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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

cd
2.3 · Atlas: Extremity Arteries
133
2
a
. Fig. 2.59a–d (Atlas) Stenosis at origin of profunda femoris artery– TEA.
a High-grade stenosis of the profunda femoris artery (A.P.F) with a monophasic ow prole and a peak systolic velocity (PSV) of 480cm/s and
end-diastolic velocity (EDV) of 90cm/s. In the color duplex image (middle section), the ow acceleration produces aliasing. The supercial femoral
artery (A.F.S) is occluded; only the distal end (about 1cm) is patent, but the slow ow is not detected with the high PRF used, and only some retrograde ow (red) is recorded. The gray-scale image (left section) depicts plaques of dierent echogenicity with marked wall irregularities. Some of
the plaques produce posterior acoustic shadowing (A.F.C=common femoral artery).
b As a result of the proximal occlusion of the supercial femoral artery and the high-grade stenosis in the main collateral (profunda femoris),
the blood volume in the relled popliteal artery is markedly reduced. This is reected by the small lumen of the popliteal artery with chronic
narrowing and the markedly reduced ow velocity (PSV of 11 and EDV of 3cm/s). In this image (obtained with the transducer in the popliteal
fossa), a collateral arising from the posterior aspect is seen (K). In addition, the popliteal vein (V), which runs posterior to the popliteal artery (A),
is depicted closer to the transducer (blue).
c The patient underwent femoral profundaplasty with severing of the ipsilateral supercial femoral artery. Following surgical elimination of the
stenosis, the treated segment of the profunda femoris artery (A.P.F) has a PSV of 80cm/s and EDV of 10cm/s. The diastolic ow component and
the reduced pulsatility are due to collateral ow in the profunda femoris and the altered wall elasticity of the patched segment (A.F.C=common
femoral artery).
d Improved perfusion, following profunda femoris repair for supercial femoral occlusion, is reected in the waveform obtained from the relled
femoral artery at about the same site as the preoperative waveform presented above, now showing a PSV of 66cm/s and EDV of 26cm/s. The
postocclusive ow character is due to persistent supercial femoral artery occlusion
b

134
Chapter 2 · Extremity Arteries
2
a
b
c
. Fig. 2.60a–c (Atlas) Stenosis at origin of profunda femoris artery (recurrence).
a Duplex ultrasound has become the method of choice for diagnosing and grading stenosis of the profunda femoris artery, as anteroposterior
angiograms are limited for various reasons: the femoral bifurcation may be obscured by overlying vessels, variants in the course of the artery may
not be assessable, and stenosis caused by posterior wall plaque is dicult to grade. In this patient with prior TEA of the common femoral artery,
aliasing in the color ow image and a peak systolic velocity (PSV) >3m/s with a monophasic ow prole indicate recurrent high-grade stenosis.
b The corresponding angiogram depicts the stenosing plaque at the origin of the profunda femoris artery. Recurrent stenosis and wide lumen of
the common femoral artery following TEA.
Distal profunda femoris stenosis.
c Distal profunda femoris artery stenosis becomes relevant and requires treatment if it involves the main branch of the artery, which courses
parallel to the supercial femoral artery and may thus be recruited as a collateral in supercial femoral artery occlusion. The color ow image (left)
shows high-grade stenosis of the profunda femoris artery approximately 4cm from its origin with a Doppler-derived PSV>5m/s. The proximal
segment of the supercial femoral artery (A.FEM.S.) is patent. The angiogram conrms the more distal stenosis of the profunda femoris artery
and a patent proximal supercial femoral artery with an occlusion in the lower thigh. The angiogram also allows clear dierentiation between the
main trunk of the profunda femoris, which is relevant as a collateral in supercial femoral artery occlusion, and a second branch arising posteriorly. The latter plays no role as a collateral in supercial femoral artery occlusion; it supplies the upper thigh muscles and receives the circumex
artery (providing arterial ow in case of occlusion of the common femoral or external iliac artery). In a patient with supercial femoral artery
occlusion, the sonographic examination cannot be conned to the origin of the profunda femoris but must include a length of 7–8cm to also
identify any relevant stenosis more distally

ab
2.3 · Atlas: Extremity Arteries
. Fig. 2.61a, b (Atlas) Profunda femoris artery– variable origin and branching pattern.
a Two profunda femoris branches arise from the common femoral artery (A.F.C)– a proximal branch (A) supplying the upper thigh and a second
branch (A.P.F) supplying the distal thigh muscles. The second branch, with its proximal segment coursing parallel to the supercial femoral artery,
can be recruited as a collateral when the supercial femoral artery becomes occluded. Therefore, stenosis of the distal profunda branch (PSV of
170cm/s) must be ruled out in patients with supercial femoral artery occlusion. If there is stenosis of this branch, TEA is indicated (for further
illustration of the situation, see angiogram,
from the posterior, posterolateral, or lateral aspect of the common femoral artery and rarely from the medial side. Alternatively, a single profunda
femoris can arise from the common femoral artery and then divide into two branches.
b Stenosis of the proximal profunda femoris branch (A) (PSV of 3m/s) has no therapeutic relevance (no collateral function). However, this branch
is often easier to identify because it arises from the posterior aspect of the common femoral artery
. Fig.2.60c (Atlas)). The second or main profunda femoris branch has a variable origin and can arise
135
2
. Fig. 2.62 (Atlas) Stenosis at origin of profunda femoris artery in
diabetes mellitus.
Plaque with a highly irregular surface causes very turbulent ow, which
is reected both in the color ow image and in the Doppler waveform.
Medial sclerosis in diabetes mellitus reduces wall elasticity, resulting in
increased pulsatility of blood ow with a higher PSV and smaller diastolic ow components (including the site of stenosis). Therefore, reliance on absolute PSV alone for stenosis grading may result in (slight)
overestimation of the severity of stenosis in diabetic patients

136
ef
bc
Chapter 2 · Extremity Arteries
2
a
d
gh i
. Fig. 2.63a–i (Atlas) Femoral artery occlusion and sequential popliteal artery stenosis.
a Color duplex imaging is superior to conventional duplex in that it enables rapid identication of an occlusion and provides fairly reliable estimates of its length. In the example, there is a 2cm occlusion of the distal femoral artery just above the adductor canal. The left image shows the
proximal and distal ends of the occluded segment with absence of ow signals in between. The absence of ow signals is due to actual absence of
owing blood rather than inadequate instrument setting or calcied plaques, as indicated by the demonstration of ow in the opposite direction
in the femoral vein posterior to the artery. Parallel shifting of the transducer leads to the disappearance of the femoral vein from the scanning
plane, while the collateral arising from the femoral artery upstream of the occlusion and re-entering downstream comes into view. In the color
mode, the collateral (KOL) is depicted closer to the transducer than the occlusion. In this imaging plane, the plaques in the occluded artery cause
posterior acoustic shadowing.
b Femoral bifurcation: The Doppler waveform from the proximal supercial femoral artery already suggests a ow obstruction distal to the
sample volume. Flow is pulsatile but the early diastolic forward ow component following the dip is absent. In this case, the ow prole cannot
be explained by diabetic medial sclerosis. Moreover, peak systolic velocity (PSV) is reduced to 40cm/s although there is no proximal stenosis. Collateral ow is mainly through the profunda femoris artery (see angiogram).
c Supercial femoral artery occlusion: The Doppler spectrum from the origin of the collateral (KOL) arising from the supercial femoral artery just
upstream of the occlusion shows a PSV of 150cm/s. The higher ow velocity is not due to stenosis at the origin but is attributable to dierent
vessel calibers. The occluded supercial femoral artery is depicted posterior to the collateral and the vein posterior to the artery. Incomplete color
coding in the artery and vein is due to plaques (S).
d The postocclusive waveform of the relled supercial femoral artery shows monophasic ow with a PSV of 45cm/s.
e, f Just proximal to the relled segment, two further collaterals (KOL) with ow toward the transducer enter the supercial femoral artery poste-
riorly. In f a long segment of the collateral is depicted in red while the supercial femoral is shown in blue (ow away from transducer). With a PSV
of 95cm/s, this collateral is not stenosed whereas the second collateral (e) entering the artery more proximally and medially shows criteria of stenosis at its site of entry on duplex ultrasound and in the Doppler waveform (aliasing, end-diastolic velocity (EDV) of 100cm/s and PSV >250cm/s).
The occlusion is indicated by arrows in e. Retrograde ow components in the supercial femoral artery are displayed in red.
g Angiogram: Conrmation of the 2-cm occlusion of the supercial femoral artery. Also seen are the anterior collateral pathway and the two collaterals entering the posterior aspect of the artery (lower arrow). The latter are supplied by profunda femoris collaterals.
h Serial stenosis in the distal popliteal artery (P3 segment). The Doppler waveform obtained distal to the entry of the collaterals bridging the
occlusion shows monophasic postocclusive ow with a delayed systolic upstoke and a PSV of 52cm/s. The downstream stenosis is indicated by
aliasing.
i Direct spectral Doppler interrogation of the suspected stenosis (aliasing) reveals a focal increase in PSV to 116cm/s. This increase alone does not
indicate a relevant stenosis; however, in conjunction with the postocclusive decrease in ow velocity to 50cm/s between the occluded femoral
artery segment and the popliteal stenosis, a 50–60% stenosis is suggested. The PSV ratio is >2

bc d
2.3 · Atlas: Extremity Arteries
137
abc
. Fig. 2.64a–c (Atlas) Artifact due to acoustic shadowing.
a In contrast to the example presented in . Fig.2.63a–g (Atlas), the absence of ow signals along a 1-cm segment of the supercial femoral
artery in this case is not due to occlusion but to acoustic shadowing produced by a calcied plaque. Just proximal to this segment, there is pulsatile, triphasic ow with a PSV of 136cm/s.
b Neither color duplex nor the Doppler waveform depicts ow in the segment obscured by acoustic shadowing.
c The Doppler waveforms obtained distal and proximal to the obscured segment are identical, excluding a higher-grade stenosis or occlusion of the
nonvisualized segment. The slightly higher ow velocity of 152cm/s may be due to moderate luminal narrowing or a Doppler-angle-related error
. Fig. 2.65a–d (Atlas) Embo-
lizing popliteal artery plaque
before and after PTA.
a Very hypoechoic plaque (P),
which is indistinct from the
lumen in the B-mode image
(arrow), in the popliteal artery is
the source of embolism in this
patient with blue toe. The plaque
causes 75% stenosis (calculated
according to the continuity
equation; intrastenotic PSV of
301cm/s and prestenotic PSV of
79cm/s). Aniograms depicting
the stenotic segment (arrow)
before (b) and after (c) PTA.
Follow-up ultrasound 6weeks
after PTA shows residual plaque
pressed into the wall (d) without
hemodynamically relevant stenosis (PSV of 95cm/s)
a
2
. Fig. 2.66a, b (Atlas) Grading of stenosis caused by eccentric
plaque.
High-grade stenosis (PSV ratio>6) of the supercial femoral artery
(A.F.S) caused by eccentric plaque (P). Unlike the plaque in . Fig.2.65
(Atlas), the plaque in this example is hyperechoic and calcied. The
rst collateral (K) re-entering the stenosed artery is seen just distal to
the plaque. The ultrasound ndings are consistent with the eccentric
stenosis seen in the angiogram obtained before PTA (b)
a
b

138
df
bc
ab
Chapter 2 · Extremity Arteries
2
. Fig. 2.67a, b (Atlas) Bypass planning– mapping for suitable vein, target vessel.
a Ultrasound allows preoperative identication of a suitable vein for bypass grafting. This includes measurement of the diameter, which should
be over 2mm for a crural bypass. Preoperative marking of the course of the selected vein on the skin reduces the length of incision and shortens
operation time. In patients with duplication of the candidate vein, the most suitable branch in terms of diameter and course is selected sonographically. The transverse view on the left shows a suitable small saphenous vein with a diameter of 4mm and the image on the right obtained
more distally a duplicated vein with a thicker (3.4mm) and a thinner branch (2.6mm).
b Veins with postthrombophlebitic changes are unsuitable for grafting and can be identied by sonography, which will demonstrate a patent
lumen with sclerotic wall thickening, as illustrated here for the small saphenous vein. A recanalized thrombophlebitic vein shows the same features as a postthrombotic deep vein: wall sclerosis and thickening, residual thrombi, and valve incompetence. In the example, transverse and longitudinal views (left and right, respectively) depict the thickened hypoechoic wall and ow in the patent lumen of the small saphenous vein (blue)
a
e
. Fig. 2.68a–f (Atlas) Selection of recipient vessel for distal bypass procedure.
a Color duplex imaging demonstrates occlusion of the P2 and P3 popliteal segments in a woman with stage IV PAOD.A sural artery provides collateral ow (K). The Doppler waveform shows a preocclusive thump pattern.
b The search for a runo vessel to position the distal anastomosis of a femorocrural bypass reveals collaterals (KOL) resupplying ow to the proximal tibial artery (A).
c The anterior tibial artery is then followed distally down to the ankle, where a Doppler waveform is obtained. There is no stenosis, and the waveform pattern suggests good peripheral runo, conrming the anterior tibial artery to be an ideal target vessel for a bypass procedure.
d In contrast, spectral Doppler measurements show the bular artery and posterior tibial artery (with multiple stenoses and only a short patent
segment) to be inadequate target vessels for the planned bypass: high pulsatility and low PSV indicate poor peripheral runo. In this case, the
Doppler ndings already show these two arteries to be unsuitable to receive the bypass, and complete mapping is not necessary.
e Angiogram conrms popliteal artery occlusion and suitability of the anterior tibial artery for use in a distal bypass procedure.
f Doppler ndings after bypass grafting onto the anterior tibial artery suggest restoration of peripheral perfusion: the anterior tibial artery wave-
form recorded just distal to the bypass anastomosis shows pulsatile ow and a PSV of 128cm/s with a short systolic rise time

bc
2.3 · Atlas: Extremity Arteries
139
a
d e
. Fig. 2.69a–e (Atlas) Stage IV PAOD with arterial occlusion below the knee.
a Duplex examination before a planned bypass procedure in a woman with stage IV PAOD with occlusion of calf arteries. Color duplex and spectral Doppler reveal only mild to moderate stenoses in the peripheral arteries down to and including the popliteal artery. Below the knee, spectral
Doppler analysis demonstrates preocclusive ow (knocking waveform) in the proximal anterior tibial artery between the origin of a collateral (K)
and an occlusion demonstrated by color duplex. The diameter (2mm) of the occluded artery is indicated by calipers. The occlusion extends down
to the ankle joint.
b The posterior tibial artery is occluded proximally (3.5cm in length) with a collateral channel (KOL) providing ow distal to the occlusion. Flow is
diminished and very slow with a peak systolic velocity (PSV) of 8cm/s; the ow pattern resembles that in a vein, but the direction is away from the
probe, indicating that an artery is being interrogated. In a situation like this, with occlusion and collateral relling of the main artery, it is important to continuously image the artery for another 4–5cm to decide whether distal runo can be evaluated by spectral Doppler measurement,
which will be the case if there is adequate resupply of blood through the collateral pathway.
c More distally, ow is again increased due to inow from additional collaterals (PSV of 60cm/s and end-diastolic velocity (EDV) of 25cm/s; postocclusive delay in systolic upstroke).
d Two centimeters distal to the waveform presented in c, there is aliasing in the posterior tibial artery and Doppler interrogation reveals an
increase in PSV of slightly more than 100% (150cm/s), corresponding to 50–60% stenosis.
e Angiogram conrms occlusions of the anterior tibial artery and proximal posterior tibial artery. The latter is supplied via collaterals distal to the
occluded segment. The thick arrow indicates a mildly narrowed segment of the posterior tibial artery (see d) and the thin arrow the anterior tibial
artery
2

140
ab
cd
Chapter 2 · Extremity Arteries
2
. Fig. 2.70a–d (Atlas) Contrast-enhanced ultrasound (CEUS)– bypass recipient vessel in popliteal artery occlusion.
a In this patient with stage IV PAOD, diabetic medial sclerosis, and foot phlegmon, the insonation conditions are very poor as there is scatter due
to interstitial uid accumulation. Even with a low PRF and high gain, only isolated ow signals are obtained from the anterior tibial artery.
b Contrast-enhanced ultrasound (CEUS) performed with low mechanical index (MI; see 7 Sects. 1.1.5, 2.1.6.1.11, and 6.1.6.1.3) depicts reections
from microbubbles in a long segment of the anterior tibitial artery (arrow). Note, however, that when using CEUS and the artery of interest is difcult to follow in the B-mode image (right), a collateral may be mistaken for the main artery, and it is not possible to detect or rule out stenosis.
c, d Contrast-enhanced color duplex ultrasound performed with normal MI: depiction of the patent anterior tibial artery (c) and the abrupt
increase in PSV (d) allow stenosis detection and grading based on the continuity equation (in the example, there is doubling of PSV, indicating
50% stenosis). However, without use of a low-MI technique, there is rapid destruction of the microbubbles and the diagnostic window is very
short (compare intensity of waveforms and color duplex images in a versus c and d)

2.3 · Atlas: Extremity Arteries
141
2
a
cd
. Fig. 2.71a–d (Atlas) Recipient vessel for pedal bypass.
a Slow ow in the supercial pedal arteries is visualized by high-resolution duplex imaging using a high-frequency transducer and a low
PRF.Plaques and stenoses are depicted, and a Doppler waveform showing the typical postocclusive monophasic ow, often with an almost
venous prole, indicates upstream occlusion. Mean ow velocity or peak systolic velocity (PSV) and the diastolic ow component are other important parameters for determining whether an artery would provide adequate outow when used as the recipient segment of a planned bypass.
This information is important to predict bypass patency prior to surgery. The patient presented has stage IV PAOD with occlusion of all arteries
below the knee. The dorsalis pedis artery shows monophasic, postocclusive ow just above the ankle joint. There is some luminal narrowing from
a hypoechoic plaque (P).
b Further down, shortly before it enters the arch of foot, the dorsalis pedis artery has an unchanged monophasic ow prole with good perfusion,
suggesting that the artery is a suitable candidate for connection of a pedal bypass graft. In this patient, with multiple upstream occlusions, a more
pulsatile ow prole would suggest poor outow.
c Angiogram of the pedal vessels demonstrates patency of the artery though there is poor opacication due to the proximal occlusions. Angiography is inferior to color duplex in predicting whether this artery will ensure adequate runo for a pedal bypass.
d The venous graft anastomosed onto the dorsalis pedis artery has triphasic ow with a PSV of nearly 80cm/s, indicating adequate perfusion of
the foot without ischemic vasodilatation in the periphery
b

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Chapter 2 · Extremity Arteries
2
abc
d
efg
. Fig. 2.72a–g (Atlas) Bypass complications: graft infection, graft occlusion.
a A hypoechoic stula (F) some centimeters in length extends from below the skin to the distal anastomosis of a P2 bypass (composite image),
indicating graft infection, although the initial clinical appearance of the wound suggested only a supercial, subcutaneous infection.
b If gray-scale ultrasound depicts elongated hypoechoic to anechoic areas around a bypass graft (BP), an infection of the bypass has to be ruled
out, in particular if the respective clinical signs are present. The simplest test is ultrasound- guided aspiration, for which the hyperechoic needle tip
(N) is positioned in the hypoechoic zone adjacent to the graft. The needle may have to be moved about a bit under suction to reach a uid collection.
c Graft infection is often characterized by mixed echogenicity, predominantly low echogenicity, around the graft; if a stula (F) has formed, a
hypoechoic tract extending to the skin level may be identied.
d Infectious thrombosis can cause stenosis or occlusion, especially at the anastomosis (e.g., in a crossover bypass and femoropopliteal graft extension (anast)). In the case presented, there is a peak systolic velocity (PSV) of 450cm/s (hypoechoic infectious area around the graft). The slightest
clinical suspicion of bypass graft infection should prompt a sonographic examination to prevent complications and initiate timely graft revision.
Graft occlusion.
e, f, g When thrombectomy is planned in a patient with a synthetic bypass graft, it is especially important to evaluate inow and outow and
whether the recipient segment is also occluded and a bypass extension might be necessary. In this patient, the triphasic waveform with an
adequate PSV in the inow tract rules out relevant proximal stenosis (e). Outow can be evaluated by obtaining a waveform from the artery distal
to the anastomis. A higher PSV indicates better outow (f); however, PSV also depends on the recipient vessel. In the crural arteries (as in this
example of a femoroanterior tibial bypss (ATA)), blood ow is slower than downstream of a popliteal artery bypass. Bypass graft occlusion can be
due to external compression as in this case of a bypass graft (BP) onto the P3 segment of the popliteal artery (arrow, see double contour in g).
External structures compressing a bypass include tendons, scar formation, or excessive longitudinal traction of the graft during implantation. For
successful repair in such cases, thrombectomy must include elimination of the external compression
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