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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

384
Chapter 5 · Extracranial Cerebral Arteries
5
a
. Fig. 5.89 (Atlas) Distal vertebral artery stenosis.
Atherosclerotic vertebral artery stenosis typically occurs at the origin
from the subclavian artery. A more distal stenosis (in the V2 segment
between C4 and C5, as in the example presented) often has other
causes such as constriction of the passageway through the transverse
processes by exostosis or dissection. An increase in ow velocity
(here 250cm/s) indicates stenosis only if it is localized. Increased ow
throughout the vertebral artery suggests a compensatory increase in
perfusion due to hypoplasia of the contralateral branch or atherosclerotic occlusion of other arteries supplying the brain
b
c
. Fig. 5.90a–c (Atlas) Vertebral artery occlusion.
a Both color duplex and spectral Doppler fail to depict ow signals in a
tubular structure arising from the subclavian artery. The course of the
structure corresponds to that of the vertebral artery, and the ndings
are consistent with vertebral artery occlusion.
b Thin vertebral artery (2.2mm) with relling through spinal vessels
just before the atlas loop and postocclusive ow (delayed systolic rise
and slow ow with a PSV of 32cm/s).
Vertebral artery dissection.
c Following a failed endovascular intervention, an intimal ap (D) is
visible in the vertebral artery between the transverse processes. At
the site of sampling, ow in the true and false lumina is in opposite
directions (coded in red and blue; above and below the baseline in the
Doppler waveform; V=vertebral vein). The vertebral artery lumen is
indicated by calipers; the false lumen is patent in the left part of the
image and thrombosed in the right part

Vertebral artery
5.10 · Atlas: Extracranial Cerebral Arteries
385
D
S
Subclavian
artery
stenosis
a b
. Fig. 5.91a, b (Atlas) Subclavian steal syndrome with to-and-fro ow in the vertebral artery.
a The steal phenomenon in the vertebral artery varies with the severity of subclavian artery stenosis. The respective changes can be reproduced
during the examination using an arm cu to induce and release ischemia while recording a Doppler waveform. To-and-fro ow may be preserved
and only change from primarily cranial ow to primarily central ow (toward subclavian artery. In the case shown, compression of the ipsilateral
arm results in high diastolic ow in the cranial direction with only little retrograde ow in systole. Upon deation of the arm cu, there is a change
in to-and-fro ow with a large retrograde systolic ow component (S) and only little antegrade ow in diastole (D).
b Diagram of to-and-fro ow in the vertebral artery in ipsilateral subclavian artery stenosis
5
. Fig. 5.92a–c (Atlas) Sub-
clavian steal syndrome with
retrograde ow in the vertebral
artery.
a In this patient with severe
subclavian steal syndrome, retrograde ow from the ipsilateral
vertebral artery (A.V) into the
subclavian artery (A.S) is already
seen at rest (displayed in blue).
This is veried by the spectral
Doppler tracing with conrmation of the identity of the vertebral artery by transmission of
oscillations from tapping in the
mastoid region. The subclavian
artery is occluded proximal to
the site of entry of the vertebral
artery.
b Following ischemia upon
release of the arm cu, the Doppler waveform shows a marked
increase in retrograde ow, in
particular in diastole.
c Diagram of retrograde ow in
the vertebral artery in ipsilateral
subclavian artery occlusion
with complete subclavian steal
syndrome
a
Vertebral artery
retrograde
Subclavian
artery
occlusion
b c

386
Chapter 5 · Extracranial Cerebral Arteries
5
a
c
. Fig. 5.93a–d (Atlas) Subclavian steal syndrome with vertebrovertebral crossover.
a Image showing the origin of the vertebral artery in central subclavian artery occlusion. The spectral waveform recorded at the origin of the vertebral artery (A.VERT) from the subclavian artery (A.S) demonstrates to-and-fro ow with a retrograde systolic component (away from transducer,
toward heart) and an antegrade diastolic component (toward transducer, toward brain). The passage of the artery through the transverse process
(WK) is shown at the left margin of the image.
b In the provocative test, compression of the ipsilateral brachial artery with reduction of blood ow into the arm arteries leads to an increase in
antegrade diastolic ow in the ipsilateral vertebral artery compared to rest (see a). Ischemia induced by release of the cu (mid-portion of the
waveform) results in a change from to-and-fro ow to a constant reversed ow from the vertebral artery into the subclavian artery (away from
transducer).
c An increase in systolic and diastolic ow velocity (S=systole, D=diastole) in the contralateral vertebral upon release of the cu around the
brachial artery on the side of the occluded subclavian artery proves vertebrovertebral crossover in subclavian steal syndrome. In the example
shown, the increase in velocity is not very pronounced, suggesting that there are other collateral routes to bypass the occluded subclavian artery.
d Angiogram with depiction of contrast medium crossover in occlusion of the left subclavian artery. The temporal course of the contrast medium
passage shows ow from the right subclavian artery (left) into the right vertebral artery (middle) and into the left vertebral artery (right)
b
d

ab
5.10 · Atlas: Extracranial Cerebral Arteries
387
5
a
c
. Fig. 5.94a–c (Atlas) Carotid body tumor.
a Ultrasound shows a rather well vascularized carotid body tumor (TU) supplied by the external carotid artery (ECA). There is relatively high ow in
the feeding artery with a peak systolic velocity (PSV) of >80cm/s. The tumor is hypoechoic and measures 11×18mm.
b Longitudinal and axial computed tomography images of the glomus tumor (large arrow); small arrows indicate the internal carotid artery (ICA)
and ECA.
c Following transarterial tumor embolization in this 82-year- old patient, perfusion in the tumor is markedly reduced (TU) and a patent feeder
arising from the ECA has a PSV of only 15cm/s. A growing carotid body tumor typically splays the carotid bifurcation. Lateral growth, as in this
patient, is less common. Even less common are carotid body tumors encasing the vessels or developing in the back of the neck. A carotid body
tumor in atypical location, as in the case presented here, must be dierentiated from lymphoma (which is more common). The primary criterion
on duplex ultrasound is good vascularization (transverse view on the left, longitudinal view on the right)
b
. Fig. 5.95a, b (Atlas) Diagnosis of brain death.
Diastolic ow velocity determines the pulsatility of blood ow, and this in turn is governed by vessel wall elasticity and especially by the degree
of peripheral resistance. In the carotid territory, peripheral resistance can increase when there is an increase in intracranial pressure, and diastolic
ow velocity reects diastolic blood pressure as a function of intracranial pressure. An increase in intracranial pressure therefore causes a decrease
in diastolic ow velocity, and the end-diastolic ow component is eliminated when intracranial pressure matches diastolic pressure. This can result
in a ow signal resembling postocclusive ow (as shown in a): high pulsatility, no diastolic ow, and markedly reduced peak systolic velocity (PSV)
(20cm/s in the example, knocking waveform). The pressure situation can lead to to-and-fro ow with markedly reduced orthograde ow velocity
(PSV of 30cm/s in b) and retrograde diastolic ow. To-and-fro ow or a waveform showing only early diastolic peaks indicates cerebral circulatory
arrest

Visceral andRetroperitoneal
Vessels
6.1 Abdominal Aorta, Visceral andRenal Arteries – 391
6.1.1 Vascular Anatomy – 391
6.1.1.1 Aorta – 391
6.1.1.2 Visceral Arteries – 391
6.1.1.3 Renal Arteries – 392
6.1.2 Examination Protocol andTechnique – 392
6.1.2.1 Aorta – 392
6.1.2.1.1 Protocol forUltrasound Examination ofthe
Abdominal Aorta andAortic Aneurysm – 392
6.1.2.1.2 Protocol forUltrasound Follow-Up After Endovascular
Aneurysm Repair (EVAR) – 392
6.1.2.2 Visceral Arteries – 393
6.1.2.3 Renal Arteries – 395
6.1.2.3.1 Ultrasound Technique – 397
6.1.3 Normal Findings – 397
6.1.3.1 Aorta – 397
6.1.3.2 Visceral Arteries – 397
6.1.3.3 Renal Arteries – 398
6.1.4 Interpretation andDocumentation – 399
6.1.5 Clinical Role ofDuplex Ultrasound – 399
6.1.5.1 Aorta – 399
6.1.5.1.1 Abdominal Aortic Aneurysm – 399
6.1.5.1.2 Inammatory andAtherosclerotic Conditions – 400
6.1.5.2 Visceral Arteries – 401
6.1.5.3 Renal Arteries – 402
6.1.6 Measurement Parameters, Diagnostic Criteria,
andRole ofUltrasound – 405
6.1.6.1 Renal Arteries – 405
6.1.6.1.1 Role ofColor Duplex Ultrasound in the Detection
ofRenal Artery Stenosis – 406
6.1.6.1.2 Therapy-Oriented Stenosis Grading – 408
6.1.6.1.3 Contrast-Enhanced Ultrasound (CEUS) – 409
6.1.6.1.4 Ultrasound Follow-Up After Renal Artery Stenting – 409
6.1.6.1.5 Diagnostic Algorithm – 411
6.1.6.1.6 Renal Artery Occlusion – 412
6.1.6.1.7 Transplant Kidney – 412
6.1.6.2 Visceral Arteries – 414
389
6
© Springer International Publishing AG, part of Springer Nature 2018
W. Schäberle, Ultrasonography in Vascular Diagnosis, https://doi.org/10.1007/978-3-319-64997-9_6

6.1.6.2.1 Celiac Trunk – 414
6.1.6.2.2 Visceral Artery Aneurysm – 415
6.1.6.2.3 Dissection – 416
6.1.6.2.4 Superior Mesenteric Artery – 416
6.1.6.2.5 Acute Mesenteric Artery Occlusion – 418
6.1.6.3 Aorta – 422
6.1.6.3.1 Aortic Stenosis andThrombosis – 422
6.1.6.3.2 Abdominal Aortic Aneurysm – 423
6.1.6.3.3 Specic Aspects oftheUltrasound Examination
inAbdominal Aortic Aneurysm – 423
6.1.6.3.4 Comparison ofUltrasound andComputed Tomography – 426
6.1.6.3.5 Abdominal Aortic Aneurysm Screening: Rupture Risk – 426
6.1.6.3.6 Aortic Dissection – 426
6.1.6.3.7 Follow-Up After Open Surgical andEndovascular
Aneurysm Repair – 427
6.1.6.3.8 Aortitis: Retroperitoneal Fibrosis– Inammatory
Abdominal Aortic Aneurysm – 433
6.2 Visceral andRetroperitoneal Veins – 435
6.2.1 Vascular Anatomy – 435
6.2.1.1 Vena Cava – 435
6.2.1.2 Renal Veins – 436
6.2.1.3 Portal Venous System and Hepatic Veins – 436
6.2.2 Examination Technique – 436
6.2.2.1 Vena Cava – 436
6.2.2.2 Renal Veins – 437
6.2.2.3 Portal Vein andSuperior Mesenteric Vein – 438
6.2.3 Clinical Role ofDuplex Ultrasound – 439
6.2.3.1 Renal Veins – 439
6.2.3.2 Portal Venous System – 439
6.2.4 Normal Findings – 439
6.2.4.1 Vena Cava andRenal Veins – 439
6.2.4.2 Portal Venous System – 439
6.2.5 Documentation – 440
6.2.6 Abnormal Ultrasound Findings, Measurement Parameters,
andDiagnostic Role – 440
6.2.6.1 Vena Cava – 440
6.2.6.1.1 Membranous Vena Cava Obstruction – 441
6.2.6.2 Renal Veins – 441
6.2.6.3 Superior Mesenteric Vein andSplenic Vein – 442
6.2.6.3.1 Splenic Vein Thrombosis – 443
6.2.6.4 Portal andHepatic Veins – 443
6.2.6.4.1 Portal Vein Thrombosis – 443
6.2.6.4.2 Portal Hypertension – 443
6.2.6.4.3 Hepatic Veins – 447
6.3 Atlas: Visceral andRetroperitoneal Vessels – 449

Left gastric artery and veinInferior phrenic arteries
d
Right gastric artery and vein
6.1 · Abdominal Aorta, Visceral andRenal Arteries
391
6
6.1 Abdominal Aorta, Visceral
andRenal Arteries
6.1.1 Vascular Anatomy
6.1.1.1 Aorta
e abdominal aorta begins at the level of the diaphragm,
crossing it via the aortic hiatus at the T12 vertebral level, and
descends in front of or slightly to the le of the vertebral column. e diameter of the aorta decreases on its downward
course from 25 to 20mm. A diameter of up to 30mm as
a result of age-related dilatation is considered normal. An
abrupt increase in diameter to more than 1.5 times that of
the normal proximal segment is regarded as evidence of an
aneurysm. e abdominal aorta divides into the two common iliac arteries at the L4/L5 level. e three major sources
of intestinal blood supply are the celiac trunk, the superior
mesenteric artery, and the inferior mesenteric artery. ese
visceral branches arise from the anterior aspect of the aorta.
eir pattern of supply is complex and has numerous variants. e lumbar arteries originate from the lateral aspect,
and the two renal arteries course in a retroperitoneal direction. e arteries arising from the aorta, from superior to
inferior, are described in detail below (
6.1.1.2 Visceral Arteries
Just below the aortic aperture of the diaphragm, the aorta
gives o the celiac trunk, or celiac artery, which, aer 2–3cm,
divides into its two main branches, the common hepatic and
. Fig.6.1).
splenic arteries. e common hepatic artery courses between
the head of the pancreas and the lower edge of the liver into
the hepatoduodenal ligament, where it gives o the right
gastric artery and gastroduodenal artery, two important collaterals that connect to the superior mesenteric artery. It then
continues to the liver as the proper hepatic artery. e splenic
artery is in part very tortuous as it courses along the upper
border of the pancreas to the splenic hilum and supplies not
only the spleen but also the body and tail of the pancreas as
well as the greater curvature of the stomach.
Approx. 0.5–2cm below the celiac trunk lies the origin
of the superior mesenteric artery at the L1/L2 level. It arises
anteriorly at an acute angle of 15–30° relative to the aorta,
and its proximal segment runs parallel to the aorta between
the pancreas and renal vein. Aer approx. 4–5cm, it gives
o the inferior pancreaticoduodenal and middle colic arteries, which supply the proximal two-thirds of the transverse
colon. e distal superior mesenteric artery divides into the
jejunal, ileal, and ileocolic arteries supplying the small intestine.
Many anatomic variants exist. In 55% of the population,
the celiac trunk gives o the hepatic artery and splenic artery
(type I according to Michel’s classication). In type II (10%),
the replaced le hepatic artery arises from the le gastric
artery. In type III (11%), the replaced right hepatic artery,
which supplies the right hepatic lobe, arises from the superior mesenteric artery (see
. Figs. 6.3e and 6.52b (Atlas)).
ese two common variants lead to altered hemodynamics at
the origin of the superior mesenteric artery (larger diastolic
Common hepatic artery
Gastroduodenal artery
Pancreaticoduodenal
Renal artery and vein
Right gastroepiploic
. Fig. 6.1 Vascular anatomy of the upper abdomen (From Luther 2014)
artery and vein
artery and vein
artery and vein
Inferior vena cava
Proper hepatic artery
Common bile duct
Portal vein
artery
Middle colic
Right colic
Esophageal branches an
left gastric veins
Celiac trunk
Splenic artery
and vein
Posterior pancreatic
artery and vein
Superior mesenteric
artery and vein
Mesentery
Inferior mesenteric vein
Inferior mesenteric artery

392
Chapter 6 · Visceral andRetroperitoneal Vessels
component). Another variant is the presence of accessory
hepatic arteries, for example, arising from the superior mesenteric artery (7%). A rare variant is a common origin of the
hepatic, splenic, and superior mesenteric arteries from the
aorta (4.5%). ere is good collateralization of the visceral
arteries, which is why chronic proximal occlusion of a single
visceral artery usually has no adverse eect.
done gently in patients with a history of abdominal surgery
and extensive adhesions.
e examination of the abdominal and retroperitoneal
vessels begins with the identication of the aorta just below the
diaphragm. e examiner then follows the aorta in transverse
orientation down to the division into the iliac arteries, localizing the origins of the visceral and renal arteries on the way.
e inferior mesenteric artery originates at the L3 level,
approx. 4–5cm above the aortic bifurcation, and descends
6.1.2.1 Aorta
anterior to and somewhat to the le of the aorta. It is not
visualized consistently due to its small caliber of approx.
2–4mm.
6.1.2.1.1 Protocol forUltrasound Examination
oftheAbdominal Aorta andAortic
Aneurysm
6
6.1.1.3 Renal Arteries
e renal arteries arise from the aorta at right angles at the
L2 level approx. 1–2 cm below the mesenteric artery. e
right renal artery oen arises somewhat higher than the le
renal artery and crosses under the inferior vena cava, while
the le renal artery takes an almost horizontal course to the
le renal hilum. Two or more renal arteries are present in
approx. 25% of the population. e renal arteries divide into
the segmental arteries just before the hilum. e segmental
arteries successively split into interlobar, arcuate, and interlobular arteries.
6.1.2 Examination Protocol andTechnique
With a scanning depth of up to 20cm, a valid and diagnostic duplex scan of the intra-abdominal and retroperitoneal
arteries can only be obtained using a low-frequency transducer with a higher receive gain and a high enough frame
rate. Slender patients can be examined with a 5MHz transducer, but 3.5–2MHz transducers will be necessary in most
cases. Sector scanners or curved-array transducers with
a small footprint make it easier to achieve a suitable Doppler angle (<70°, ideally <60°). Spectral Doppler sampling is
impaired by the longer pulse delay with increasing depth of
the vessel of interest.
e examiner is confronted with a dilemma here since a
high pulse repetition frequency (PRF) is required to detect
fast ow, while the depth of the target vessels necessitates the
use of a low PRF, making aliasing a more common problem
when evaluating stenosis of an abdominal vessel. is problem can be overcome by reducing the transmit frequency
and scanning at a smaller insonation angle. To achieve an
adequate frame rate in the color mode, a small color box just
large enough to cover the area of interest must be chosen (as
the frame rate is lower when more scan lines are processed).
e patient is positioned supine with the arms along
the side of the body and a relaxed abdominal wall. Other
preparations are usually not necessary. To reduce artifacts,
the examiner can apply gentle pressure with the transducer
and push interfering gas-lled bowel loops out of the way
or compress them. Exerting pressure with the transducer
additionally reduces the scanning depth (skin level– aorta).
However, exerting pressure may be painful and should be
e sonographic evaluation of the abdominal aorta begins
by following its course in transverse orientation from the
diaphragm to the bifurcation. Adequate characterization of
dilated aortic segments and their extent includes the common and internal iliac arteries in longitudinal and transverse
planes.
An abdominal aortic aneurysm (AAA) is dened as a
focal increase in diameter to twice that of the proximal segment or a diameter>3cm. e length of an aneurysm is not
relevant for the decision when to operate and only adds to
the confusion in the numbers game. What is relevant though
is whether an aneurysm begins above or below the renal
artery origins and how close an infrarenal aneurysm extends
to the renal artery origins. e peripheral extent of an AAA
is of interest in terms of involvement of the common iliac
artery and possibly of the internal iliac artery. e iliac arteries are evaluated in transverse and longitudinal orientation
(oblique abdominal view). is information is important for
therapeutic decision making and preoperative planning.
To measure an AAA, the examiner rst localizes the
largest diameter and then moves the transducer around to
identify a plane depicting a circular structure with a small
diameter. is maneuver will avoid overestimation of the
aneurysm, which would result from measuring the size in
oblique orientation and which is a common pitfall, especially in the presence of dilatative atherosclerotic processes
with elongation and arching of the aorta. With its exible
selection of scan planes, ultrasound is superior to computed
tomography, which relies on the acquisition of standardized
axial slices.
diagnostic evaluation of patients with suspected
In the
stenosis, a spectral Doppler tracing of the aorta is obtained in
longitudinal orientation. Occlusion of the aorta is most easily
identied by the absence of ow in the duplex mode and then
conrmed by acquisition of a Doppler waveform. e vena
cava to the right of the aorta can serve as a landmark.
6.1.2.1.2 Protocol forUltrasound Follow-Up After
Endovascular Aneurysm Repair (EVAR)
Color duplex ultrasound (CDUS) (. Figs.6.77, 6.78, 6.79, 6.80,
6.81,
and 6.82 (Atlas)) and contrast-enhanced ultrasound
(CEUS)
(. Fig.6.36 and . Figs.6.82 and 6.38 (Atlas)) rely on
dierent mechanisms to detect owing blood. Endoleaks are
a common complication of endovascular aneurysm repair
(EVAR) for abdominal aortic aneurysm (AAA). CDUS

6.1 · Abdominal Aorta, Visceral andRenal Arteries
393
6
requires a minimum Doppler shi frequency to detect owing blood and thus fails to detct very slow ow or ow in
anatomic areas where a suciently small Doppler angle cannot be accomplished. Recall that, according to the Doppler
equation, a smaller angle of insonation results in a higher
Doppler shi frequency. Hence, a small angle improves the
detection of slow ow.
Following intravenous injection, ultrasound microbubbles enhance the signal from owing blood, rendering CEUS
more sensitive to low ow and slow ow within a stent gra
and in the extravascular space following escape through an
endoleak compared with conventional color duplex imaging.
When CDUS is used for endoleak detection, it is important
to use a lower PRF (as for the sonographic examination of
veins), possibly in conjunction with a longer persistence
and higher gain. For hemodynamic characterization of an
endoleak, ow should be characterized by spectral Doppler
interrogation at the site of entry into the residual aneurysm
sac. When the B-mode image shows inhomogeneous echogenicity, hypoechoic areas should be scrutinized closely in
the color duplex mode.
CEUS for endoleak detection is performed aer bolus
injection of 1.2–2.4mL SonoVue. e abdominal aorta including the stent gra and its limbs is examined in transverse orientation. Following arrival of the contrast microbubbles, the
examiner rst scrutinizes the proximal and distal anchorage
of the stent gra to identify a possible type I endoleak using a
low mechanical index (MI) to avoid rapid destruction of the
microbubbles (transmit power reduced to 10–20% of the output power). Type II endoleaks (patent lumbar arteries, inferior mesenteric artery) will typically become apparent aer a
short delay (late arterial to venous phase) following arrival of
the contrast agent in the stent gra. For identication of a type
II endoleak, the entire residual aneurysm sac is rst imaged in
transverse orientation, which may be supplemented by longitudinal and oblique planes as required (video). To avoid misinterpretation of the CEUS scan, it is important to compare
the ndings with the corresponding B-mode image (special
soware). Especially in patients with a complex stent gra,
the nal step is to examine the renal artery origins and mesenteric arteries for patency and stenosis.
e microbubble contrast solution is supplied along with
large-lumen cannulas and glass syringes to minimize microbubble destruction (shear stress and wall adherence) during
handling. e dynamic examination of the target anatomy
begins immediately aer administration of the microbubble
bolus and saline ush. e arterial phase begins 10–20s aer
injection; aer 30s, the venous phase begins.
Also in transverse orientation, the course of the
artery
to the spleen can be followed. e hepatic and splenic
splenic
arteries are characterized by rather large diastolic ow components as they supply parenchymal organs. From a clinical
point of view, sonographic examination of these arteries is
performed for two reasons only: to evaluate patients with
suspected iatrogenic vascular complications aer major
abdominal surgery and to search for aneurysm. Visceral
artery aneurysms are rare and most commonly occur in the
splenic artery, followed by the hepatic artery.
e superior mesenteric artery is identied at its origin in longitudinal orientation and tracked as far as possible
along its course parallel to the aorta. In inammatory bowel
disease, B-mode imaging enables evaluation of intestinal wall
thickening, while blood ow velocity in the superior mesenteric artery provides a measure of inammatory activity.
Inammatory bowel disease is associated with an increased
peak systolic velocity (PSV) and above all with an increased
diastolic velocity.
e superior mesenteric artery arises at the level of the
celiac trunk or as far as 2cm below it. It descends parallel to
the aorta and is thus seen as a round structure with a smaller
diameter anterior to the aorta in transverse images. Doppler
spectra are sampled in transverse planes in the celiac trunk
and the hepatic and splenic arteries and longitudinally in
the superior mesenteric artery. A better Doppler angle is
achieved when the transducer is moved downward and tilted
(
. Figs.6.2 and 6.3). Patients with an elongated and arched
proximal segment of the superior mesenteric artery should
be asked to breathe in slightly, which will shi the mesentery downward, thereby stretching the proximal segment for
improved Doppler angle correction.
An atypical origin of the hepatic artery from the superior
mesenteric artery aects the hemodynamics of the superior
mesenteric artery (larger diastolic component). erefore,
the celiac trunk must always be included in an examination
75º
25º
SMA
Ao
6.1.2.2 Visceral Arteries
e short celiac trunk with the division into the hepatic and
splenic arteries is oen identied in the transverse view as
a conspicuous palm-leaf-shaped structure. Slight angulation
of the transducer may be necessary to identify and visualize
the origins of these arteries. e proper hepatic artery can be
followed along its course anterosuperior to the portal vein in
the hepatoduodenal ligament.
. Fig. 6.2 Diagram of the origin of the superior mesenteric artery
(SMA) from the aorta (Ao), illustrating how the Doppler angle can be
improved from 75° to 25° by moving the transducer distally and then
tilting it cranially

394
ab
ab
Chapter 6 · Visceral andRetroperitoneal Vessels
6
CT
CHA
SMA
30–40%
5–10%
c
LGA
SA
15–25%
1–2%1%
de
c
0.5% 2–3%
f
gh
3%
3%
d
. Fig. 6.3 a Sonoanatomy of the celiac trunk and superior mesenteric artery. The left image shows the origin of the celiac trunk (T.C) from the
aorta (A) in transverse orientation. The celiac trunk varies in length from 1 to 4cm and divides into the hepatic artery (A.H) and splenic artery (A.L).
The hepatic artery is contained within the hepatoduodenal ligament, coursing beneath the liver to the liver hilum. The right image shows the
origins of the celiac trunk (T.C) and superior mesenteric artery (A.M.S) from the aorta in longitudinal orientation. The mesenteric artery descends
in front of the aorta (sometimes slightly to the left or to the right of the aorta). The celiac trunk divides early, leaving the scan plane, so that only a
short segment is typically seen on longitudinal abdominal scans. b–d Variants of hepatic artery (A.H) anatomy. The example shows an individual
with two hepatic arteries: one hepatic artery arising from the celiac trunk (T.C) and supplying the left hepatic lobe (b) and a second hepatic artery
arising from the superior mesenteric artery (A.M.S) and supplying the right hepatic lobe (c). The hepatic artery arising from the superior mesenteric artery aects the pulsatility of blood ow in the latter (larger diastolic component, see waveform in d). PPZ=pancreatic pseudocyst,
P=pancreas, PV=portal vein, V.C=vena cava, A=aorta. e Diagram illustrating variants of visceral artery origins from the abdominal aorta.
CT, celiac trunk; SMA, superior mesenteric artery; CHA, common hepatic artery; SA, splenic artery; LGA, left gastric artery
i
e
12–20%
jk
1%
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