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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

6.3 · Atlas: Visceral andRetroperitoneal Vessels
465
. Fig. 6.72a–c (Atlas) Transplant kidney– rejection– stula.
Analysis of the Doppler waveform from the renal artery is an integral component of the diagnostic evaluation of kidney graft function and rejection. The renal artery of a transplant kidney anastomosed to the iliac artery is often more easily accessible to sonographic evaluation than the
native renal artery.
a The two renal arteries supplying the kidney are depicted at their origins from the iliac artery (A.I.). A highly pulsatile waveform comparable to
that of an extremity artery is obtained from the origin of the second renal artery (A.REN.2). This ow prole indicates rejection.
b Surprisingly, the other transplant artery, inserted above the rst one, has a monophasic waveform with the low-resistance ow typical of normal
kidney function.
c The Doppler waveform of the renal vein (ow toward transducer in the direction of the iliac vein) depicts a pulsatile ow prole with marked turbulence, which is typical of venous ow downstream of an arteriovenous stula. The patient had a history of repeated biopsy for suspected graft
rejection, which led to the formation of a stula and explains why the artery (A.REN.1) supplying the stula shows low-resistance ow despite
rejection (as documented in the second artery, labeled A.REN.2in a, b)
6
. Fig. 6.73a–c (Atlas) Abdominal aortic and iliac artery aneurysm.
a Partially thrombosed infrarenal abdominal aortic aneurysm (AAA) shown in transverse orientation (left section) and longitudinally (middle section). Evaluation of the perfused lumen is improved in the color duplex mode. The total AAA diameter is 62mm. The mural thrombosis lining the
lumen appears hypoechoic around the patent lumen. The aneurysm (right section, arrowheads) involves the common iliac artery (A.I.C) and the
proximal internal iliac artery (A.I.I). The elongated external iliac artery (A.I.E) leaves the scanning plane. At this level, the aneurysm has a total diameter of 47mm with a patent lumen of 14mm.
b Angiogram showing aneurysmal dilatation of the aorta and of the common iliac arteries. Due to mural thrombosis, the origin of the internal iliac
artery on the right (arrow) seems not to be dilated.
c Contrast-enhanced CT: Aneurysm on the right (arrow) extending into the proximal internal iliac artery with mural thrombosis surrounding the
perfused lumen. The internal iliac artery arises from the posterior aspect of the common iliac artery (see a)

466
Chapter 6 · Visceral andRetroperitoneal Vessels
6
. Fig. 6.74a, b (Atlas) Abdominal aortic aneurysm with arterial embolism.
a While the risk of rupture correlates with the diameter of the aneurysm, the risk of embolism associated with the presence of thrombosis in an
aneurysm is independent of its size. The saccular aneurysm shown has a size of only 4cm with mural thrombosis reducing the size of the lumen to
that of the normal vessel, especially in the saccular portion; nevertheless, this aneurysm was the source of distal emboli (see b). This is an indication for surgery irrespective of aneurysm size. Angiography shows no abnormalities as the perfused lumen of the aneurysm corresponds to that
of the normal width of the aorta. The white outline in the left image indicates the extent of the aneurysm; the longitudinal image on the right
depicts the saccular anterior outpouching and the thrombotic lining.
b Isolated occlusion of the profunda femoris artery with a patent supercial femoral artery (A.F.S) and common femoral artery (A.F.C) is typically
due to embolism rather than atherosclerosis. Neither color duplex nor the Doppler waveform demonstrates ow in the profunda femoris artery.
The gray-scale mode shows not only a posterior plaque with acoustic shadowing but also hypoechoic thrombotic material extending from the
profunda femoris artery (sample volume) into the bifurcation
. Fig. 6.75a, b (Atlas) Abdominal aortic aneurysm.
a The therapeutic management of an abdominal aortic aneurysm (AAA) is mainly dictated by its diameter, involvement of the iliac artery, presence of thrombosis, and infrarenal extent, including the distance to the renal artery origins, which is important when endovascular aneurysm
repair (EVAR) is contemplated. Since the renal artery origins are best seen transversely, and the segment between the origins and the end of the
aneurysm longitudinally, it is helpful to rst identify the superior mesenteric artery in the longitudinal view and then use it as a guiding structure.
The renal arteries arise 1–2cm distal to the origin of the mesenteric artery. The segment between the end of the aneurysm and the superior mesenteric artery origin can thus be measured in longitudinal orientation. This value minus 2cm is the distance between the renal artery origin and
the aneurysm. This AAA cannot be eliminated by EVAR with a simple, nonbranched stent graft because thrombotic deposits in the aneurysm neck
(posterior to the caliper in the left image) preclude rm proximal anchorage of the stent graft.
Contained perforation of abdominal aortic aneurysm.
b Infrarenal, partially thrombosed AAA measuring 6cm (D3+D4). The transverse lower abdominal scan reveals a contained perforation with com-
plete thrombosis of the spilled blood at the time of the examination. The contour of the thrombosed aneurysm (arrow) is distinct from the clotted
perivascular blood. The site of perforation is indicated by the contour disruption anterolaterally. The blood that escaped through the perforation
into the psoas muscle has a total extent of 12cm (D1). There are no ow signals at the site of perforation at the time of the examination

6.3 · Atlas: Visceral andRetroperitoneal Vessels
467
. Fig. 6.76 (Atlas) Abdominal aortic aneurysm due to nonatherosclerotic cause.
Aneurysms of nonatherosclerotic or nonbacterial/noninfectious origin can grow to giant size before they rupture. In this young African woman
(examined in Uganda) who presented with a tense abdomen, an aneurysm with a cross-sectional diameter of over 15cm arising from the infrarenal aorta and extending to the iliac bifurcation on both sides lled most of the intra-abdominal cavity. The aneurysm is shown on a composite
scan in longitudinal orientation. There is suprarenal kinking of the aorta, which thus extends from the vertebral column to the abdominal wall.
The intestine is pushed to the side. Further down in the lower abdomen, with the transducer slightly rotated, the common iliac artery is shown
to be aneurysmatically dilated to the level of the origin of the external iliac artery (normal lumen). Posterior to the common iliac artery, the common iliac vein is dilated due to congestion. There are no atherosclerotic lesions of the arterial wall. The patient has AIDS, making Cytomegalovirus
infection (induced by immunodeciency) the most likely cause of the aneurysm
6
. Fig. 6.77a, b (Atlas) Follow-up after endovascular aneurysm repair (EVAR).
a B-mode ultrasound follow-up after EVAR shows the stent graft (S) in the lumen of the abdominal aortic aneurysm (AAA) with properly connected left modular limb (longitudinal image on the left, transverse image on the right). The aneurysm diameter has decreased from 63 to 55mm.
Stent migration is dicult to identify by B-mode imaging.
b The aneurysm and stent graft are scrutinized carefully for endoleaks in longitudinal (leftmost section) and transverse orientation (middle and
right sections) using color duplex imaging with a low pulse repetition frequency (in order not to miss low-ow endoleaks). In addition, the entire
sac must be searched for ow from patent lumbar arteries (typically entering the aneurysm posterolaterally) or from a patent inferior mesenteric
artery entering the sac anterolaterally (type II endoleak). The third step is to search for failure of the modular limb seal (type III endoleak) in longitudinal and transverse orientation. S indicates the two iliac limbs in longitudinal and transverse orientation (left and middle sections) and the
main stent graft body in transverse orientation (right section). V.C, vena cava

468
Chapter 6 · Visceral andRetroperitoneal Vessels
6
. Fig. 6.78a–c (Atlas) Type Ib endoleak.
a Following implantation of a straight stent graft to isolate an infrarenal abdominal aortic aneurysm (AAA), there is ow in the distal aneurysm
sac (V.C, vena cava; A, aorta; ST, stent). The middle section shows failure of the distal anastomotic seal at the level of the aortic bifurcation (type Ib
endoleak, arrow). The Doppler waveform from this site shows high-frequency to-and-fro ow (with a PSV of 250cm/s). Blood enters the aneurysm
sac in systole and, in diastole, ows back into the distal aorta.
b Closer evaluation of ow within the aneurysm sac reveals that part of the blood ows along the stent graft toward the origin of the inferior
mesenteric artery (coded in red, toward transducer). Directly at the origin of the inferior mesenteric artery (A.M.I), there is orthograde ow from
the aneurysm (blue, away from transducer; below the baseline in the Doppler waveform). Flow at the origin of the inferior mesenteric artery is
slow with a PSV of 30cm/s. In the transverse image, the aneurysm sac is indicated by a white outline; the stent graft is visualized with color-coded
ow, and bright echoes indicate the stent graft wall (S). The normal ow direction in the inferior mesenteric artery suggests that this is not a
typeII endoleak, but rather a type I endoleak with blood draining from the aneurysm sac through the inferior mesenteric artery. This example
underscores the importance of evaluating blood ow directions for comprehensive evaluation after endovascular aneurysm repair (EVAR) and
reliable identication of inow and outow. This information is important for correct interpretation of the situation and adequate management.
c 3D CT angiogram conrms the type I endoleak (arrow)

6.3 · Atlas: Visceral andRetroperitoneal Vessels
469
6
. Fig. 6.79a, b (Atlas) Type I endoleak after endovascular aneurysm repair (EVAR).
a The color ow image shows ow within the stent graft (S) but also large color-coded areas indicating ow within the hypoechoic aneurysm sac.
Blood enters the sac through a leak at the anastomotic seal below the renal artery origins (middle section), which is a type I endoleak (arrow). The
Doppler waveform from the site of the leak shows high-frequency monophasic ow with a peak systolic velocity (PSV) of over 1m/s. The to-andfro ow characteristic of endoleaks and false aneurysms (identical hemodynamic situation) is absent here. Unidirectional ow into an aneurysm
through an endoleak will lead to rupture within a short time if there is no adequate drainage, underscoring the importance of searching for an
outow in such situations.
b Here, blood leaves the aneurysm through the inferior mesenteric artery (A.M.I; coded in blue, away from transducer, indicated by arrow) visualized along the hypoechoic aneurysm sac with the stent graft (S) and the two iliac limbs (R and L). Farther to the left, the origin of the inferior
mesenteric artery is seen with ow coded in red. The corresponding Doppler waveform from the inferior mesenteric artery reveals a rather large
diastolic ow component
. Fig. 6.80 a, b (Atlas) Type II endoleak– high-ow.
a When the color ow image shows ow in the residual sac following endovascular aneurysm repair (EVAR), true ow must be dierentiated from
artifacts (migration artifact, mirror artifact, and artifact from pulsatile stent graft movement in the thrombosed aneurysm sac, especially shortly
after EVAR). Artifacts can be identied by insonation from dierent directions and spectral Doppler evaluation. Similar to false aneurysms in terms
of hemodynamics, endoleak jets should exhibit to-and-fro ow from the lumbar artery perfusing the aneurysm sac (ow into the sac during systole and back into the lumbar artery during diastole).
b Contrast-enhanced CT scan demonstrates blood ow into the aneurysm sac from a lumbar artery (type II endoleak)

470
Chapter 6 · Visceral andRetroperitoneal Vessels
a
6
Pulsation 2,5 mm
bc
d e
f
. Fig. 6.81a–f (Atlas) Type II endoleak– when to treat.
a The example shows ow into the residual aneurysm sac from a lumbar artery on the right (coded in red, toward transducer); also visible is ow in
both iliac limbs (blue). The waveform shows to-and-fro ow of very low frequency with a peak systolic velocity (PSV) <20cm/s. The slow ow (measured at the site of entry of the feeding artery), combined with the small caliber of the feeding artery, means that the amount of blood entering the
aneurysm is small. Such aneurysms often thrombose spontaneously, and there is no risk of rupture. They do not require treatment and can be managed by close monitoring (at 3-month intervals) to rule out further sac growth.
b, c Endoleak requiring repair– pulsation in time-mode mode.
b In the gray-scale image, inhomogeneous areas in the residual aneurysm sac already suggest an endoleak (EL) (S, stent). The diameter variation of
2.5mm through the cardiac cycle (time-motion mode) indicates relevant blood ow into the residual sac. This endoleak requires repair.
c The color ow image conrms this diagnosis, showing blood ow in most of the residual aneurysm sac.
d–f Small type II endoleak.
Patient with a small type II endoleak fed by a patent posterolateral lumbar artery, which is identied by to-and-fro ow in the Doppler waveform (d)and
by contrast-enhanced ultrasound (CEUS) (e). The absence of diameter variation of the residual aneurysm sac in the time-motion mode (f)indicates that
there is no relevant pressure build-up in the aneurysm sac during systole

6.3 · Atlas: Visceral andRetroperitoneal Vessels
471
6
a
c
fg
. Fig. 6.82a–g (Atlas) Type II endoleak– high-ow versus low-ow (comparison with CT ndings).
a Most endoleaks fed by an inferior mesenteric artery are high-ow endoleaks. In the case shown, peak systolic velocity (PSV) is 138cm. Such
high-ow endoleaks rarely close spontaneously, even if only a small portion of the excluded aneurysm sac shows ow signals.
b The CT angiogram conrms that ow is conned to a small portion of the aneurysm sac; however, ow into the sac is already seen during the
arterial phase. Follow-up 3months later conrmed a persistent high-ow endoleak (based on duplex ultrasound criteria) and an 8-mm increase in
the diameter of the residual aneurysm sac (not shown). Endoleak embolization was performed.
c Follow-up 6months later shows a new low-ow endoleak with a PSV of 27cm/s (fed by a lumbar artery, ow coded in blue). The endoleak is
located more peripherally, posterior to one of the iliac limbs. There is a mirror artifact with red-coded ow (same ow direction as within the stent
graft). The waveform demonstrates to-and-fro ow with systolic inow (S) and diastolic outow (D), conrming the endoleak (as this is a ow pattern that does not occur physiologically). This small endoleak requires monitoring but no treatment.
d In the CT angiogram, the small endoleak cannot be identied with certainty. In addition, there is a small posterior plaque, which may be
mistaken for an endoleak (in conjunction with the ndings of contrast-enhanced ultrasound (CEUS)). Note that, in contrast-enhanced CTA, an
endoleak fed by a patent lumbar artery may be opacied rather late, i.e., during the venous phase or even later (due to longer transit time of the
contrast microbubbles through lumbar arteries). As a result, such endoleaks may even be missed by CTA.
e The type II endoleak identied by color duplex imaging in this patient and fed by a lumbar artery is more conspicuous in the CEUS examination
(arrow) compared with CTA.
f,g Patent inferior mesenteric artery, not classied as a relevant endoleak.
f Sonographic mapping of an isolated aneurysm sac after EVAR for ow (using a low pulse repetition frequency) should also include a search for
patent lumbar arteries supplying the sac or for a patent inferior mesenteric artery. Retrograde ow in the inferior mesenteric artery (A.M.I; redcoded ow toward transducer) is always suspicious for an endoleak even if no ow is detectable in the aneurysm sac. Here, the Doppler waveform
demonstrates to-and-fro ow in the patent inferior mesenteric artery.
g CT angiogram conrms patency of the inferior mesenteric artery but without passage of contrast medium into the aneurysm sac, conrming
the sonographic ndings (this constellation of ndings is very rare)
b
de

472
Chapter 6 · Visceral andRetroperitoneal Vessels
6
. Fig. 6.83a–d (Atlas) Endoleak– stepwise diagnostic workup by CDUS, CEUS, CTA.
Stepwise diagnostic workup of a patient with unchanged diameter of abdominal aortic aneurysm (AAA) one year after endovascular aneurysm
repair (EVAR): search for endoleak and evaluation of therapeutic relevance.
a Color duplex ultrasound (CDUS) identies a small type II endoleak with to-and-fro ow.
b The endoleak is conrmed by contrast extravasation in the contrast-enhanced ultrasound (CEUS) examination.
c CT angiogram also shows contrast medium extravasation into the aneurysm sac.
Type II endoleak missed by CDUS but detected with CEUS.
d Color duplex examination (left image) following EVAR fails to identify an endoleak despite adequate settings. The two iliac limbs are depicted in
the posterior portion of the aneurysm sac with the patent vena cava laterally (power mode display, which is less angle-dependent and improves
the detection of slow-owing blood; see . Table1.8). In the color duplex image obtained after contrast medium administration (middle), the
signal enhancement reveals ow (arrow) in the aneurysm sac, consistent with a type II endoleak. The contrast-enhanced CT scan (right) conrms
the endoleak (arrow) (Images courtesy of K.Pster)

6.3 · Atlas: Visceral andRetroperitoneal Vessels
473
6
. Fig. 6.84a, b (Atlas) Stent graft rupture after EVAR.
a The B-mode image already shows stent graft rupture; the color duplex images (transverse and longitudinal planes) conrm a type IV endoleak;
and the waveform shows to-and-fro ow with a peak systolic velocity (PSV) of 60cm/s.
Follow-up after EVAR– complication versus retroperitoneal brosis.
b Ultrasound follow-up 6months after endovascular aneurysm repair (EVAR) identies a margin of low echogenicity around the residual aneu-
rysm sac. The residual diameter of the aneurysm sac in this plane (D2) is 48mm (marked with calipers). The 1-cm margin around the stented
aneurysm is most conspicuous anteriorly. Neither duplex ultrasound nor CT (rightmost image) demonstrates an endoleak. The Doppler waveform
obtained from the area showing isolated color-coded ow signals within the hypoechoic margin (see sample volume) indicates normal intravascular blood ow and no to-and-fro ow (dierential diagnosis: contained perforation). New-onset retroperitoneal brosis is suspected (dierential
diagnosis: perigraft reaction) and conrmed by ultrasound-guided biopsy. A.S = main stent graft body, V.C = vena cava.
The center right image (obtained at a slightly lower level) shows occlusion of the more anterior stent graft limb adjacent to the 1-cm hypoechoic
margin surrounding the aneurysm sac (indicated by calipers); this is a complication occurring after EVAR.P.S = stent limb, V.C = vena cava.
The contrast-enhanced CT scan shows enhancing tissue around the aneurysm sac (interpreted to indicate inammatory hyperemia). Retroperitoneal brosis also explains why shrinkage of the aneurysm sac after EVAR is minimal, even though neither contrast-enhanced CT nor color duplex
imaging reveals an endoleak. Another CT nding consistent with retroperitoneal brosis is the demonstration of perfused arteries (arrow) coursing partially within the thickened margin and then being pushed back toward the aorta by perivascular brosis (see . Figs.6.37 and 6.85 (Atlas))

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Chapter 6 · Visceral andRetroperitoneal Vessels
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. Fig. 6.85a, b (Atlas) Retroperitoneal brosis– dierential diagnosis: perforated abdominal aortic aneurysm.
a Retroperitoneal brosis (Ormond’s disease) may be visualized as a hypoechoic cap-like structure anterior to the aorta. This condition diers from
aortitis and inammatory aortic aneurysm in that the process also involves the vena cava, which is ensheathed by brotic tissue. The origin and
proximal course of the inferior mesenteric artery are evaluated to establish the dierential diagnosis. In the presence of retroperitoneal brosis,
the mesenteric artery, after arising from the left lateral aspect of the aorta, is pushed against the aortic wall, where it runs for some centimeters
before piercing through the hypoechoic brotic layer and continuing its intra-abdominal course in the mesentery. The image on the left depicts
the inferior mesenteric artery arising from the aortic wall and the hypoechoic cap above. The image on the right obtained in slightly oblique orientation documents the course of the inferior mesenteric artery with ow displayed in blue (away from transducer). It is pushed against the aortic
wall by the hypoechoic structure. The middle section shows the corresponding Doppler waveform.
b After a few months of cortisone treatment, the hypoechoic layers around the aorta and vena cava have markedly decreased in thickness, from
1cm (see a) to 4mm. However, the brotic tissue still pushes the inferior mesenteric artery against the aorta and its course remains unchanged.
The Doppler waveform is from the inferior mesenteric artery
. Fig. 6.86 (Atlas) Inammatory abdominal aortic aneurysm.
Transverse image (left) and longitudinal image (right) showing the
typical appearance of an inammatory abdominal aortic aneurysm
(AAA). The aneurysm has a luminal diameter of 3.5cm and exhibits atherosclerotic wall changes. The circumferential hypoechoic layer (1cm)
around the AAA conrms the inammatory origin of the aneurysm.
Furthermore, the presence of hyperechoic plaque allows identication
of the intima and thus provides further evidence that the thickening
is not due to thrombus (as it involves the arterial wall layer external to
the intima; see . Fig.6.38)
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