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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

ab
6.3 · Atlas: Visceral andRetroperitoneal Vessels
475
. Fig. 6.87a, b (Atlas) Abdominal aortic aneurysm in a patient with horseshoe kidney.
a A horseshoe kidney is seen as a hypoechoic cap-like structure extending over the distal aorta. In the presence of a concomitant abdominal
aortic aneurysm (AAA), as in this case, the abnormal kidney must be sonomorphologically dierentiated from the aortic wall as well as from other
retroperitoneal structures or contained aneurysm rupture.
b CT conrming AAA and horseshoe kidney
6
a b
. Fig. 6.88a–h (Atlas) Aortic dissection– dynamic versus static blood ow reduction.
a Aortic dissection can be demonstrated by B-mode ultrasound when the intimal ap is insonated at a right angle (transverse view on the left,
longitudinal view in the middle). The time-motion mode on the right shows the systolic-diastolic ap movement in the lumen. Imaging at a perpendicular angle enables dierentiation of the true (WL) and false lumen (FL). The false lumen is compressed as pressure increases during systole
and expands again in diastole.
b The natural course and therapeutic measures in aortic dissection depend on the extent and involvement of aortic branches. Involvement of
the superior mesenteric artery is associated with high-grade stenosis at the origin. Morphologically, the course of the intimal tear is dicult to
identify. When the false lumen is located on the anterior side as in the case presented (see a), the superior mesenteric artery arises from the true
lumen, and its origin is compressed by the false lumen or an intimal ap, resulting in ow obstruction with a typical stenotic waveform and a peak
systolic velocity (PSV) of over 3m/s (interpolated due to aliasing) (static ow reduction due to dissection membrane).
c Poststenotic Doppler waveform with the typical delay in systolic upstroke, turbulent ow, and a larger diastolic component. The color ow
image shows the aorta (A) with the ap deep to the superior mesenteric artery.
d The Doppler waveform from the celiac trunk of the patient shows systolic deceleration with near-zero ow. This decrease in systolic ow velocity
is due to intermittent obstruction of the celiac artery origin by the aortic intimal ap; normal orthograde ow during diastole occurs because of
pressure reversal pushing the ap back into the lumen. This dangerous situation with imminent arterial occlusion cannot be adequately visualized
by any of the merely morphologic imaging modalities and can only be identied on the basis of the hemodynamic information provided by spectral Doppler measurement (dynamic ow reduction due to dissection membrane).
e Diagram of type III aortic dissection according to De Bakey (examples in b and c). The mesenteric arteries arising from the true lumen are compressed by the false lumen or the intimal ap (From Heberer and van Dongen 1993).
f If dissection involves the origin of a renal artery, there may be superimposition of the Doppler frequency spectra from the true and false lumina
or– depending on the re-entry site or the position of the sample volume in the dissected segment– to-and-fro ow as in the left renal artery
shown.
g The waveform from a segmental artery in the left renal hilum demonstrates the typical postocclusive ow pattern with a reduced systolic
upstroke and low PSV (25cm/s) due to ow obstruction by the dissection.
h The right renal artery is not involved in the dissection and has a typical monophasic waveform with a PSV of 1m/s. The further infrarenal course
of the aortic dissection is shown in longitudinal (right center) and transverse planes (rightmost). The change in color coding may be due to the
position of the re-entry site or physiologic ow reversal (early diastolic reux)

476
cd
Chapter 6 · Visceral andRetroperitoneal Vessels
True lumen
False
lumen
6
e
f
h
g
. Fig. 6.88 (continued)
. Fig. 6.89 (Atlas) Infrarenal
dissection.
Rare example of isolated infrarenal dissection with partial thrombosis. There is marked to-and-fro
ow at the entry site (systolic
inow and diastolic outow with
additional forward and backward
ow during diastole). A re-entry
site is not identiable. D indicates
the dissection membrane; the
true lumen (WL) is compressed;
and the false lumen (FL) is partially thrombosed

6.3 · Atlas: Visceral andRetroperitoneal Vessels
477
6
. Fig. 6.90a–g (Atlas) Aortic dissection.
a Blood ow to the renal arteries is a crucial issue in the diagnostic evaluation of aortic dissection. At the level of the renal arteries (left image),
both lumina of the dissected aorta exhibit antegrade ow, and the left renal artery (A.REN.LI) is displayed with blue-coded ow. The image on the
right obtained 5cm below clearly depicts the ap between the two lumina. The overall diameter is dilated to 42mm due to aneurysmal changes.
b CT scan of dissected aortic aneurysm with visualization of the intimal ap.
c The second important diagnostic task in aortic dissection is to determine the relationship to the origins of the iliac arteries. Here, the dilated and
dissected aorta with thrombotic wall deposits gives o the common iliac artery (A.I.C) on the right side, and the dissected aneurysm (A) extends
into the left common iliac artery. The gray-scale image (left) depicts the ap and the thrombotic portion, while the color duplex image (right)
shows the perfused lumina.
Aortic dissection after intervention.
d Aortic dissection as in the preceding example but with red-coded ow in the true lumen and blue-coded, retrograde ow in the false lumen.
The image on the left fails to depict the intimal ap about 3cm below the renal artery origins The image on the right demonstrates partial thrombosis of the false lumen just above the bifurcation. These ndings reect the status post surgery with closure of the thoracic entry.
e Following closure of the thoracic entry, the false lumen supplying the renal artery is lled retrogradely through the abdominal re-entry. The longitudinal image (right) demonstrates forward, red-coded ow in the true lumen and retrograde, blue ow in the false lumen (transducer moved to
the left side).
f Patency of the false lumen is maintained through the outow of blood into the left renal artery arising from it. The false lumen and the left renal
artery are depicted with ow coded in blue. The Doppler waveform shows decreased ow with a peak systolic velocity (PSV) of 60cm/s in the left
renal artery compared to the contralateral side.
g The true lumen (red) gives o the blue-coded right renal artery, which arises from the posterior aspect and has a PSV of 165cm/s and an enddiastolic velocity (EDV) of 45cm/s

478
Chapter 6 · Visceral andRetroperitoneal Vessels
6
. Fig. 6.91a–d (Atlas) Aortic perforation.
a Diagnostic evaluation of suspected perforation in the abdomen and pelvis may be impaired by a poor insonation window or the occurrence of
artifacts. Color duplex imaging is useful for demonstrating leakage, but the high susceptibility to artifacts in the abdomen makes it necessary to
always conrm the color ow ndings by spectral Doppler interrogation. In the example, color duplex imaging of a patient presenting with back
pain identies a leak in the posterior aortic wall with color-coded ow signals distal to it. Alternatively, these signals may represent mirror artifacts
caused by the strong reection of the aortic wall.
b The Doppler waveform (right) obtained from this area conrms the perforation by demonstrating to-and-fro ow (systolic inux with reux
throughout diastole), as it is also typical of pseudoaneurysm.
Dierential diagnosis: aortic perforation– lumbar artery.
c Posteroinferior to a 41-mm infrarenal abdominal aortic aneurysm (BAA) a hypoechoic area is depicted adjacent to the aortic bifurcation (dif-
ferential diagnosis: hematoma– retroperitoneal brosis– inammatory vascular disease). As in b above, color ow imaging depicts blood ow
signals coming out of the aorta (blue with sample volume) and passing the hypoechoic area. The Doppler waveform (right) shows the typical ow
pattern of a lumbar artery, thus ruling out contained aortic perforation with typical to-and-fro ow.
Mycotic aortic perforation.
d The transverse and longitudinal color ow images show ow coded in red posterior to the aorta (P in the longitudinal image). Part of the
escaped blood posterior to the aorta (A) is thrombosed and has low echogenicity. The Doppler waveform from the site of the leak (indicated by
D3in the transverse image) shows the characteristic to-and-fro ow of contained perforation (same as in pseudoaneurysm) with ow out of the
artery in systole (S) and back into the artery in diastole (D). The longitudinal CT reconstruction of the aorta shows the site of perforation (arrow)
in the distal aorta just above the bifurcation. The axial CT scan conrms the contained perforation (arrow) with perfused and thrombosed portions

6.3 · Atlas: Visceral andRetroperitoneal Vessels
479
6
. Fig. 6.92a–c (Atlas) Suture aneurysm after placement of a straight stent graft.
a Sonographic follow-up after aortic stent graft placement (e.g., for aneurysm) is indicated at 6-month intervals because an untreated suture aneurym,
in particular at the superior anastomosis (N.AN), can lead to duodenal perforation, a potentially life-threatening complication. The anastomoses are
evaluated in longitudinal and transverse planes for the presence of hypoechoic mushroom-like structures indicating a contained perforation or suture
aneurysm. Color duplex imaging shows paravascular ow at the anastomosis, and the Doppler waveform from this site shows the ow prole characteristic of a pseudoaneurysm.
b With progressive thrombosis, the color-coded area becomes smaller and the aneurysm is more dicult to dierentiate from other hypoechoic perivascular structures. In this setting, a suture aneurysm is suggested by a color-coded area extending beyond the wall directly next to the suture line (arrow).
c CT conrming the suture aneurysm with nearly complete thrombosis (2)
. Fig. 6.93a, b (Atlas) Suture aneurysm after placement of a straight stent graft.
a Patient with suture aneurysm after implantation of a straight stent graft. The B-mode image shows a large hypoechoic area at the level of the
renal artery origins with ow in the color duplex examination, consistent with a large retroperitoneal suture aneurysm. Doppler measurement in
this area allows good dierentiation of the suture aneurysm (NA) and renal artery (A.R).
b Unlike the waveform from the renal artery origin (A, see a), the Doppler waveform from the site of aortic leakage into the suture aneurysm
(arrow) shows to-and-fro ow

4806 Chapter 6 · Visceral andRetroperitoneal Vessels

6.3 · Atlas: Visceral andRetroperitoneal Vessels
481
. Fig. 6.95a–c (Atlas) Vena cava
a The cross-sectional area and ow velocity in the vena cava (V.C) vary with respiration. Blood ow is markedly faster during inspiration. In addition, blood ow is subject to cardiac (atrial) pulsatility. The Doppler waveform typically shows two peaks, one during systole and the other upon
opening of the atrioventricular valves (W-shaped waveform). There is marked reduction, cessation, or even a short reversal of ow during atrial
contraction.
b The usual oval cross section of the vena cava can show diameter variation due to changes in intravascular pressure during the respiratory cycle
(W-shaped waveform); in addition, there may be variation due to cardiac pulsatility, indicated by “<<CM” in the time-motion display (right).
Situs inversus.
c There are some extreme anatomic variants of the vena cava; these are rare and include absence, doubling with one vena cava on either side of
the aorta, and a single vena cava to the left of the aorta as in the case shown (here, in accordance with ultrasound convention, the left-lying vena
cava is displayed to the right of the aorta). In complete situs inversus, the liver is located in the left upper abdomen, and the portal vein (PV) also
ascends toward the liver hilum on the left side
6
. Fig. 6.94a–f (Atlas) Aortic thrombus (thrombolytic treatment)– aortic stenosis.
a 35-year-old woman presenting with very severe acute foot and calf pain due to bilateral occlusion of the below-knee arteries. For illustration,
the occlusion of the anterior tibial artery is shown in transverse orientation. The artery blocked by a hypoechoic thromboembolus exhibits no
ow, while there is ow coded in red in the paired anterior tibial vein (V) to the right and left of the artery. The acoustic shadow to the left of the
tibial vein is caused by the bula.
b In this case, embolic occlusion of the below-knee arteries is due to a thrombus in the distal aorta. The transverse image (left) depicts the thrombus 4cm above the bifurcation. It is attached to the wall posteriorly with ow being conned to its anterior aspect (blue with aliasing). The right
image depicts the hypoechoic thrombus in the aorta just above the bifurcation surrounded by ow with turbulent and high-frequency components on all sides.
c The longitudinal image shows the thrombus occupying most of the aortic lumen with some residual ow anteriorly. The Doppler waveform
demonstrates marked ow acceleration with an end-diastolic velocity (EDV) of 50cm/s and a peak systolic velocity (PSV) of 210cm/s (aliasing);
the waveform is monophasic. (Only the proximal segment of the aorta is depicted with color coding due to the small color box used.).
d On the basis of the duplex ultrasound ndings obtained in this patient, angiography of the aorta was dispensed with because the manipulations might have triggered further distal embolism. Instead, bilateral intra-arterial thrombolytic treatment was initiated, which led to resolution of
the thromboemboli in the below-knee arteries, as illustrated by the Doppler waveform from the recanalized anterior tibial artery. The waveform
still shows abnormally increased diastolic ow, which is due to residual stenosis of the aorta and reactive hyperemia.
e Local thrombolytic treatment also had a systemic eect, resulting in dissolution of the thrombus in the aorta. The transverse image (left) and
longitudinal image (right) still depict residual marginal thrombotic deposits. The color coding shows the patent lumen with aliasing (yellow– light
blue) due to residual stenosis. The Doppler waveform indicates high-grade residual stenosis with a PSV of 300cm/s and a monophasic ow prole.
f The patient refused further treatment. Follow-up 2weeks later demonstrated autolysis of the residual thrombus in the distal aorta. The longitudinal image (middle section) shows hyperechoic posterior plaque and some residual, hypoechoic thrombotic deposits on the left wall with little
luminal narrowing. Neither the Doppler waveform nor color duplex imaging demonstrates hemodynamically signicant stenosis

Chapter 6 · Visceral andRetroperitoneal Vessels
482
. Fig. 6.96a–c (Atlas) Right renal vein.
a Cardiac pulsatility and respiratory phasicity of blood ow are transmitted as far as the right renal vein at the hilum (vein: blue, segmental
artery:red).
Left renal vein.
6
b Cardiac pulsatility is typically lost in the left renal vein due to the narrow passage between the superior mesenteric artery and aorta. Instead,
its ow variation is determined by the aortic pulse. Posterior to the red-coded renal vein, the renal artery is depicted in blue. The renal vein has a
rather large caliber in front of the narrow passage and then continues as a relatively thin vessel (blue) to the vena cava.
Retroaortic left renal vein.
c If the left renal vein (V.R.L; red, ow toward transducer) is not identied between the aorta and superior mesenteric artery, the examiner must try
and locate its entry into the vena cava (V.C) posterior to the aorta (AO). Identication of a retroaortic left renal vein is important prior to resection
of an aortic aneurysm but is often an incidental nding, as in the case presented, where the atypical entry was identied in a patient in whom
vascular sonography was performed prior to ultrasound-guided biopsy of a lymphoma (L)
. Fig. 6.97 (Atlas) Normal and abnormal Doppler waveforms of hepatic veins.
a W-shaped Doppler waveform with a rst hepatofugal ow peak in systole, a second hepatofugal peak upon opening of the atrioventricular
valves, and hepatopedal ow during atrial contraction. An abnormal waveform resembling a sinus wave with to-and-fro ow in the extreme case
is seen in patients with right ventricular failure.
Abnormal waveform of hepatic veins in liver cirrhosis.
b The right hepatic vein in a patient with Child A liver cirrhosis scanned from the intercostal approach shows only residual cardiac pulsatility. The
associated loss of parenchymal elasticity primarily prevents the decrease in ow velocity during atrial contraction, resulting in an increasingly
band-like spectrum from the entry into the vena cava to peripheral branches (intermediate hepatic vein in blue, portal vein branch in red).
Waveform of hepatic vein in liver cirrhosis.
c Biphasic ow prole in the hepatic vein in a patient with liver cirrhosis (intercostal approach). Though the curve is attened due to stiening of
the liver, some residual cardiac pulsatility is still present, and the curve is not as at as in b (A, ascites) (same patient as in .
. Fig. 6.98a–c (Atlas) Portal vein and its tributaries.
a The Doppler waveform from the portal vein is characterized by relatively wide variation in ow velocity, but ow is typically hepatocentral and
slower during inspiration.
b The respiratory variation in blood ow velocity continues into the superior mesenteric vein, which is depicted to the right of the superior mesenteric artery.
c The splenic vein (V.L) is depicted at the lower edge of the pancreas with ow in red. It crosses over the root of the superior mesenteric artery
(A.M.S) to enter (displayed in blue) the portal vein (V.P). The respiratory variation in ow velocity may continue into the splenic vein
Fig.6.101 (Atlas))

6.3 · Atlas: Visceral andRetroperitoneal Vessels
483
. Fig. 6.99a, b (Atlas) Mesenteric vein thrombosis– surrounded by owing blood.
a The extent of thrombosis and collateralization determine whether the clinical manifestation will be mild with u-like symptoms or severe with
an acute abdomen due to intestinal necrosis. A 38-year-old patient with diuse abdominal pain was treated conservatively for several days.
Sonography was performed to rule out appendicitis and pancreatitis. Closer evaluation of the superior mesenteric vein by color duplex imaging revealed thrombosis of individual jejunal vein branches with protrusion of a thrombus into the trunk of the superior mesenteric vein. Mural
mesenteric vein thrombosis obstructs blood ow. Prompt initiation of full heparinization is necessary to prevent further appositional thrombus
growth and intestinal necrosis.
b Digital subtraction angiogram conrms partial mesenteric vein thrombosis
6
. Fig. 6.100a–d (Atlas) Superior mesenteric vein thrombosis.
a Complete thrombosis of the superior mesenteric vein (V.M.S) is indicated by the absence of ow signals despite a low pulse repetition frequency
(indicated by aliasing in the vena cava, V.C). The vena cava is depicted posterior to the superior mesenteric vein.
b The superior mesenteric artery (A.M.S, red) comes into view when the transducer is moved to the left side. There is aliasing in the aorta posteriorly (A). With this transducer position, the superior mesenteric artery appears deep to the conuence of the superior mesenteric vein (V.M.S) and
the splenic vein. Occluding thrombosis of the superior mesenteric vein aects ow in the artery, giving rise to a preocclusive thump pattern. Peak
systolic velocity (PSV) is markedly reduced (50cm/s) and, along with the loss of diastolic ow, suggests high outow resistance. Surprisingly, the
17-year-old woman had only mild diuse abdominal pain (of the enteritic type) and mild meteorism, but no signs of peritonitis; there was mild
leukocytosis without acidosis, and lactate levels were normal. The clinical symptoms persisted for 6weeks before the diagnosis was made. Preexisting portal vein thrombosis in an abnormal vein with severe ectasia led to the formation of collateral pathways, mainly via the inferior mesenteric vein, which is why acute mesenteric vein thrombosis did not cause intestinal necrosis in this patient.
c, d Portal vein thrombosis.
c In portal vein thrombosis, there is a marked compensatory increase in blood ow in the hepatic artery with a peak systolic velocity (PSV) of
approx. 2m/s and an end-diastolic velocity (EDV) of 90cm/s. The thrombosed portal vein (PV) is indicated by calipers.
d Good collateral drainage through small veins is conrmed by the depiction of ow in the hepatoduodenal ligament (continuous high-frequency
ow with a velocity of 50cm/s) and around the gallbladder

Chapter 6 · Visceral andRetroperitoneal Vessels
484
6
. Fig. 6.100 (continued)
. Fig. 6.101a–c (Atlas) Portal hypertension.
a Loss of respiratory diameter variation in gray-scale ultrasound is a sign of portal hypertension. In the example, the time-motion mode demonstrates a constant diameter of 14mm of the portal vein (PV).
b The patient presented has portal hypertension and Child C liver cirrhosis. The peak ow velocity is markedly reduced to 11.2cm/s with a mean
ow velocity of 8.4cm/s (intercostal transducer position). Other signs of liver cirrhosis depicted by ultrasound are perihepatic ascites (A) and the
enlarged caudate lobe (LC). The congestion index is markedly increased to 0.2cm×s.
c A reduced increase in postprandial ow velocity (mean ow velocity of 10.8cm/s) is another sign of portal hypertension. With an unchanged
diameter of 14mm, postprandial ow velocity increases by only 20% (versus >60% in normal individuals). For didactic purposes, views of the
portal vein from two transducer positions (c: subcostal; b: intercostal, from the ank) are shown with identical sample volumes in the vein. The
intercostal approach permits smaller Doppler angles (38° versus 67° in the example), thus yielding more accurate ow velocity measurements.
Serial examinations should be performed with identical transducer positions
. Fig. 6.102 (Atlas) Portal vein
aneurysm.
Gray-scale image (left, arrow) and
color duplex image (right) show a
portal vein aneurysm measuring
25mm in diameter; which is more
than 4 times the normal portal
vein (PV) diameter adjacent to
the aneurysm (VC, vena cava; M,
stomach; L, liver)
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