) (Strauss etal. 1991). Later
investigators applied absolute PSV cutos for stenosis grading in the entire femoropopliteal territory. ese studies used
dierent cutos and reported the following results:
5 PSV cuto of 150cm/s: 94.5% sensitivity and 99%
specicity (Khan etal. 2011)
5 PSV cuto of 180cm/s: 66% sensitivity and 80%
specicity (Ranke etal. 1992)
5 PSV cuto of 200cm/s: 70% sensitivity and 96%
specicity (Leng etal. 1993)
Some authors used surprisingly low cuto velocities for the
detection of therapeutically relevant stenosis (>70%). One
study, for instance, found 89% sensitivity and specicity for a
. Fig. 2.16b), are dicult to esti-
ROC
. For the origin of the
PSV cuto of 200 cm/s (Khan et al. 2011), while another
study reported 74% sensitivity and 83% specicity for a cuto of 250 cm/s (Favaretto et al. 2007) (see, however,
. Fig.2.16b).
For stenosis grading based on focally increased blood
flow velocity
cutos for 50% and 75% stenosis, respectively (Khan etal.
2011; Ranke etal. 1992). Studies reported in the literature
investigated PSV ratios ranging from 1.5 to 2.4 to identify
50% stenosis compared with angiography. For a PSV ratio
of 1.5, Khan et al. (2011) reported 90.8% sensitivity and
97% specicity. For a ratio of 2, Polak etal. (1990) found
88% sensitivity and 95% specicity, while Aly etal. (1998)
found 92% sensitivity and 99% specicity. For the highest
PSV ratio of 2.4, Ranke etal. (1992) reported 87% sensitivity and 94% specicity. Most studies found the best results
for identication of >50% stenosis when using a PSV
ratio>2 (Alexander etal. 2002; Flanigan etal. 2008; Kohler
et al. 1987; Sensier et al. 1996). For identication of
>70(−75)% stenosis, most investigators use velocity ratios
of 3.5–4.0 (Alexander et al. 2002; Favaretto et al. 2007;
Legemate etal. 1991; Polak etal. 1990; Schlager etal. 2007),
while Khan etal. (2011) propose a surprisingly low ratio of
2. One factor accounting for this low ratio appears to be the
choice of the prestenotic sampling site (segmental classication).
2.1.6.1.6 Role ofCollateralization
, PSV ratios of 2 and (3-)4 have emerged as
inStenosis Grading
roughout its course, the supercial femoral artery gives o
arteries supplying muscles. ese arteries can be recruited as
collaterals in patients with steno-occlusive disease in this vascular territory, giving rise to intricate hemodynamic patterns
and variability in blood ow directions and velocities, which
must be taken into account when interpreting Doppler waveforms (. Fig.2.15). Good collateral circulation reduces blood
ow in the main artery, resulting in a lower intrastenotic peak
systolic velocity (PSV) than in a stenosis of the same degree
with poor or absent collateralization (. Fig.2.16b).
e pressure gradient across a higher-grade stenosis leads
to pressure reversal in muscle arteries arising distal to the
stenotic segment. ese arterial branches in turn are supplied
by collateral pathways bridging the obstructed main artery,
resulting in reversed blood ow into the main artery, where
pressure and blood ow are reduced due to the obstruction.
erefore, PSV and pulsatility in the poststenotic segment
will be higher distal to the origin of a muscle artery recruited
as a collateral than proximal to it.
Collateralization also aects blood ow velocities in the
prestenotic segment of the main artery (femoral artery).
Good collateralization results in a higher PSV in the main
artery upstream of the origin of relevant collaterals than
when measured closer to the stenosis and downstream of the
collateral origin (see
taken into account when choosing the prestenotic spectral
Doppler sampling site for PSV measurement. Using the
higher, more proximal prestenotic PSV to calculate the PSV
. Figs. 1.46 and 2.16b). is must be

78
a b
Chapter 2 · Extremity Arteries
2
Good Poor
collateralization
. Fig. 2.15 a With poor collateralization, the Doppler waveform obtained in the postocclusive segment (right) is damped with a large diastolic
component, resulting from distal dilatation in response to chronic peripheral ischemia. With increasing collateralization, blood ow distal to an
occluded segment becomes more pulsatile (left), approaching normal ow when there is optimal collateralization and postocclusive pressure
approximates preocclusive pressure. b The pulsatility of the Doppler spectrum recorded distal to an occlusion is determined by the magnitude of
collateral ow. Good collateral pathways can compensate for an occluded main artery and ensure adequate perfusion, at least at rest. For instance,
if an isolated occlusion of a pelvic artery or the supercial femoral artery develops slowly over years, one may occasionally obtain a triphasic waveform from the popliteal artery, but with reduced PSV and delayed acceleration. Conversely, the poorer the collateral situation, the more monophasic
the waveform and the lower the PSV (relative to end-diastolic ow velocity) become. The rst example illustrates the ndings in supercial femoral
artery occlusion with good collateralization (left): the Doppler waveform from the popliteal artery shows pulsatile ow with short retrograde ow in
early diastole and zero diastolic forward ow (ABI of 0.8). The second example (right) shows a monophasic waveform from a patient with poor collateralization of supercial femoral artery occlusion: it is characterized by persistent diastolic ow and a low PSV (ABI of 0.5)
ratio for stenosis grading results in lower PSV ratios and
explains why some investigators found lower cuto ratios for
relevant stenosis (e.g., Khan etal. 2011). For consistency of
results, it is therefore important to always measure preste-
notic PSV 2–5cm proximal to the obstructed segment of
the main artery
and distal to the origins of relevant collaterals (. Fig. 2.16b). If this recommendation is followed, the
continuity equation applies and an increase by a factor of 4
identies stenosis with 75% cross-sectional area reduction
(which is inversely related to PSV). Note though that this is
only an approximation based on the assumptions that hold
for the behavior of Newtonian uids.
Little or no attention has so far been paid to how the site
of prestenotic PSV measurement can aect stenosis grading.
is is one factor explaining why dierent PSV ratios have
been proposed as cutos for stenosis grading in this vascular
territory. And what is more, some investigators even deliberatedly aimed at using a prestenotic sampling site farther away
from the stenotic segment (Polak et al. 1990; Khan et al.
2011).
A nal aspect to be considered is that, because collaterals
divert blood away from the obstructed main artery, absolute
intrastenotic PSV may be lower
than expected from the
degree of luminal narrowing alone (see study results discussed in the preceding section). Blood ow in the main
artery between the origin of a collateral and an obstruction
decreases as ow in the collateral increases (Schäberle etal.
2013). Ignoring the eect of good collateralization on intrastenotic PSV in high-grade stenosis (. Fig.2.16b) can lead to
underestimation of stenosis severity when an absolute PSV
cuto >180cm/s is used. is pitfall can be avoided by using
PSV ratios instead.
2.1.6.1.7 Eects ofCollateralization
onPre- andPostocclusive
SpectralDoppler Waveforms
In the peripheral arteries, postocclusive perfusion pressure is
determined by preocclusive systemic pressure and, above all,
by ow resistance in the collateral circulation (. Fig.2.16a).
Collateral resistance, in turn, depends on the number and
size of collateral vessels, the length of the occluded segment
to be bridged, and blood viscosity. When collateral resistance
is low, the eect on peripheral perfusion is less dramatic, and
there is only moderate peripheral vasodilatation. As a result,
postobstructive ow remains pulsatile, and a fairly normal
triphasic Doppler waveform is obtained. Whether the postocclusive waveform becomes monophasic thus depends on
the degree of stenosis or length of occlusion and collateralization. Both the Doppler waveform and the ankle-brachial
index (ABI) thus reect not only the severity of stenoocclusive disease but also the magnitude of collateralization.
Better collateralization (e.g., at the pelvic level) results in less
abnormal spectral Doppler ndings.
is also explains why the postocclusive Doppler waveform
correlates well with the ABI and the severity of the patient’s
clinical condition. A damped but still triphasic postocclusive
waveform suggests that, at least at rest, peripheral perfusion is
still adequate. ese patients also have a longer walking distance.
e spectral Doppler ndings, along with the ABI, can thus help
dierentiate pain due to PAOD from other underlying causes.

∆
∆
2.1 · Pelvic andLeg Arteries
Preocclusive pressure
P
1
P
1/2
Q
k
P
2
P
2/3
Q
p
Collateral resistance
R
c
Postocclusive pressure
Peripheral resistance
R
p
Muscle
Skin
79
2
ab
. Fig. 2.16 Eects of collateralization on spectral Doppler ndings in and around steno-occlusive arterial lesions. a Postocclusive arterial pres-
sure depends on the degree of stenosis or length of occlusion as well as on collateral resistance. Collateral resistance is low when there is good
collateralization, which in turn results in higher postocclusive pressure in the main artery. With good collateralization, the postocclusive waveform
is less abnormal with a higher peak systolic velocity (PSV) and low end-diastolic velocity (EDV). A nearly normal triphasic waveform may be seen
in patients with pelvic artery occlusion and good collateralization (from Rieger and Schoop 1998). b With little or no collateralization (or in bypass
graft stenosis), the prestenotic waveform will show a reduced PSV.In this situation, ow in the prestenotic segment is less aected by compensatory peripheral vasodilation, and a knocking waveform (thump pattern) may be obtained in very high-grade stenosis (left diagram). In case of
good collateralization, PSV proximal to the origin of a collateral vessel is relatively normal; however, in patients with reduced peripheral perfusion
and compensatory vasodilation, there will be some diastolic ow transmitted through the collateral. Flow is more pulsatile between the origin of
a collateral and the stenosis; some to-and-fro ow may be seen immediately proximal to a high-grade stenosis (right diagram). If there are no collaterals, intravascular pressure leads to a higher intrastenotic ow velocity (left). The lower pressure in a collateral vessel diverts blood ow from
the stenotic artery. The resultant decrease in pressure in the main artery reduces intrastenotic ow velocity compared with the velocity expected
in a stenosis of the same degree without collateral circulation (right). This is why the severity of a stenosis using absolute PSV may be underestimated if the eects of collateralization are ignored. The intrastenotic-to-prestenotic PSV ratio is independent of the magnitude of collateralization
(see . Fig. 1.46)
Spectral Doppler interrogation provides a wealth of
information reecting the complex hemodynamic situation
around a stenotic or occluded arterial segment. With the
development of collateral pathways in patients with chronic
vascular obstruction, postocclusive ow becomes more pulsatile (
the ow prole upstream of the stenosis. How collaterals
inuence the waveform depends on where they arise and
enter relative to the site of Doppler sampling. In the prestenotic segment proximal to the origin of collaterals, loss of
peripheral resistance results in a monophasic waveform with
persistent diastolic ow through the collaterals. However, in
contrast to the poststenotic situation, PSV is high and there is
a steep systolic upstroke. A prestenotic waveform from the
segment between the origin of a collateral and a high-grade
stenosis will show more pulsatile ow (. Fig.2.16) because
resistance is higher than upstream of the collateral origin (see
. Fig. 1.46).
P
3
Venous pressure
. Fig. 2.15). Collaterals also aect ow velocity and
2.1.6.1.8 Plaque Conguration
andStenosis Degree
Systematic dierences in stenosis grading between angiography and color duplex ultrasound may result from ignoring the eect of plaque conguration (concentric versus
eccentric). Stenosis in the common femoral artery is typically due to eccentric plaque. When an eccentric plaque
causes 50% diameter reduction, the corresponding crosssectional area reduction is only 50% (. Figs.2.17 and 5.27)
as opposed to 75% when the stenosis is caused by concentric plaque with the same diameter reduction. Hence, a concentric plaque has a greater hemodynamic and clinical
eect than an eccentric plaque. is dierence in terms of
hemodynamic relevance is reected by the fact that the
increase in intrastenotic PSV is twice as high (PSV ratio of 4
versus 2) (. Fig.2.17d). In other words, the increase in PSV
within the stenosis reects the cross-sectional area reduction (. Fig. 2.18). e hemodynamic stenosis severity

80
Maximum diameter reduction (%)
100
Chapter 2 · Extremity Arteries
2
a
b
. Fig. 2.17a–d Eects of plaque conguration. a Common femoral artery stenosis with an intrastenotic peak systolic velocity (PSV) of 220cm/s.
The longitudinal gray-scale image shows luminal narrowing caused by eccentric posterior wall plaque with the appearance suggesting high-grade
stenosis, while the PSV is consistent with 50–60% stenosis. A PSV ratio of 2 is calculated from the intrastenotic PSV of 220cm/s and the prestenotic
prestenotic PSV of 110cm/s, which corresponds to focal doubling of blood ow velocity and indicates 50% stenosis. The waveform was obtained
by moving the transducer along the artery and includes the sites of prestenotic and intrastenotic PSV measurement. b Gray-scale and color duplex
images of the same stenosis as in c. The gray-scale image shows eccentric, calcied plaque on the posterior wall. Planimetric measurement of
the cross-sectional area reduction yields 50% luminal reduction (measured using the built-in software: 0.68cm2 cross-sectional area of the vessel– 0.34cm2 cross-sectional area of plaque → 50% area occlusion). While the method yields a correct estimate in this case, it is discouraged, and
hemodynamic stenosis grading based on spectral Doppler interrogation should be preferred. Good plaque delineation in the gray-scale image as
in this example (left) is rarely accomplished, and activation of the color ow mode does not improve dierentiation of plaque from owing blood.
On the contrary, color duplex is prone to color spillover, obscuring plaque and the vessel wall. The perpendicular insonation angle for adequate
visualization of the plaque area in the transverse view is a poor Doppler angle (close to 90°). A higher gain setting is not an option either and
would even increase color blooming. c The anteroposterior angiogram does not allow adequate identication of this stenosis, and the only hint of
luminal narrowing caused by the eccentric plaque at this site is some brightening in the otherwise opacied vessel. In a lateral view, this plaque
b would mimic high-grade stenosis. Technically, only oblique rather than lateral angiographic projections can be obtained in this territory. d Dia-
gram illustrating the relationship between cross-sectional area reduction and diameter reduction as a function of plaque conguration (concentric– eccentric). Diameter reduction is the basis for stenosis grading in angiography, while the cross-sectional area reduction, which determines
the hemodynamic relevance of a stenosis (see . Fig. 5.27), is the basis for sonographic stenosis grading. The drawing illustrates that 50% diameter
reduction (in angiography) corresponds to 75% cross-sectional area reduction when caused by a concentric plaque versus 50% reduction when
caused by an eccentric plaque. Grading by spectral Doppler measurement would yield a PSV ratio of 4 for the circumferential stenosis, corresponding to a higher-grade stenosis, and a PSV ratio of 2 for the eccentric stenosis, corresponding to a lower-grade stenosis (according to the continuity
equation). In both cases, angiography would yield a 50% stenosis in terms of diameter reduction. As the cross-sectional area reduction is what
determines the hemodynamic eects of a stenosis and hence the patient’s clinical symptoms, the hemodynamic stenosis grade determined by
ultrasound is a more adequate measure of the clinical relevance of a stenosis (see
7 Sect. 1.2.3)
c
Cross-sectional area reduction (%)
100
80
60
40
20
0
20 40
0
d
60 80
determined by duplex ultrasound is thus a more adequate
measure of the plaque-related blood ow obstruction and
also of the patient’s clinical situation than angiography,
which solely relies on morphologic appearance.
Angiographic stenosis grading is additionally limited by
the fact that it oen relies on a single (anteroposterior) projection, while exact grading requires two planes, especially
when stenosis is caused by eccentric plaque. is limitation is
especially relevant in the angiographic evaluation of the
common femoral artery, where stenosis is typically caused by
posterior wall plaque and even relevant stenosis may be
missed when only anteroposterior projections are obtained.
Despite these limitations, even scientic studies still use
angiography as the gold standard and report poor agreement
of duplex ultrasound with anteroposterior angiograms
(Schlager etal. 2007). Overall, though, duplex ultrasound is
judged to provide adequate accuracy for detecting >50% stenosis in the routine clinical setting.

500
Angiographic diameter reduction (%) Angiographic diameter reduction (%)
100
100
100
PVR: calculated diameter reduc
PSV ratio (intrastenotic PSV divided by
ab
cd
2.1 · Pelvic andLeg Arteries
81
2
y = 5.19.10
400
300
200
Intrastenotic PSV (cm/s)
100
0
0204060
500
y = (2.49.10
y = (3.73.10
400
300
-4
Angiographic diameter reduction (%) Angiographic diameter reduction (%)
-3
-10
.
x
.
x
2.92
1.62
5.26
.
x
+ 112.8
) + 1; x<80
) + 1; x≥80
y = 18.0 + 0.65x
n = 106
80
60
40
20
PSV: calculated diameter reduction (%)
80 100 020406080
0
100
80
tion (%)
60
r = 0.81
SEE = 10.4
y = 10.9 + 0.79x
n = 106
r = 0.93
SEE = 6.9
200
prestenotic PSV)
100
0
020406080 100
. Fig. 2.18a–d Correlation of absolute intrastenotic peak systolic velocity (PSV) (a, b) and of the PSV ratio (intrastenotic PSV divided by preste-
notic PSV) (c, d) with the percentage diameter reduction at angiography (graphs from Ranke etal. 1992). a Correlation of intrastenotic PSV and
angiographic diameter reduction (%) in 106 femoral artery stenoses using a PSV cuto of 180cm/s for >50% stenosis (correlation r=0.81).
b Linear regression analysis of percentage diameter stenosis calculated from PSV versus angiographic diameter stenosis. c The PSV ratio (PVR) cor-
relates better with angiographic diameter reduction (r=0.93) because it is less susceptible to variations in systemic factors (systolic blood pressure) or other eects such as vessel wall elasticity. According to this analysis, the best results were achieved using a PSV ratio cuto of 2.4, which
identied >50% stenosis with 87% sensitivity and 94% specicity. d Linear regression analysis of percentage diameter reduction calculated from
the PSV ratio (PVR) versus angiographic diameter reduction
It is not surprising that two imaging modalities based on
dierent principles yield discrepant results. Angiography
(but also IA DSA and X-ray densitometry) is primarily based
on morphologic features, while duplex ultrasound assesses
the hemodynamic signicance of a stenosis. In addition to
which is common at the pelvic level and in the femoral bifurcation and is dicult to assess on anteroposterior views (see
. Figs. 5.27, 5.14, and 2.55 (Atlas)). Despite its limitations,
however selective angiography continues to be the gold standard against which new methods are evaluated.
40
20
0
020406080
the limitations already mentioned, other drawbacks include
that angiograms depict only the perfused lumen and not the
vessel wall and that the angiogram reduces the threedimensional lumen to the two dimensions of the lm. Specic
drawbacks in the iliofemoral territory include limited evaluability of the femoral bifurcation due to superposition and
underestimation of stenosis caused by posterior wall plaque,
2.1.6.1.9 Profunda Femoris Artery
Absolute peak systolic velocity (PSV) thresholds of 180cm/s or
greater have been proposed for stenosis grading in arterial bifurcations (e.g., origin of profunda femoris artery) (. Fig. 2.19),
where the more reliable PSV ratio with focal doubling of intrastenotic PSV relative to prestenotic PSV does not apply

82
Sensitivity
Specificity
1.0 0.9 0.8 0.7 0.6 0.5 0.4
Chapter 2 · Extremity Arteries
1.0
2
0.9
0.8
0.7
0.6
0.5
a b
. Fig. 2.19 a Profunda femoris artery stenosis: ROC curve for determining the sensitivity and specificity of different intrastenotic peak sys-
tolic velocity (PSV) cutoffs in the profunda femoris artery measured by duplex ultrasound in comparison with angiography. b Stenosis at the
profunda femoris origin is suggested by aliasing in the color flow image and confirmed by spectral Doppler interrogation (monophasic flow
with a PSV of 403cm/s). The gray-scale and color flow images show the femoral bifurcation with the common femoral artery (A.F.C), superficial
femoral artery (A.F.S), and profunda femoris artery (A.P.F) in one scan plane. While evaluation of the superficial femoral artery is impaired by
acoustic shadowing due to plaque, presence of a second stenosis in this artery is suggested by aliasing (blue indicates flow away from the
transducer, toward the periphery)
170
180
200 190
210
160
150 cm/s
abc
. Fig. 2.20a–c Grading of supercial femoral artery stenosis. a Hypoechoic plaque (P) causes 50–70% stenosis of the supercial femoral artery.
Spectral Doppler measurement yields an intrastenotic peak systolic velocity (PSV) of 290cm/s (sample volume placed in the stenotic jet identied
by aliasing in the color ow image). b A continuous Doppler tracing was obtained from the supercial femoral artery (A.F.S.) by moving the tilted
transducer (acute Doppler angle) across the skin starting 2cm proximal to the stenosis. This Doppler tracing yields a PSV of 290cm/s in the stenotic jet versus 110cm/s in the prestenotic segment. The PSV ratio calculated from these values (intrastenotic to prestenotic PSV) is greater than 2
but less than 4, indicating 50–70% stenosis. The stenosis is not a high-grade stenosis, which is why the Doppler waveform shows normal triphasic
ow (no arteriolar dilatation and hence adequate peripheral perfusion). c Angiogram conrms 50–70% stenosis
(7 Sect. 1.2.3). e indirect signs of hemodynamically relevant
stenosis (pre- and poststenotic waveform changes) discussed
above (7 Sect. 2.1.6.1.4) can be used as supplementary criteria.
e main trunk of the profunda femoris artery is of particular signicance in the diagnostic evaluation of patients
with steno-occlusive disease of the supercial femoral artery,
for several reasons: it is the most important collateral and
concomitant profunda femoris involvement is common. At
the same time, blood supply to the calf and foot can be
improved by a minor surgical intervention (profunda femoris repair, TEA). Stenotic lesions at the origin of the pro-
funda femoris artery
are therefore important to identify but
may be obscured on angiograms by superimposed vessels.
Reliable angiographic assessment is only possible when an
additional oblique projection is obtained (. Fig.2.20).
A study conducted by the author’s group (Strauss and
Schäberle 1988) investiged the hemodynamics at the origin of
the profunda femoris with determination of the degree of stenosis from PSV and found a positive predictive value (PPV)
and a negative predictive value (NPV) of 86% and 91%, respectively, compared with angiography as the reference method.
ROC analysis identied a PSV of 180cm/s as the optimal cuto for dierentiating normal ow and low- grade stenosis from
higher-grade stenoses (>50%) (
. Figs.2.20 and 2.21).
As already discussed above, interpretation of ow velocities must take into account whether the artery being exam-
ined acts as a collateral
. As the main collateral in occlusion
of the supercial femoral artery, the profunda femoris may
show an increase in mean ow velocity of over 100% at its
origin without itself being stenosed. Moreover, ow in a
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