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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

Esophagus
gastric
Splenic artery origin
Weight loss, epigastric/abdominal pain
k
(demonstration of steal)
MAL division
6.1 · Abdominal Aorta, Visceral andRenal Arteries
Diaphragm
MAL
Color duplex ultrasound
415
6
T11
T12
L1
L2
Left renal artery origin
Left renal vein
Superior mesenteric artery
. Fig. 6.19 Topographic relationships between the median arcuate
ligament (MAL), aorta, celiac trunk, superior mesenteric artery, and
celiac ganglion. Mechanism of compression of the proximal celiac
trunk by the arcuate ligament (From Schwilden 1987)
Celiac
gangilon
Left
artery
Aorta
>70% stenosis (PSV >250 cm/s)
Fixed stenosis
in inspiration/expiration
Change eating habits
(several small meals)
No improvement
angiography
. Fig. 6.20 Diagnostic and therapeutic decision algorithm in median
arcuate ligament (MAL) syndrome
Intermittent stenosis
no steal
Celiac ganglion bloc
Median arcuate ligament division is indicated if a xed
stenosis is present, identied by a PSV exceeding 280cm/s
during both inspiration and expiration. Surgery is promising
and likely to eliminate the compression-related symptoms,
especially in patients in whom a steal eect has been demonstrated by duplex ultrasound or by mesentericography and
celiacography and in whom the clinical symptoms are due
to this eect (abdominal angina with epigastric and postprandial pain and weight loss) and not to compression of the
hypogastric plexus (pain).
Other possible causes such as atherosclerotic stenosis of
the mesenteric arteries, tumor compression, or chronic pancreatitis must be ruled out (
. Fig.6.20).
6.1.6.2.2 Visceral Artery Aneurysm
Aneurysms of the visceral arteries are rare and most commonly aect the splenic artery (see . Fig. 6.61 (Atlas)). A
ruptured visceral artery aneurysm is a life-threatening emergency. e risk of rupture increases exponentially with the
aneurysm diameter. Visceral aneurysm is congenital in rare
cases. Other underlying mechanisms include atherosclerosis,
trauma, mycosis, and inammation. Up to 5–10% of patients
with a many-year history of chronic pancreatitis develop a
visceral artery aneurysm as a complication of this condition.
Visceral artery aneurysms are oen detected incidentally
and occasionally cause nonspecic symptoms with upper
abdominal pain. ey are conspicuous on B-mode scans as
hypoechoic to anechoic round structures (see . Fig. 6.27).
. Fig. 6.21 Course of the hepatic artery in the hepatoduodenal liga-
ment. There is a small aneurysm (AN) with turbulent ow (diameter of
16mm)
Mural thrombosis is seen as echogenic layering. Aneurysms
are
dierentiated from tumors or pseudocysts of the pan-
creas by the demonstration of ow in the color ow mode
(. Fig.6.21 and . Fig.6.61 (Atlas)). However, a large, mostly
thrombosed aneurysm can be mistaken for a malignant
tumor. A hepatic artery aneurysm requires precise preoperative localization, which determines the surgical approach
(. Fig. 6.60 (Atlas)): an aneurysm of the common hepatic
artery proximal to the origin of the gastroduodenal artery
can be ligated without reconstruction because the liver will
be supplied with blood via the gastroduodenal artery, while
elimination of a more distal aneurysm (proper hepatic artery)
additionally requires vascular reconstruction. Surgery can be
planned on the basis of sonographic localization of the aneurysm and determination of its relationship to the origin of
the gastroduodenal artery.

()
()
Chapter 6 · Visceral andRetroperitoneal Vessels
416
6
. Fig. 6.22 Patient with approx. 50% stenosis of the superior mesenteric artery (A.M.S) with a peak systolic velocity (PSV) of 242cm/s (left
image and waveform) and >70% stenosis of the celiac trunk (T.C) with a PSV of 344cm/s (right image and waveform). The high diastolic ow in
this patient is due to a replaced right hepatic artery arising from the superior mesenteric artery (see . Fig.6.3b–d and . Figs.6.51 and 6.52 (both
Atlas)). Note that enhanced ow may also be seen when the examination is performed after eating and that Doppler angle correction is dicult in
the curved artery
6.1.6.2.3 Dissection
Dissections of the visceral arteries (see . Fig.6.88 (Atlas)),
and of the renal arteries, occur either as extensions of aortic
dissections (discussed in more detail in 7 Sect. 6.1.6.3.6) or as
iatrogenic complications of endovascular procedures (PTA).
e severity depends on the dissection membrane, ranging
from relatively asymptomatic cases to ischemic problems or
even vascular occlusion. A dissection membrane extending
from the aorta can be identied by color duplex ultrasound
only if insonation conditions are very good. However, in most
cases, there will be a characteristic abnormal ow signal due
to the oating membrane in the bloodstream (see . Fig.6.88
(Atlas)) and the dissection-related ow obstruction (which
may be static or dynamic).
6.1.6.2.4 Superior Mesenteric Artery
Hemodynamics and Measurement Technique
z
Because blood ow volumes and velocities in the mesenteric
artery vary widely with demand, it is essential to examine
patients in the fasting state in order to obtain standardized
measurements and reliable results when applying velocity
thresholds (. Fig.6.51 (Atlas)).
Mesenteric blood ow increases aer eating (widening of the
artery and increase in blood ow velocity) and is also aected
by other physiologic and disease states as well as by pharmacologic agents. Decreases in blood ow velocity and volume
are observed aer physical exertion and under the inuence
of vasopressin. An increase in mesenteric peak systolic velocity
(PSV) and blood ow volume can be observed aer glucagon
administration and in individuals with severe hyperthyroidism
or during acute episodes of inammatory bowel disease involving large segments of intestine (Derko 2001).
Quantication of mesenteric blood ow requires calculation of averaged ow velocity and precise measurement of
the vessel diameter. Diameter measurements in the superior
mesenteric artery by our group demonstrated variations of
approx. 10% between systole and diastole with ensuing dierences in the cross-sectional area of up to 35%. erefore, accurate blood ow measurement makes it necessary to measure
systolic and diastolic diameters separately and to calculate a
mean vessel diameter according to the following formula, representing the two diameters according to their relative weight:
Mean vessel diameter radius R
=´´+13 2
RRR
/
(
/
diastolicsystolic
For vessels up to 12mm in diameter, the diameter can be
measured most reliably using the leading-edge method (see
. Fig. 1.28) and scanning with a low transmit power. is
method results in slight overestimation of the diameter but,
for diameters of up to 10mm, the overestimation is smaller
than the underestimation that would result from using the
inner-wall-to-inner-wall method. Also, the method enables
systematization of the measurement error, which is important for serial measurements.
Color duplex imaging facilitates the identication of the
mesenteric and renal arteries. Once the target artery has
been brought into view, a Doppler waveform is obtained for
hemodynamic evaluation. Under good insonation conditions, color ow imaging will suggest a stenosis, but verication by spectral Doppler is necessary. Depending on the
clinical question to be answered, spectral Doppler tracings
should be sampled at the vessel origins, the preferred sites of
atherosclerotic stenosis of the visceral arteries.
Atherosclerotic stenosis of visceral branches usually
occurs at the origins from the aorta (. Fig.6.22). Involvement of the peripheral branches is only seen in diabetics
with generalized medial sclerosis. If there is high-grade atherosclerotic stenosis of only one of the three visceral artery
origins, compensatory dilatation of the preformed collateral
pathways will ensure adequate perfusion in most cases.

Common
Aorta
Celiac trunk
ry
pancreaticoduodenal
6.1 · Abdominal Aorta, Visceral andRenal Arteries
417
6
hepatic artery
Gastroduodenal
artery
Middle colic
artery
Inferior
artery
. Fig. 6.23 Diagram of collateral pathways in occlusion of the celiac
trunk and/or superior mesenteric artery: the Riolan anastomosis
(dashed lines) between the superior mesenteric artery and the middle
colic artery is the main collateral pathway in superior mesenteric artery
occlusion. Collaterals between the celiac trunk and superior mesenteric
artery include the pancreaticoduodenal artery and the gastroduodenal
artery, which joins the hepatic artery
Splenic artery
Superior mesenteric artery
Inferior mesenteric arte
Left colic artery
In general, chronic intestinal ischemia manifests as
abdominal angina only if there is occlusion or stenosis of
more than one visceral artery or in case of poor collateralization. e typical symptom is postprandial pain. Calcied
plaques suggest a stenosis in the B-mode image, but denitive evidence is provided only by ow acceleration with turbulence or the absence of ow signals in case of occlusion.
Chronic mesenteric artery occlusion is due to athero-
sclerosis and is associated with extensive collateralization
through the celiac trunk (primarily involving the pancreaticoduodenal artery) and the inferior mesenteric artery
(Riolan anastomosis; . Fig.6.23). While the main collaterals
(gastroduodenal, splenic, and inferior mesenteric arteries)
are oen detectable by ultrasound (
. Figs. 6.58b,c (Atlas)
and 6.23), angiography provides a better overview and overall picture of collateral pathways. Specically, the dilated gastroduodenal artery is visualized by duplex ultrasound at the
pancreatic head. Ultrasound evaluation is facilitated by the
fact that patients with chronic mesenteric ischemia tend to
be thin because they suer from abdominal angina (abdominal pain aer eating). e superior mesenteric artery is lled
distally and shows postocclusive ow with a delayed and
reduced systolic rise and a decreased Pourcelot index (see
. Fig.6.58 (Atlas)).
Color Duplex Ultrasound Grading
z
of Mesenteric Artery Stenosis
Several studies, mostly in small series, report good results for
color duplex ultrasound (CDUS) in the detection of hemodynamically relevant mesenteric artery stenosis in patients
presenting with abdominal angina. While investigators consistently describe good sonographic evaluability of the mesenteric artery trunk and especially of the superior mesenteric
artery origin, there is disagreement regarding the best velocity
parameter (peak systolic velocity (PSV) versus end-diastolic
velocity (EDV)) and optimal cuto values (
. Table 6.7).
Some authors advocate PSV as the most suitable parameters
for mesenteric stenosis grading (Moneta etal. 1991; Bowersox etal. 1991; AbuRahma etal. 2012; Mitchell etal. 2009),
while others opt for EDV (Zwolak 1999; Perko etal. 1997).
PSV is well known to be inuenced by a variety of factors
including systolic blood pressure during the examination,
. Table 6.7 Sensitivity, specicity, positive predictive value (PPV), negative predictive value (NPV), and overall accuracy (OA) of duplex ultra-
sound in the diagnosis of stenosis at the origin of the mesenteric artery. Results obtained with dierent cutos for peak systolic velocity (PSV),
end-diastolic velocity (EDV), and PSV ratio. Cutos were identied using ROC curve analysis with angiography as the standard of reference
Parameter (study) (cuto) Sensitivity Specicity PPV NPV OA
PSV
≥70% stenosis (Moneta 1993) (PSV ≥275cm/s) 92% 59% 56% 93% 71%
≥50% stenosis (Bowersox 1991) (PSV ≥300cm/s) 86% 89% 91% 83% 87%
>50% stenosis (Perko 1997) (PSV >275cm/s) 93% 80%
>50% stenosis (AbuRahma 2012) (PSV >295cm/s) 87% 89% 90% 84% 88%
>70% stenosis (AbuRahma 2012) (PSV >400cm/s) 72% 93% 81% 85% 85%
EDV
≥50% stenosis (Zwolak 1998) (EDV ≥45cm/s) 79% 79% 84% 72% 79%
≥50% stenosis (Perko 2001) (EDV ≥70cm/s) 47% 98% 97% 57% 68%
>50% stenosis (AbuRahma 2012) (EDV >45cm/s) 79% 79% 82% 69% 79%
>70% stenosis (AbuRahma 2012) (EDV >70cm/s) 65% 95% 86% 81% 84%
PSV ratio (superior mesenteric artery origin/aorta)
>50% stenosis (AbuRahma 2012) (PSV ratio>3.5) 69% 78% 79% 68% 73%
>70% stenosis (AbuRahma 2012) (PSV ratio>4.5cm/s) 67% 83% 65% 84% 78%

418
Chapter 6 · Visceral andRetroperitoneal Vessels
sympathetic tone, medications, and time since last meal.
Even the respiratory phase appears to play a role, as some
authors found a higher PSV during expiration (van Petersen
etal. 2013; Seidl et al. 2010). is observation may be due
intrastenotic PSV >300cm/s. is PSV appears rather low,
and most asymptomatic patients with in-stent restenosis
do not need a reintervention as long as intrastenotic PSV
remains below 400cm/s.
to transient compression of the artery by the diaphragmatic
crura (mild form of median arcuate ligament syndrome). A
pitfall to be considered is that the proximal superior mesenteric artery segment may be more arched during expiration,
leading to errors in setting the Doppler angle (see . Fig.6.55
(Atlas)).
To account for systemic factors aecting absolute PSV,
some authors explored a PSV ratio calculated from intrastenotic PSV at the superior mesenteric artery origin and PSV
6
in the aorta. However, AbuRahma etal. (2012) found poorer
accuracies on the order of 70–80% using a PSV ratio>3.5 as a
cuto for identifying >50% stenosis and a ratio>4.5 for >70%
stenosis compared with absolute PSV thresholds.
Another alternative velocity parameter, the EDV, also
failed to improve accuracies (AbuRahma etal. 2012). EDV
is inuenced by even more additional factors than PSV
(inammatory bowel disease, heart rate). Anatomic variants also aect EDV.Of note, EDV is higher when the right
hepatic artery arises from the superior mesenteric artery.
Errors in Doppler angle correction can cause errors
in both PSV and EDV measurement. Aligning the angle
correction cursor with the direction of blood ow is difcult when the proximal superior mesenteric artery takes
an arched course. With downward movement of the diaphragm during inspiration, the bowel pulls down the
mesenteric root, straightening the mesenteric artery and
improving adjustment of the Doppler angle (see . Fig.6.55
(Atlas)).
e author’s practical experience suggests that a PSV cuto of 280cm/s for >50% stenosis and of 350cm/s for >70%
provides adequate accuracies in the clinical setting. e
relatively low sensitivity of 74% in conjunction with a high
specicity of 93%, which AbuRaham etal. (2012) identied
when using a PSV cuto of 4m/s for identifying 70% stenosis
(. Table6.7), indicates that this cuto is slightly too high. It
should also be noted that identication of 50% mesenteric
stenosis is of little clinical relevance. Abdominal angina is
caused by higher-grade stenosis, and because of good collateralization in this territory, steno-occlusive disease becomes
relevant only when several arteries are aected (celiac trunk,
inferior mesenteric artery). Finally, angiographic evaluation
of the mesenteric artery origin in two planes is also technically challenging.
A stent alters hemodynamic parameters, and higher
velocity thresholds should be used when evaluating
restenosis
. A stent reduces wall elasticity and the lumen
in-stent
of the artery, resulting in more pulsatile blood ow and a
higher PSV. AbuRahma etal. (2012) propose a 20–30cm/s
higher velocity cuto for stented mesenteric arteries, corresponding to a 10% higher PSV compared with stenosis in
the native arteries (. Fig.6.24a). Armstrong (2007) recommends angiography with reintervention in patients with an
EDV of 50–70cm/s or a poststenotic PSV <40cm/s and an
6.1.6.2.5 Acute Mesenteric Artery Occlusion
Acute mesenteric occlusion due to embolism is easily and
reliably demonstrated by (color) duplex imaging as the
absence of ow if the occlusion is located near the origin of
the mesenteric artery from the aorta. Peripheral mesenteric
artery occlusions, on the other hand, pose a diagnostic problem. If there is extensive infarction of the small intestine but
the mesenteric artery trunk is patent, the embolus is typically
lodged at the divisions into jejunal branches or further distally at the origins of the ileocolic and right colic arteries. If
there are patent branches such as the middle colic artery or
proximal segments of the jejunal branches, the trunk of the
mesenteric artery is patent as well. e overall reduction in
blood ow and peripheral dilatation in the territory of the
patent branches, which provide collateral ow via the arcades,
is reected in the corresponding spectral Doppler waveforms
(
. Fig.6.25; see . Figs.6.56 (Atlas) and 6.57 (Atlas)). Peak
systolic velocity (PSV) is reduced, and the lower peripheral
resistance results in a larger diastolic component and a lower
Pourcelot index.
e waveform changes become more conspicuous with
the number of occluded branches, which in turn increases
the more proximal an embolus is located (see . Fig. 6.57
(Atlas)). Consequently, these spectral Doppler changes in
conjunction with the above-described decreases in the Pourcelot index and PSV should prompt a careful evaluation of
the individual mesenteric branches distally in longitudinal and transverse planes using color duplex ultrasound to
identify ow (. Fig. 6.26). e Doppler waveform changes
are less marked when the mesenteric artery is occluded more
distally (e.g., aecting only a few jejunal branches). However,
the number of vessels involved has little clinical relevance
and does not aect the patient’s prognosis because the loss
is compensated for by collateral ow through the patent
branches and the arcades.
In the abdomen,
color duplex ultrasound usually pro-
vides adequate resolution for evaluation of blood ow in
the mesenteric artery trunk including its peripheral segment and the origins of the jejunal branches arising from
it (. Figs.6.26 and 6.57 (Atlas)). However, the sonographic
detection of individual jejunal branch occlusions is of no
therapeutic consequence. e foremost aim is the timely
detection of mesenteric artery occlusion and surgical restoration of blood ow before ischemia causes extensive necrosis
of the small bowel. For this, it is sucient that the mesenteric
artery trunk can be evaluated for ow from its origin to the
umbilical level. When required, ultrasound of the mesenteric artery should include the origins of jejunal branches
(. Fig.6.26). Nonocclusive mesenteric ischemia (NOMI) is
not detectable by duplex ultrasound; however, other imaging modalities such as CTA or angiography do not consistently detect NOMI either. NOMI oen leads to necrosis and

6.1 · Abdominal Aorta, Visceral andRenal Arteries
419
6
. Fig. 6.24 a High-grade superior mesenteric artery in-stent restenosis with a peak systolic velocity (PSV) of 580cm/s in a patient with a history
of right-sided hemicolectomy for ischemic perforation (same patient as in . Fig.6.13). b There is concomitant celiac trunk occlusion, and the liver
is supplied via the splenic artery, which shows reversed ow, i.e., ow toward the hepatic artery (red, toward transducer). The waveform from the
splenic artery (A.L) shows little pulsatility. The splenic artery is supplied by small dilated arteries coursing from the pancreatic tail to the mesentery
of the transverse colon. These arteries, in turn, are supplied by branches of the inferior mesenteric artery. The patient refused reintervention. c One
year later, the patient presented with intestinal ischemia and occlusion of the stented superior mesenteric artery. The distal superior mesenteric
artery is supplied via pancreaticoduodenal collaterals. The splenic artery (with regrograde ow) now supplies not only the liver but also the distal
superior mesenteric artery (see . Fig.6.23). In conjunction with the patient’s clinical presentation, these ultrasound ndings prompted immediate endovascular reintervention
resection of aected bowel segments regardless of the time
elapsed between symptom onset and surgery.
e role of ultrasound is conrmed by the author’s expe-
rience in 101 consecutive patients seen from 1997 through
2004. ese patients had a high clinical suspicion of mesenteric artery occlusion and a history of characteristic pain of
less than 24-h duration. Suspected mesenteric artery occlusion was conrmed by duplex ultrasound using the abovedescribed criteria in 19 patients (19%), who proceeded to
surgical embolectomy based on the sonographic ndings.
e sonographic ndings were conrmed intraoperatively.
Nine of the patients operated on had occlusion of the peripheral mesenteric artery trunk only. Another four patients
(4%) had NOMI due to obstruction of peripheral segments,
which did not cause spectral waveform changes and was not
detected by duplex ultrasound. In most of these cases, only
a short intestinal segment had to be removed. In 62 patients
(61%), ultrasound ruled out acute embolic mesenteric occlusion, and the ndings were conrmed by the further clinical
course or during surgery performed for other causes of acute
abdomen. In 16 of the 101 patients (16%), angiography or
CTA was performed because of poor insonation conditions
or inconclusive spectral Doppler ndings.
e results of Danse etal. (1996) conrm the ability of
Doppler sonography to diagnose acute mesenteric artery
occlusion. In this study of 770 patients with emergency
admissions for acute abdominal pain, ultrasound correctly
diagnosed superior mesenteric artery occlusion in 5 cases.
e author of another, rather general overview (Cappell
1998) describes ultrasound as a nonstandard diagnostic test
in acute mesenteric ischemia, though without providing
sound scientic evidence for this conclusion.
B-mode imaging features can also provide clues in patients
presenting with acute intestinal ischemia. Rapid development

420
Vasa recta Occlusion of 2nd and 3rd order branches
ab
cd
Chapter 6 · Visceral andRetroperitoneal Vessels
. Fig. 6.25a–d Acute mes-
enteric artery occlusion. The
extent of intestinal necrosis
varies with the level of occlusion.
Occlusion of individual jejunal
branches only will not lead to
acute intestinal ischemia as the
arcades ensure collateral ow
from patent jejunal branches
(d).The vasa recta are involved in
nonocclusive intestinal ischemia
(c). Proximal occlusions in which
the mesenteric trunk is still patent are associated with necrosis
of long intestinal segments and
6
have a poor prognosis. The Doppler waveform from the patent
mesenteric artery shows abnormal changes (a, b). The remaining
patent branches dilate to provide
maximum blood supply via the
arcades, resulting in less pulsatile,
low-resistance ow. Nevertheless,
overall ow through the patent
mesenteric trunk is reduced
(decreased PSV)
Main trunk
Ileocolic artery/part of main trunk
of intestinal wall edema is identied by the so-called bull’s
eye sign. e further course is characterized by intestinal wall
necrosis and cessation of peristalsis along with further intestinal wall thickening and the appearance of free uid around
aected bowel loops. In the late phase, air bubbles appear in
the intestinal wall and portal vein (Seitz and Rettenmaier 1994).
Ischemic bowel wall changes detected with B-mode
ultrasound and unenhanced CT (Gebhardt etal. 1989; Danse
etal. 1996, 2009) typically indicate irreversible damage, and
no therapeutic measures can salvage the aected bowel segments. Nevertheless, color duplex ultrasound evaluation of
intestinal wall thickening in acute abdomen may be helpful
in that detection of ow signals near the wall rules out ischemia as the underlying cause.
When ultrasound identies thickened bowel loops and
ischemia is a possible dierential diagnosis, a high-resolution ultrasound transducer can be used to search for ow
signals in the bowel wall or in the adjacent mesentery (high
gain without artifacts and low PRF). Flow detected by color
duplex imaging should then be conrmed by obtaining a
Doppler waveform from this area. Conrmation of ow
rules out ischemia as the underlying cause, and a large diastolic ow component in the Doppler waveform points to an
inammatory cause (see
A contrast-enhanced ultrasound (CEUS) examina-
tion
can also contribute useful information in patients with
suspected mesenteric ischemia. Studies report sensitivities,
specicities, PPV, and NPV of 94%, 100%, 100%, and 97%
. Fig.6.59 (Atlas)).

branches
6.1 · Abdominal Aorta, Visceral andRenal Arteries
Middle colic artery
Pancreaticoduodenal
artery
Right colic artery
Jejunal
Ileocolic
artery
. Fig. 6.26 Divisions of the superior mesenteric artery with side
branches. Under good conditions, color duplex imaging visualizes the
main trunk, the division into jejunal branches, the right colic artery,
and ileocolic artery (visible area outlined) (According to Kubale 1994)
(Hamada et al. 2007) and of 85%, 100%, 100%, and 91%
(Hata etal. 2005). However, in these studies, the authors did
not investigate the mesenteric artery trunk but searched for
enhancing ow (or absence of owing blood) in the bowel
wall of segments showing morphogic abnormalities on
B-mode imaging (widening or wall thickening). CEUS is
more time-consuming, and a literature search identied only
one case report that describes the diagnosis of mesenteric
artery trunk occlusion based on the use of ultrasound microbubbles (Giannetti etal. 2010).
It follows from the above that color duplex ultrasound is
not the generally recommended rst-line diagnostic imaging test, as it has several limitations including its examiner
dependence, the reliance on good insonation conditions, and
incomplete evaluability of the mesenteric territory. However,
when performed by an experienced examiner with good
methodological skills and use of adequate instruments settings, color duplex is a very time-ecient and accurate tool
for identifying those forms of early acute mesenteric artery
occlusion that are amenable to treatment in emergency
patients. An ultrasound examination is routinely performed
in patients presenting with abdominal pain, and supplementing this examination by a color duplex evaluation of the
mesenteric artery trunk requires little extra time (<5min).
When color duplex yields a condent diagnosis, treatment
can be initiated, while inconclusive ndings need to be conrmed by CTA.
Insonation conditions are inadequate in the late phase of
acute mesenteric artery occlusion, due to overlying air, pain,
421
and poor patient compliance. At this stage, the indication for
surgery is established on clinical grounds (but the prognosis
is poor), and the sonographic ndings are of little relevance.
Conversely, in the earlier phase, when the clinical presentation alone would not necessarily justify emergency surgery
(see
. Table6.3), the insonation conditions in most patients
allow adequate sonographic evaluation of the mesenteric
artery trunk and its proximal divisions.
e resistive index (Pourcelot index) in the superior
mesenteric artery is also decreased in patients with abdominal conditions associated with peritonitis or in patients
with septicemia. However, in these patients, the RI is not
required as a diagnostic marker, and the indication for
surgery is established on clinical grounds or on the basis
of additional diagnostic tests (B-mode ultrasound or other
imaging modalities). e Doppler waveform in septicemia
or peritonitis diers from that obtained in patients with distal mesenteric artery occlusion in that, while the diastolic
component is increased, the PSV is still rather high and
close to normal (while it is decreased in mesenteric artery
occlusion).
Indirect sonographic criteria cannot be quantied and,
if present, should prompt further diagnostic testing (angiography) or, if warranted in conjunction with the clinical
presentation, laparotomy. Hypotension and tachycardia, as
in septic shock, or generalized peritonitis also cause marked
hemodynamic changes, resulting in abnormal Doppler
waveforms. us, the spectral waveform from the mesenteric artery must always be interpreted in conjunction with
the clinical presentation. However, the combination of a
lower Pourcelot index with decreases in PSV and averaged
blood ow velocities, demonstrated by spectral Doppler
interrogation of the proximal superior mesenteric artery,
always indicates peripheral occlusion of several mesenteric
branches.
e duplex ultrasound ndings in steno-occlusive disease of the superior mesenteric artery can be summarized
as follows:
5 Stenosis:
5 PSV >250–280cm/s (fasting)
5 Proximal occlusion:
5 Absence of ow signals at the origin of the superior
mesenteric artery
5 Distal occlusion:
5 Absence of ow in distal mesenteric artery trunk or
occluded mesenteric branch (on condition that
insonation conditions are adequate)
5 Indirect evidence from proximal Doppler interroga-
tion:
Ȥ Decrease in PSV when hemodynamically relevant
ow obstruction is present distally
Ȥ Reduced RI
Ȥ ump pattern immediately upstream of occlusion
e resistive index (RI), derived by spectral Doppler analysis,
in the superior mesenteric artery is decreased or increased
in the following physiologic and pathologic situations.
6

422
Chapter 6 · Visceral andRetroperitoneal Vessels
. Fig. 6.27 Small aneurysm (<AN; arrow) with a diameter of 2.2cm of the superior mesenteric artery (A.MES.S). The ndings are presented in
transverse and longitudinal views in the gray-scale mode on the left and in the color ow mode on the right. In addition, there is aortic dissection
6
(A) with the dissection membrane (<D) visualized in the transverse gray-scale and color images. The corresponding axial abdominal CT image
(rightmost) shows the mesenteric aneurysm (arrow) with a diameter of 2cm and the aortic dissection with the dissection membrane to the left of
the aneurysm
5 Lower RI (Pourcelot index; . Fig.1.28c) with absolute or
relative increase in diastolic ow component:
5 With increase in averaged ow velocity:
Ȥ Postprandial
Ȥ Medication-induced
Ȥ Inammatory
Ȥ Tumor-related
Ȥ Replaced hepatic artery (or the branch supplying
the right liver) arising from the superior mesenteric
artery (
. Fig.6.3e)
5 With decrease in averaged ow velocity:
Ȥ Distal mesenteric artery occlusion (widening of
arteries recruited as collaterals)
5 Higher RI with absolute or relative decrease in diastolic
ow component:
5 Diabetes mellitus (medial sclerosis)
5 Acute severe mesenteric vein thrombosis.
In individuals with an abberrant hepatic artery arising
from the superior mesenteric artery, the Doppler waveform
obtained upstream of the origin will show a large diastolic
component with a decrease in RI, because the ow pattern
in this case is aected by the supply of a parenchymal organ.
is must be borne in mind in interpreting the Doppler
waveform (see . Fig.6.52 (Atlas)).
Nonocclusive intestinal ischemia (NOMI) has a poor
prognosis and frequently occurs in patients with considerable
comorbidity. e examiner must be aware of this condition as
a dierential diagnosis of proximal mesenteric occlusion.
Circulatory insuciency, sepsis, and diabetes mellitus play a
role in the development of NOMI.Ultrasonography has no
role in the diagnosis since only the smaller, distal mesenteric
branches are aected, while the superior mesenteric artery
and the proximal segments of the main branches are patent.
e diagnosis is conrmed angiographically before therapy
with intra-arterial vasodilators is initiated.
An increased pulsatility of the mesenteric artery may be
due to reduced wall elasticity in diabetes mellitus or indicate
disturbed peripheral venous drainage, as in extensive mesenteric vein thrombosis.
diagnostic value of color duplex ultrasound in
e
evaluating infarction of the liver, spleen, or kidneys
due to
acute peripheral artery occlusion depends on the insonation
conditions. e extent of infarction varies with the site
of occlusion and blood supply through collateral routes.
B-mode ultrasound shows poorly delineated, inhomogeneous, and hypoechoic areas, but not earlier than 1–3days
aer the acute event (Seitz and Rettenmaier 1994). ere are
some case reports describing the use of color duplex imaging
in patients with renal or splenic infarction, but ultrasound is
most benecial in guiding interventional procedures such as
abscess drainage in superinfection of necrotic areas.
Aneurysms of the visceral arteries are very uncommon
but may present as emergencies when they rupture. ey are
typically detected incidentally in patients undergoing B-mode
ultrasound for diagnostic workup of abdominal symptoms
(which may be due to aneurysm-related pressure). ey are
dierentiated from pseudocysts or other cystic tumorous
lesions of the upper abdomen by their characteristic color
duplex appearance. Locating the aneurysm to the splenic,
superior mesenteric, or hepatic artery is important for planning the surgical procedure (see . Fig.6.61 (Atlas)). As with
all other vascular territories, the diagnostic evaluation of
aneurysms is the domain of color duplex ultrasound: the exibility in choosing the orientation of the scan plane enables
reliable diameter measurement, identication of thrombotic
wall deposits, and assessment of the patent residual lumen.
Aneurysm of the superior mesenteric artery is rare
(. Fig. 6.27). Even less common are aneurysms of the gastroduodenal, pancreaticoduodenal, and inferior mesenteric
arteries. ey are typically mycotic aneurysms (staphylococci, salmonellae). Sonographically, they are located and
measured as in other vascular territories. In planning the surgical procedure, it is crucial that their course and relationship
to other vessels be determined exactly. Visceral aneurysms
appear to be more common in patients with aberrant arteries.
6.1.6.3 Aorta
6.1.6.3.1 Aortic Stenosis andThrombosis
Bilateral intermittent claudication may be caused by stenosis
of the distal aorta. erefore, the aorta should be evaluated
if the Doppler waveform from the iliac artery shows poststenotic changes. High-grade stenosis of the abdominal aorta

6.1 · Abdominal Aorta, Visceral andRenal Arteries
423
6
is indicated in the color duplex scan by a mosaic pattern
resulting from perivascular vibration, as in an arteriovenous
stula. Severe atherosclerosis with calcied plaques impairs
the detection of the stenosis jet in the duplex mode. On the
other hand, extensive plaque with acoustic shadowing and
poor delineation of the lumen in the B-mode scan oen suggests high-grade stenosis of the aorta. e Doppler waveform
sampled distal to the high-grade stenosis will show the typical postocclusive ow prole with a delayed systolic rise and
large diastolic component.
Abdominal aortic stenosis occurs chiey in the distal
infrarenal segment including the bifurcation
ting, collateral supply with relling of the iliac territory is
mainly ensured by the inferior mesenteric artery, which will
become dilated and show high peak systolic velocities (PSV)
(oen >200cm/s) and end-diastolic velocities (EDV).
In acute occlusion of the distal aorta (Leriche’s syndrome),
the lumen is discriminated in the B-mode image by virtue of
its being lled with hypoechoic material. If the occlusion is
due to atherosclerosis, on the other hand, the aorta is difcult to dierentiate from surrounding tissue. Flow is absent
in both cases. In patients with poor visualization, chronic
occlusion can be dierentiated from high-grade stenosis by
the absence of the mosaic pattern, caused by perivascular
vibration, that is typical of stenosis.
rombosis of the aorta is visualized as a hypoechoic
cone-like structure in the lumen. e tail of the thrombus is
typically surrounded by owing blood on all sides. Signs of
luminal narrowing are seen on duplex scanning only when
there is nearly complete occlusion. Most patients with aortic
thrombosis present with embolism, oen in both legs. Demonstration of ow around the hypoechoic thrombus on color
ow images dierentiates aortic thrombosis from an embolizing aneurysm (see
6.1.6.3.2 Abdominal Aortic Aneurysm
B-mode ultrasound (real-time gray-scale imaging) is the
screening method of rst choice for abdominal aortic aneurysm (AAA). e reported diagnostic accuracy approaches
100% (Beales et al. 2011; Hartshorne etal. 2011; Lindholt
etal. 1999; Vidakovic etal. 2007; Mastracci and Cinà 2007;
anos etal. 2008). To determine the true maximum diameter of the aneurysm, the largest transverse extension is
identied to then rotate the transducer for measurement
perpendicular to the vascular axis. Other important diagnostic features include the aneruysm shape, its topographic
relationship to the renal artery origins, and possible iliac
artery involvement. e therapeutically relevant
tures to be evaluated by color duplex
as follows:
5 Maximum AAA diameter (to establish surgical indica-
tion)
5 Shape (saccular, spindle-shaped)
5 Partial thrombosis
5 Involvement of (common, internal) iliac arteries
5 Infrarenal– suprarenal
5 Other relevant features if endovascular repair is
contemplated:
. Fig.6.94 (Atlas)).
can be summarized
. In this set-
AAA fea-
5 Distance from renal artery origins
5 Degree of angulation of elongated infrarenal aorta and
possible iliac artery elongation
5 Conically shaped aneurysm neck
Color duplex ultrasound is only required to evaluate the
patent lumen and dierentiate it from mural thrombi and to
obtain additional information in the dierentiation of rare
vascular conditions such as inammatory AAA and aortitis
(giant cell arteritis). However, the color ow information
may facilitate evaluation of the topographic relationship to
the renal artery origins and possible extension of a very long
AAA aneurysm to the internal iliac artery origin.
Compared with angiography, which only depicts the residual lumen of an aneurysm, ultrasound provides much more
detailed information regarding localization and extent as well
as dierentiation of thrombosed and patent portions. And the
exibility of ultrasound in selecting the scanning plane relative to the course of the abdominal aorta facilitates measurement of the
that use standardized axial sections may overestimate aneurysm size when the section in which the diameter is measured
corresponds to an oblique (elliptical) plane through the aneurysm (. Fig.6.30). is pitfall is attributable to concomitant
elongation of the distal abdominal aorta, which is common in
patients with atherosclerotic AAA (see . Figs.6.29 and 6.31).
AAA is a rare source of embolism. ese aneurysms and
aortic aneurysms with a very saccular shape require surgical
management irrespective of their size. Saccular aneurysms
tend to exhibit turbulent ow on color duplex imaging,
while laminar ow is more likely in smaller, spindle-shaped
aneurysms. e local pressure peaks occurring in turbulent
ow are associated with more rapid growth and a higher risk
of rupture. In the sonographic evaluation of patients with
embolic occlusion of the leg arteries, thrombi in an aortic
aneurysm should be ruled out as a source of embolism (see
. Fig.6.74 (Atlas)).
In inammatory AAA, concentric wall thickening is
sonographically distinct from owing blood in the patent
lumen and, in patients with concomitant atherosclerotic
lesions of the intima, also from thrombus in the aneurysm
sac. In patients with inammatory AAA, wall thickening
tends to be conned to the aneurysmally dilated segment.
Conversely, wall thickening in giant cell arteritis also
involves the proximal abdominal aorta (and may be associated with concomitant aortic widening) (see
6.1.6.3.3 Specic Aspects oftheUltrasound
true aneurysm diameter. Imaging modalities
. Fig.6.38).
Examination inAbdominal Aortic
Aneurysm
Diameter Variation Through the Cardiac Cycle and
z
Eect of Measurement Method
Exact sonographic measurement of the maximum diameter
of the abdominal aorta is essential for identifying patients
whose abdominal aortic aneurysm (AAA) should be operated on and for obtaining reliable serial measurements of
AAA diameter in patients assigned to surveillance programs
or undergoing follow-up aer treatment. In addition, AAA

424
Chapter 6 · Visceral andRetroperitoneal Vessels
6
. Fig. 6.29 Measurement of abdominal aortic aneurysm (AAA)
diameter in a patient with elongation of the aorta and deviation to the
left. Measurement in the transverse abdominal view (right image, see
. Fig. 6.28 Diameter variation of the abdominal aorta during the
cardiac cycle in the time-motion mode. This mode systematically
captures the full diameter range from 48mm during systole to 44m
during diastole. In contrast, a single B-mode image (left) captures the
diameter at a single point in time. In this example, the B-mode image
incidentally shows the diameter during systole, which is 48mm (measured using the leading-edge method)
diameter is an important parameter in assessing the interobserver variability of ultrasound measurement and in comparing ultrasound with computed tomography (CT) or other
imaging modalities. No standard exists for ultrasound- or
CT-based aortic diameter measurement, and discrepancies
resulting from the use of dierent methods are oen ignored
in the context of scientic investions (Long etal. 2012; Beales
etal. 2011; Chiu etal. 2014).
ere are several pitfalls the examiner should avoid. First,
there is variation in the diameter of the normal aorta and of
AAA during the cardiac cycle, resulting in a diameter dierence
of 1.5–4.3mm from systole to diastole (. Fig.6.28) (Schäberle
etal. 2014). In a small series of 30 patients with AAA analyzed
by the author, the mean diameter variation through the cardiac
cycle was 2.8mm with diameters ranging from 3.6–7.6cm. is
issue is hardly ever addressed in sonographic studies (Grondal
etal. 2012), and it simply cannot be considered due to inherent
methodological limitations in static CT-based aortic diameter
measurement (Chiu et al. 2014). Aortic diameter variation
through the cardiac cycle explains some of the dierences in
serial measurements and in studies comparing dierent methods. ECG-gated ultrasound diameter measurement has been
proposed to reduce variability and overcome this limitation
(Bredahl etal. 2013); however, it is not feasible in clinical practice or in the setting of screening programs.
Another source of variability in sonographic aortic diameter measurement is whether the inner or outer wall reection
is used for measurement (see . Fig.1.28; Chiu et al. 2014).
Investigators tend to uncriticially compare data from studies measuring the outer-to-outer-edge diameter (Ellis etal.
1991; Pleumeekers etal. 1998; Hartshorne etal. 2011) with
results based on inner-to-inner-edge measurement (Lanne
etal. 1997). While these sonographic methods were found to
body marker) yields a diameter of 62.2mm (D3). In contrast, measurement perpendicular to the longitudinal vessel axis after rotation of the
transducer at the same level (left image) yields a diameter of 51.8mm
(D1). This is the orthogonal aneurysm diameter and reects the true
diameter. The anteroposterior (AP) diameter is the same in both views
(50.5mm (D2) and 51mm (D4))
have good inter- and intraobserver agreement, the inner-edge
method underestimated the diameter by an average of 4mm
compared with the outer-edge method (Chiu etal. 2014).
Measurement series in other vascular territories and in
ultrasound phantoms show that the leading-edge method
(see
. Figs. 1.28 and 6.28) yields the most reliable results
because it avoids or systematizes errors resulting from
blooming at interfaces between tissues with large dierences
in acoustic impedance such as the vessel wall (Schäberle
2009). With the leading-edge method, the vessel diameter is
measured from the bright reection of the outer wall close
to the transducer to the inner wall reection of the opposite
wall (see . Fig. 1.28).
Taken together, these limitations can result in a total
variability in AAA diameter measurements of 5–6mm. is
variation is not harmful in initial screening but becomes
relevant in patients with borderline AAA size and patients
undergoing regular surveillance for AAA (where a size
increase of 5mm over 6months is generally considered to
be an indication for surgery). ese issues are also relevant
when AAA size is measured using CT and should be borne
in mind when interpreting the results of studies comparing
the diagnostic accuracy of ultrasound and CT.
Transducer Position and Multiplanar Reconstruction
z
e error resulting from measuring AAA diameter in the
transverse abdominal view with oblique visualization of the
aortic axis is more serious. When an AAA is present and
increases in size, the aorta tends to become elongated and tortuous with lateral and sometimes anterior deviation. In this
situation, measurement of the largest aortic diameter in the
transverse upper abdominal view will overestimate AAA size.
e same holds true for axial CT measurement. e elliptical
slice of the aneurysm may overestimate its size by 1–2cm
compared with its true orthogonal diameter (
. Fig.6.29). In
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