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6.1 · Abdominal Aorta, Visceral andRenal Arteries
405
6
for angiographic stenosis of 50% was 24mmHg. Other investigators found a signicant upregulation of renin even for a
10% transstenotic pressure gradient (De Bruyne Manoharan
etal. 2006; Hirsch etal. 2006).
Besides the need for a generally accepted threshold for
clinically relevant RAS, the other issue to be resolved is the
degree of stenosis above which an attempt at revascularization is justied (percutaneous transluminal angioplasty
(PTA) with stenting/surgery). In the past, when surgery
was the only treatment option, a higher cuto was used
because of the higher rate of morbidity compared with PTA.
Catheter dilatation with stenting can be used more gener-
ously given the low complication rate and high success rate
(internal quality assurance). It must be noted, however, that
although studies show dilatation of RAS to be slightly superior to medical treatment in terms of lowering arterial blood
pressure and improving renal function, there is no evidencebased proof for this superiority (Balk etal. 2006; Jaarsveld
etal. 2003). e disagreement about the stenosis threshold
that justies interventional or surgical treatment is also at the
root of the controversy regarding sonographic cuto velocities and the diagnostic criteria to be used (direct or indirect):
the largest group of authors advocate higher cuto velocities,
recommending PTA mainly for patients with higher-grade
stenosis and severe renal dysfunction. Conversely, lower cuto velocities are used by proponents of early PTA (typically
to prevent xed hypertension or parenchymal damage). e
advocates of early PTA cannot make use of indirect sonographic criteria for diagnosis as these criteria yield reliable
results only for higher-grade stenosis. Note also that PTA has
no eect on essential hypertension in patients with secondary atherosclerotic wall lesions and RAS.
Aer RAS has been conrmed by duplex ultrasound, no
further diagnostic tests are needed prior to angiography with
simultaneous PTA. In patients having undergone PTA with
or without stenting, ultrasound is also the follow-up method
of choice for identifying residual or recurrent stenosis.
Color duplex ultrasound should be routinely used
after kidney transplant and can help to prevent gra loss
by timely detection of early postoperative vascular complications (Aschwanden et al. 2006; Urbancic and ButurovicPonikvar 2001). e sonographic parameters determined in
this examination, in particular the resistance index (RI), also
serve as baseline for subsequent follow-up examinations. In
the further posttransplant course, a color duplex scan should
be performed whenever a deterioration of gra function or
an increase in arterial blood pressure is noted.
6.1.6 Measurement Parameters, Diagnostic
Criteria, andRole ofUltrasound
6.1.6.1 Renal Arteries
A skilled examiner using a state-of-the-art high-end ultrasound machine should be able to identify and evaluate
the renal arteries for stenosis in about 90% of cases. However, accessory renal arteries are more dicult to identify
(Krumme etal. 1996). In the hands of an experienced examiner, sonographic evaluation of the renal arteries takes
10–20 min, depending on the acoustic window and clinical question to be answered (atherosclerotic stenosis: renal
artery origins; bromuscular dysplasia: middle thirds).
A wide range of dierent duplex scanning techniques and
parameters have been proposed to dierentiate normal ndings and low-grade renal artery stenosis (RAS) from hemodynamically signicant higher-grade stenosis. is situation
shows that all methods have their specic limitations, which
one tries to overcome by using dierent approaches. e fact
that the poor visualization of the proximal and middle thirds
of the renal arteries precludes velocity measurement for direct
demonstration of stenosis has prompted some investigators
(Bönhof etal. 1990; Schwerk etal. 1994) to measure and compare peripheral resistance indices in both renal arteries. is
is done by spectral Doppler sampling in the distal thirds of
the arteries from the ank approach (see
In normal, unobstructed renal arteries, the
index
(Pourcelot index, see . Fig. 1.28) is roughly the same
on both sides on condition that there is no unilateral renal
parenchymal damage, which would lead to more pulsatile
ow and thus aect the Pourcelot index as well. Distal to
high-grade stenosis, ow is characterized by a delayed systolic upstroke and lower peak systolic velocity (PSV), while
diastolic ow is increased, resulting in a lower Pourcelot
index (. Fig.6.8). A Pourcelot index <0.5in the distal renal
artery at the hilum suggests postocclusive changes due to
upstream ow obstruction (. Fig.6.6).
However, this method has poor sensitivity in patients
with more pulsatile ow and higher Pourcelot indices resulting from a loss of vascular compliance due to atherosclerosis
or medial sclerosis. In these patients, not even high-grade
stenosis is associated with a Pourcelot index <0.5. On the
other hand, unilateral reduction of the Pourcelot index of
>0.05 (i.e., 10% decrease) compared with the contralateral
side (. Fig.6.67 (Atlas)) was found to have 82% sensitivity
and 92% specicity for identifying >70% RAS using angiography as the gold standard (Schwerk etal. 1994). is method
takes into account elasticity losses as well as systemic factors
such as the eects of hypercirculation or hypertension, which
may be a source of error in ow velocity measurements for
stenosis quantication.
ese indirect methods are limited by the fact that they
will miss bilateral RAS.Moreover, the results are inuenced
by the presence of parenchymal damage, which aects the
RI. Although renal damage with loss of parenchyma and
renal atrophy can be identied by B-mode imaging and thus
taken into account in the measurements, some uncertainty
will remain. Parenchymal damage can also be caused by
long-standing RAS.In these cases, a high resistance index
is an indicator of parenchymal damage and can be used to
identify those patients who will not benet from renal artery
recanalization due to the extent of kidney damage that has
already occurred at the time of diagnosis. is is assumed
to be the case if the ipsilateral intrarenal Pourcelot index is
>0.8–0.85 (Radermacher etal. 2000).
7 Sect. 6.1.2.3).
resistive
Sensitivity
100
100 80 60 40 20 Specificity
AT: 40 ms AT: 90 ms AT: 400 ms
ab
Chapter 6 · Visceral andRetroperitoneal Vessels
406
AG
90
30 30 30
AT
75
AT
60
6
RI: 0.66 RI: 0.6 RI: 0.5
c
. Fig. 6.8 a Atherosclerotic renal artery stenosis (at origin). Changes
in postocclusive waveform: less pulsatile ow with delayed systolic
upstroke, lower peak systolic velocity (PSV), and corresponding
increase in diastolic ow. Lower resistance index (RI, Pourcelot index) as
compared with nonstenosed, contralateral artery (see . Figs.6.6 and
6.68 (both Atlas)). b Fibromuscular dysplasia of renal artery. Prestenotic
and poststenotic waveforms with changes resulting from stenosis in
the middle third. Flow is more pulsatile upstream of the stenosis and
becomes less pulsatile downstream with a markedly larger diastolic
component and decreased RI (AG, adrenal gland). c Poststenotic renal
artery Doppler waveforms obtained at renal hilum (evaluation for
indirect stenosis criteria). Diagrams illustrating the changes seen with
increasing stenosis severity (from left to right): normal to mild stenosis,
moderate stenosis (60–70%), high-grade stenosis. The poststenotic
decrease in pressure is associated with a decrease in peak systolic
velocity (PSV), resulting in a lower RI (Pourcelot index). With increasing
stenosis severity, the systolic upstroke (i.e., time to peak or acceleration
time, AT) is delayed
e resistance index can be regarded as a sensitive indicator of an early, relevant loss of kidney function. Especially in
patients with signs of a hepatorenal syndrome, higher-grade
liver cirrhosis is associated with vasoconstriction in the renal
cortex, which is reected in an increased RI.In these patients
with advanced cirrhosis, the RI is increased before laboratory tests show any signs of impaired kidney function (Götzberger etal. 2008).
6.1.6.1.1 Role ofColor Duplex Ultrasound in the
Detection ofRenal Artery Stenosis
Direct Criteria
z
As outlined above, various criteria have been proposed for
detecting and grading renal artery stenosis (RAS), and the
diagnostic accuracy reported for color duplex ultrasound
(CDUS) depends on the criteria used. For peak systolic velocity (PSV), published sensitivities range from 71% to 98% with
specicities of 62–98% compared with angiography as the
gold standard. ese ranges were obtained in studies dening hemodynamically relevant RAS as either >50% or >60%
stenosis and using PSV cutos ranging from 100 to 220cm/s
(. Tables 6.5 and 6.6). It is noteworthy that earlier investigators, using a combination of B-mode and Doppler ultrasound
rather than CDUS, tended to identify lower PSV thresholds
AG
100 cm/s
80
60
AT
40
20
0
. Fig. 6.9 Receiver-operating characteristic (ROC) curve for identify-
ing the optimal peak systolic velocity (PSV) cuto for dierentiating
a normal renal artery or low-grade stenosis from hemodynamically
signicant stenosis (>50%). A PSV threshold of 140cm/s yields a sensitivity of 86% and a specicity of 83% compared with 75% and 93%,
respectively, for a PSV of 160cm/s (investigated in 170 renal arteries,
including 44 with signicant stenosis, and using X-ray densitometry as
an additional reference method because reliable angiographic stenosis
grading (in 2 planes) is generally not possible in the renal arteries)
(Schäberle etal. 1992)
140 cm/s
160 cm/s
(<150cm/s) (Avasthi etal. 1984; Schäberle 1989, 1992; Ferretti etal. 1988; Hansen etal. 1990) (
. Fig.6.9, . Table6.5).
Without the color mode for visualization of owing blood
(ow jet), however, PSV measurement is more prone to
errors because angle correction is more dicult, especially in
the more curved right renal artery (see . Fig.6.62d (Atlas)).
Some studies conducted in the early 1990s (Berland etal.
1990; Breitenseher etal. 1992; Desberg etal. 1990) used PSVs
of 100–120cm/s to discriminate hemodynamically relevant
RAS from moderate stenosis (based on PSV cutos used for
grading internal carotid artery stenosis).
Later studies (especially aer 1993; . Table 6.6) using
color duplex for placing the Doppler angle correction cursor mostly relied on higher PSV cutos on the order of 180–
200cm/s (Staub etal. 2007; Karasch etal. 1993; Motew etal.
2000; Conkbayir etal. 2003; Krumme etal. 1996; Solar etal.
2011). When cutos are dened using ROC curve analysis,
the value identied to strike the best balance between sensitivity and specicity or positive predictive value (PPV) and
negative predictive value (NPV) to some extent also reects
subjective bias and the specic situation for which the cuto is dened. A more recent study (AbuRahma etal. 2012)
found sensitivity, specicity, PPV, NPV, and overall accuracy
(OA) to be 89, 54, 56, 88, and 68% for a PSV of 200cm/s
versus 67, 90, 81, 80, and 81% for a PSV of 285cm/s. Based
on their results, the authors proposed 285cm/s as the ideal
PSV cuto for 60% RAS.Staub etal. (2007) reported a sensitivity, specicity, PPV, NPV, and accuracy of 96%, 69%, 81%,
93%, and 85% for a PSV of 180cm/s; 92%, 81%, 87%, 88%,
and 87% for a PSV of 200cm/s; and 78%, 92%, 93%, 75%,
6.1 · Abdominal Aorta, Visceral andRenal Arteries
and 84% for a PSV of 250cm/s. Based on published data and
clinical experience, the author considers 200cm/s to be the
best cuto
. ROC curve analysis using angiography as the
standard of reference will invariably yield lower sensitivity
and higher specicity for higher PSV cutos and higher sensitivity with lower specicity for lower cutos.
Other factors contributing to the identication of dier-
ent PSV thresholds
in published studies are:
5 the ultrasound technique used
5 angle-correction errors (especially in the more curved
right renal artery)
5 the composition of the study population investigated
(impact of greater rigidity of the vessel wall, chronic renal
parenchymal damage, poorly controlled hypertension).
407
6
Published studies rarely discuss how the PSV is aected by
systemtic factors such as blood pressure during the examination (a case in point is presented in . Fig. 5.50 (Atlas)) and
vessel wall rigidity.
Another issue that deserves more attention is how the
results obtained for the method under investigation are
degraded by
ence
. As a rule, only oblique angiographic projections of the
inherent limitations of the standard of refer-
renal arteries are obtainable (while 2 projections are required
for adequate stenosis grading). In most studies, sonographic
PSV-based RAS grading is compared with anteroposterior
angiograms. While angiography reportedly has good accuracy in the detection of RAS, interrater agreement regarding
stenosis grading is poor (Van Jaarsveld etal. 1999). For this
reason, radiodensitometry was used as an additional reference
method in a study conducted by the author’s group (Schäberle
etal. 1992). In this study, a PSV cuto of 140cm was found to
have 86% sensitivity and 83% specicity (. Fig.6.9). Moreover,
this study revealed good correlation (R=0.84) in RAS grading
before and aer PTA between PSV-based sonographic grading and X-ray densitometry (see . Figs.6.66 (Atlas) and 6.14).
Discrepancies between angiographic and sonographic
grading are especially large for eccentric RAS. e reason is
that an eccentric plaque causing the same angiographic diameter reduction as a concentric plaque has a less severe hemodynamic eect (because the hemodynamic eect of a stenosis
is based on the cross-sectional area reduction, which is 75%
when caused by concentric plaque with 50% diameter reduction versus 50% when caused by eccentric plaque with the same
diameter reduction). Duplex ultrasound evaluates the hemodynamic eect of a stenosis as a function of the cross-sectional
area reduction. erefore, the PSV measured in a concentric
stenosis may be up to twice as high as the PSV in an eccentric
stenosis with the same angiographic diameter reduction.
e other major direct parameter for predicting RAS is
renal-aortic ratio (RAR). For identication of >60% RAS
the
using an RAR >3.5, older studies reported 84–91% sensitivity and 95–97% specicity (Kohler etal. 1986; Taylor etal.
1988; Hawkins etal. 1989; Hansen etal. 1990). More recent
studies found poorer diagnostic accuracies of 76–78% with
sensitivities of 73–84% and specicities of 72–81% for this
parameter (AbuRahma etal. 2012; Staub etal. 2007).
. Fig. 6.10 Fibromuscular dysplasia causing 50–60% stenosis of
the middle third of the renal artery (the preferred site of stenosis in
patients with this condition). In this patient, renal artery stenosis (RAS)
was graded based on the ratio of intrastenotic PSV to prestenotic PSV
at the renal artery origin (continuity equation). The PSV ratio was 2.7
(from a PSV of 80cm/s at the renal artery origin and an intrastenotic
PSV of 220cm/s)
Some investigators explored
end-diastolic velocity (EDV)
as a criterion for RAS.However, caution is in order because
EDV strongly depends on the patient’s heart rate and peripheral resistance and therefore becomes unreliable once renal
parenchymal damage has occurred (which is associated with
higher peripheral resistance and hence a decrease in EDV).
Studies specicially validating the use of color duplex
ultrasound (CDUS)
cular dysplasia
in patients with RAS due to bromus-
have not been conducted. e main challenge is overlying bowel gas, which may preclude adequate
evaluation of the middle segment of the le renal artery. is
diagnostic limitation can be overcome by comparing Doppler waveforms and resistive indices (RIs) from the origin
of the renal artery and the hilum (. Fig.6.8). In all patients
with adequate evaluation of the mid-renal artery, calculation of the ratio of intrastenotic PSV and prestenotic PSV
(in the proximal third of the artery) allows reliable stenosis grading according to the continuity equation (Schäberle
. Fig. 6.10). A ratio >2 indicates >50% RAS and a
2015) (
ratio> 4 indicates >75% RAS (for concentric stenosis). As
in the peripheral arteries, the PSV ratio is a more reliable
parameter than absolute PSV.
Indirect Criteria
z
Experience with waveform analysis in other vascular territorities suggests that indirect stenosis criteria do not
change appreciably unless higher-grade stenosis is present. erefore, it is not surprising that a side-to-side difference in the resistive indice (∆RI) of >0.05 (. Fig.6.8c;
. Table6.6) only has 31% sensitivity and 97% specicity
(Staub etal. 2007) with a PPV of 93% and NPV of 50%
for predicting 50% RAS versus 42% sensitivity and 91%
specicity for predicting 70% stenosis (PPV of 69% and
NPV of 77%). e poor sensitivity, even for >70% RAS,
was conrmed by Zeller et al. (2001), who found 77%
408
Chapter 6 · Visceral andRetroperitoneal Vessels
sensitivity but 99% specicity, and by Ripolles etal. (2001),
who reported only 50% sensitivity but 90% specicity (69%
PPV, 92% NPV). Inerestingly, Ripolles et al. found the
∆RI >0.05 to yield adequate results in patients <50years
of age. In this age group, the parameter had 90% sensitivity and 99% sensitivity as opposed to 0% sensitivity and
100% specicity in patients >50 years. e poststenotic
waveform strongly depends on vessel wall rigidity and
renal parenchymal function. In elderly patients with atherosclerosis and parenchymal kidney damage, the typical
poststenotic ow changes (markedly reduced PSV relative
to EDV, delayed systolic upstroke) are less pronounced.
Errors in interpreting ∆RI may also result in patients with
6
asymmetrical parenchymal kidney damage.
Another indirect criterion is a delayed systolic rise
(prolonged acceleration time) or a reduced acceleration
index
at the renal hilum (Kliewer etal. 1997; Stavros and
Harsheld 1994; Postman etal. 1996; Nazzal et al. 1997;
Patriquin etal. 1992). An acceleration time (AT) of >0.07s
is abnormal and indicates greater than 60% stenosis (Baxter etal. 1996; Kliewer etal. 1997; Stavros etal. 1992; Isaacson et al. 1995; Nazzal etal. 1997; Martin et al. 1991).
However, recall that the indirect criteria are not helpful in
identifying moderate stenosis (<70–80%) as the poststenotic blood ow abnormalities must reach a certain level
before they are reliably reected in changes in the indirect
criteria that can be determined by sonographic evaluation
at the renal hilum. is also holds true for AT, which shows
poor sensitivity (on the order of 50%) but good specicity
(around 95%) for <80 RAS (Conkbayir etal. 2003; Motew
etal. 2000).
Many renal diseases and the renal damage they cause lead
to an increase in the vascular RI; these include both acute
and chronic conditions, glomerulonephritis, pyelonephritis,
urinary tract obstruction, and steno-occlusive disease of the
renal veins. AT is also aected by dierent factors such as
arterial wall compliance and disturbed microcirculation in
dierent conditions associated with renal parenchymal damage (in particular diabetic nephropathy).
Ipsilateral comparison of Pourcelot indices at the renal
artery origin and at its distal end near the renal hilum is a
useful criterion for identifying stenosis due to bromuscular
brosis if overlying bowel gas or obesity precludes adequate
sonographic evaluation of the middle third of the artery.
Obstruction by high-grade stenosis will lead to more pulsatile ow with a higher Pourcelot index upstream and a lower
index downstream due to a decreased PSV and a corresponding increase in EDV (. Fig.6.8a, b).
of direct and indirect parameters (
. Table6.6). For the com-
bination of PSV (>180 or 200cm/s) and a renal-aortic ratio
(RAR) of >3.5, three studies found sensitivities and specicities on the order of 90% (Staub etal. 2007; Conkbayir etal.
2003; Krumme etal. 1996).
AbuRahma et al. (2012) identied the combination of
PSV >285cm/s and RAR >3.5 to allow adequate RAS evaluation. is combination had only 60% sensitivity but 94%
specicity using 60% angiographic stenosis for comparison.
ROC curve analysis for a lower PSV of >180cm/s in combination with the same RAR cuto in this study by necessity
resulted in a markedly better sensitivity of 73%, albeit at the
cost of a lower specicity of 81% (. Table6.6).
Determination of a combination of parameters is not
feasible on a routine basis, which is why RAS grading in
patients should primarily rely on PSV measurement. Additional parameters such as RAR or ∆RI can be determined in
patients with inconclusive ndings or in borderline cases.
In patients with higher-grade RAS, color duplex ultrasound
using PSV, or the other criteria discussed here, is superior to
angiography.
e poststenotic pressure drop with decreased perfusion
aer higher-grade RAS simulates low systemic blood pressure, which is counterregulated by the renin-angiotensin
system of the aected kidney. It was long assumed that this
regulatory mechanism is not triggered unless severe RAS
stenosis of at least 70% is present (corresponding to a PSV
>280 cm/s). Hence, it was also assumed that only these
higher-grade stenoses require treatment and need to be diagnosed reliably (Textor 1994; May et al. 1963; Muster etal.
1998; Guo and Fenster 1996). A stenosis of this magnitude
can be diagnosed by additionally taking into account indirect
criteria such as (audible) turbulence. For a therapy-oriented
approach, the denition of a precise velocity cuto for identifying stenosis with beginning hemodynamic eects (on the
order of 50%) is less relevant, and the search for the best PSV
cuto becomes a purely academic pursuit.
Later studies including measurement of intra-arterial
systolic pressure gradients suggest that renovascular hypertension can already be triggered by lower-grade stenosis
(Gross etal. 2001; Staub etal. 2007). For a PSV of >200cm/s
(i.e., 50% angiographic stenosis), Staub etal. (2007) found
a mean pressure gradient of >22 mmHg, which indicates
signicant stenosis with beginning upregulation of renin
production (De Bruyne 2006). A limitation of these studies
is that poststenotic pressure was measured with the transstenotic catheter in place (articially contributing to luminal
narrowing).
Strauss et al. (1993) found the intrastenotic pressure
6.1.6.1.2 Therapy-Oriented Stenosis Grading
Although peak systolic velocity (PSV) with a cuto of
180cm/s (to 200cm/s) is regarded as the most reliable parameter for detecting and grading renal artery stenosis (RAS),
some investigators achieved inadequate sensitivities and
specicities and therefore recommend various combinations
drop, validated by PSV measurement for iliac artery stenoses, to yield reliable results only when high-grade stenosis
is present (simplied Bernoulli equation: pressure gradient
dP=4× intrastenotic PSV
2
), for which the prestenotic PSV
is considered negligible. When the stenosis is at the origin
of the renal artery, the PSV measured in the aorta cannot be
6.1 · Abdominal Aorta, Visceral andRenal Arteries
409
6
used as the prestenotic value. On the other hand, the poststenotic PSV occasionally used in the Bernoulli equation (Stock
2009) instead of the prestenotic PSV (dP=4 × (intrastenotic
2
– poststenotic PSV2)) is inaccurate and neglects fric-
PSV
tional and inertial losses across the stenosis.
e study of Staub etal. (2007) impressively illustrates
the problems encountered in defining cutoffs for the
major ultrasound-derived parameters of RAS (PSV, RAR,
RI). A high sensitivity is achieved at the cost of specicity, and vice versa. For a therapy-oriented approach it thus
follows that an ideal velocity cuto for the renal arteries should detect all stenoses causing at least 70% diameter reduction, that is, it should have a high sensitivity
combined with a high negative predictive value in order
to reliably identify all patients for whom the majority of
investigators advocate intervention (Zeller etal. 2003). In
those cases where RAS can be treated by PTA with stenting,
the diagnostic test should also reliably identify lower-grade
stenosis (50%); the rationale here is that it has been shown
that 50% stenosis is already associated with a poststenotic
pressure drop and renin response. In these patients, PTA
is an option if a benet is expected based on the patient’s
clinical presentation and the eectiveness of other bloodpressure-lowering treatments. Hence, in this subset of
patients, in whom PTA is contemplated as a realistic and
benecial treatment option, a lower PSV cuto can be used
even when it comes at the cost of a certain number of possibly unnecessary angiographies being performed, that is,
in those patients who proceed to angiography with PTA
(standby) based on the sonographic results (see graph in
. Fig.6.9). However, note that in patients with borderline
RAS, there are as yet no adequate evidence-based data
available to prove any benets of PTA over antihypertensive
. Fig. 6.11 Stenosis of the left renal artery with very turbulent
ow and a peak systolic velocity (PSV) of 230cm/s, corresponding to
approx. 60% stenosis. Based on scientic data, this is a borderline nding with regard to whether or not PTA should be performed. The high
resistive index (RI) of 0.9 indicates renal parenchymal damage. Therefore, no benet in terms of blood pressure lowering is expected from
interventional treatment of RAS in this patient
drug treatment (
. Fig.6.11). A high RI of >0.9in the renal
artery (. Fig.6.11) indicates that parenchymal kidney dam-
age has already occurred, and no blood-pressure-lowering
eect can be expected from PTA (Radermacher etal. 2000);
However, PTA may be indicated to maintain kidney function when there is very severe RAS.
6.1.6.1.3 Contrast-Enhanced Ultrasound (CEUS)
Surprisingly good results were reported by the authors of
a study investigating the clinical role of contrast-enhanced
ultrasound (CEUS) in 120 patients with 38 stenotic renal
arteries in comparison to color duplex ultrasound (CDUS)
using angiography as the reference standard (Ciccone etal.
2011). is study reported a sensitivity, specicity, PPV, and
diagnostic accuracy of 100% for CEUS compared with 84%,
0%, 80%, and 94% for CDUS.Claudon etal. (2000) described
a 20% improvement in the detection of renal artery stenosis (RAS) by CEUS compared with CDUS (from 63.9% to
83.9%). In an earlier study, Missouris et al. (1996) found
an increase in sensitivity from 85% to 94% and in specicity from 79% to 88% based on a 20dB increase in Doppler
intensity following administration of contrast microbubbles.
Taken together, these study results indicate that CEUS can
help resolve inconclusive CDUS ndings in patients with
suspected RAS.
CEUS is also highly sensitive in demonstrating active
bleeding in patients with subcapsular renal hemorrhage and
hematoma (posttraumatic or iatrogenic) (
6.1.6.1.4 Ultrasound Follow-Up After Renal
. Fig.6.12).
Artery Stenting
Duplex ultrasound is the method of choice for the follow-up
of patients aer endovascular treatment of renal artery stenosis (RAS) (Schäberle 1993). In the postinterventional patient,
the target site is known, and a spectral Doppler waveform
enables good hemodynamic quantication of residual or
recurrent RAS.Good visualization of the stent contributes to
the good diagnostic performance of ultrasound in the identication of stent complications (. Figs.6.13 and 6.14).
Data on recurrent RAS aer stenting suggest that peak
systolic velocity (PSV) and renal-aortic ratio (RAR) cutos
dened for native arteries may overestimate in-stent reste-
. Fig. 6.13) (Chi et al. 2009; Fleming et al. 2010).
nosis (
However, published reports present conicting results. In
the carotid territory, the need to use higher cutos for grading in-stent restenosis has been attributed to greater rigidity of the stented wall compared with native arteries and a
narrower lumen of the stented segment. For >70% in-stent
restenosis of the renal arteries, Chi etal. (2009) obtained
optimal results using cutos of >395cm/s for PSV and of
>5.1 for RAR.Fleming etal. (2010) performed ROC curve
estimates using PSV cutos of 180, 200, and 250cm/s for
identication of >60% in-stent RAS.ey reported a sensitivity, specicity, PPV, and accuracy of 73%, 80%, 64%, and
77% for a PSV of 180cm/s, 68%, 80%, 63%, and 76% for a
Chapter 6 · Visceral andRetroperitoneal Vessels
410
6
. Fig. 6.12 a Iatrogenic renal injury (as a complication of abscess puncture in the paracolic gutter) with subcapsular renal hematoma and addi-
tional retroperitoneal hematoma. Contrast-enhanced ultrasound (CEUS) shows active bleeding from the puncture channel into the subcapsular
hematoma (arrow); however, there is no diuse bleeding into the surrounding tissue but to-and-fro ow at the site of the puncture channel. The
bleeding stopped following thrombin injection treatment (for details of the method see 7 Sect. 2.1.6.3). Directly after thrombin injection into
the area of active bleeding (right CEUS image and corresponding gray-scale image), with the needle still in place (<<), bright spots are apparent
lateral to the needle in the gray-scale image, indicating that the corresponding bright spots in the CEUS image are reections of the injected
thrombin and not due to the presence of microbubbles. The two images before (left) and after (right) thrombin injection show the same area;
however, the left image was obtained from a more anterior approach (subcostal view) and the right image from a more posterior approach (intercostal view). b, c, d CT scans before thrombin treatment show bleeding from the puncture channel into the subcapsular renal hematoma during
the arterial phase (b and c, arrow). The situation 7days after ultrasound-guided thrombin injection is shown in d (compare a)
. Fig. 6.13 a High-grade
in-stent restenosis of the left
renal artery with a peak systolic
velocity (PSV) of 5.5m/s and
very turbulent ow (hyperechoic
stent is seen extending into the
aortic lumen). b Angiogram of
the high-grade in-stent restenosis
(proximal end of renal artery
stent extends into the aorta). The
patient has a second stent at the
mesenteric artery origin (projected onto the aorta)
400
Duplex ultrasound (cm/s)
X-ray densitometry (% stenosis)
100
6.1 · Abdominal Aorta, Visceral andRenal Arteries
PSV of 200cm/s, and 59%, 95%, 87%, and 83% for a PSV
of 250cm/s. Again, published ROC curve estimates suggest
that there is no single cuto for all situations. If the aim of
sonographic evaluation is to identify all restenoses, a PSV
cuto of 180cm/s yields the best results (highest sensitivity).
However, if the aim is to identify the subset of patients with
higher-grade stenosis who should have a reintervention,
results are best when the PSV cuto with the highest PPV
and specicity is used (i.e., PSV of 250cm according to the
results of Fleming etal.).
Other investigators found similar velocity cutos for both
stented and native arteries, for example a PSV of >200cm/s
and an RAR of >3.5 (Nolan etal. 2005) or a PSV >225cm/s
and a RAR >3.5 (Rocha-Singh etal. 2008). Napoli etal. even
used lower cutos compared with the native renal arteries
to improve the sensitivity and specicity for identifying instent RAS (PSV of 144cm/s instead of 180 cm/s, RAR of
2.53 instead of 3.5). It may be speculated that, in this study,
there was a larger proportion of patients with eccentric RAS
(
. Fig. 6.13). An eccentric stenosis with the same angio-
graphic diameter reduction as a concentric stenosis causes
a smaller cross-sectional area reduction and thus has a less
severe hemodynamic eect, reected in a smaller intrastenotic PSV increase (. Figs. 2.17 and 5.27).
e limitations resulting from the use of angiography
as the gold standard in studies evaluating the diagnostic
performance of ultrasound in native arteries also apply to
studies investigating in-stent RAS, which are hampered by
a number of additional factors. ese additional limitations
include small patient populations, a retrospective single-center design, selection bias (angiography only in patients with
clinical and sonographic abnormalities), no information on
insonation conditions (sonographic evaluability, angle correction errors), and failure to consider eects of systemic factors on hemodynamics. Some investigators are aware of these
limitations and thus caution readers about generalizing their
results (Chi etal. 2009; Fleming etal. 2010).
411
300
200
100
before PTA
after PTA
0
02550
. Fig. 6.14 Correlation of duplex ultrasonography and X-ray den-
sitometry in 14 patients before and after percutaneous transluminal
angioplasty (PTA) (R=0.84). Hemodynamically signicant stenosis
is assumed at a peak systolic velocity (PSV) of >140cm/s for duplex
ultrasound and at >50% stenosis for X-ray densitometry (Schäberle
etal. 1992)
75
6
6.1.6.1.5 Diagnostic Algorithm
Color duplex ultrasound (CDUS) is well suited as a rst-line
diagnostic test in patients with suspected renal artery stenosis (RAS). e most reliable parameter for identifying RAS is
a peak systolic velocity (PSV) of >180 (to 200) cm/s. Inconsistenciens of published data on the best PSV cuto reect
dierences in study design and limitations of the standard
of reference. In patients with inconclusive sonographic ndings based on intrastenotic PSV, sensitivity and specicity can be improved by supplementary contrast-enhanced
ultrasound (CEUS) or the additional use of indirect criteria
(Schäberle 2015). If this extended sonographic approach still
yields inconclusive ndings or sonographic evaluation of the
renal arteries is limited, magnetic resonance angiography
(MRA) or computed tomography angiography (CTA) can
be used for further diagnostic workup. Studies report sensitivities and specicities of 88–100% for MRA (Vasbinder
etal. 2001) and 90–100% sensitivity and 92–98% specicity
for CTA (Beregi etal. 1997; Kim etal. 1998; Wittenberg etal.
1999; Rountas etal. 2007). For CTA, the prospective multicenter Renal Artery Diagnostic Imaging Study in Hypertension (RADISH) reported a lower sensitivity of 64% and
specicity of 92%.
Clinical experience can be at odds with the results
obtained in trials with standardized study designs. As in
other vascular territories, MRA tends to overestimate RAS
severity by 26–32% (Glifeather et al. 1999; Krinsky et al.
1996; Steens etal. 1997), and CT is limited in the identication of calcied plaque.
When the sonographic ndings show borderline stenosis
and a correct diagnosis is clinically warranted, angiography
with PTA standby can be performed instead of supplementary CTA or MRA (
. Fig.6.15).
Diagnostic algorithm for RAS with
Chapter 6 · Visceral andRetroperitoneal Vessels
412
essential to use adequate settings including a low PRF and
high enough gain (
. Fig.6.16).
Renal artery occlusion may be missed if the acoustic window is poor or there is perfusion of the renal capsule and
subcapsular parenchyma via collaterals, in particular from
the retroperitoneum or the adrenal gland. However, in this
situation, ow velocity is markedly reduced, and the ow
prole shows characteristics of postocclusive ow as indirect
No RAS
(or mild RAS)
(PSV <180 cm/s)
indication for PTA/surgery
CDUS
Based on intrastenotic
PSV (and indirect
criteria as required)
Inconclusive findings
Borderline PSV
Poor insonation conditions
>60-70% RAS
(PSV >260 cm/s)
signs. An additional contrast-enhanced ultrasound examina-
MRA
No RAS
6
(or mild RAS)
CTA
CEUS
Relevant RAS
(or inconclusive findings)
tion (CEUS) may be helpful and improve diagnostic accuracy
(>95%), especially in patients with peripheral renal infarction or infarction due to occlusion of a segmental artery or
lower pole artery.
6.1.6.1.7 Transplant Kidney
No further
diagnostic tests
Angiography
with PTA standby
Two types of complications may occur aer a kidney transplant: vascular complications and gra failure.
. Fig. 6.15 Diagnostic algorithm for the sonographic workup of
suspected renal artery stenosis (RAS) with indication for PTA/surgery.
CDUS, color duplex ultrasound; CEUS, contrast-enhanced ultrasound;
CTA, computed tomography angiography; MRA, magnetic resonance angiography; PSV, peak systolic velocity; PTA, percutaneous
transluminal angioplasty
Vascular complications include:
5 Postoperative occlusion of the anastomosed artery or
vein in the early postoperative phase
5 Transplant renal artery stenosis (TRAS) as a late compli-
cation (incidence of 2–25%)
5 Aneurysm and arteriovenous stula.
Anastomotic stenosis can occur during the rst weeks
aer surgery or aer many years. e connection of the
transplant artery to the iliac artery (see
. Fig.6.71 (Atlas))
and the more supercial localization of the transplant vessels
facilitate evaluation by duplex ultrasound. Stenosis criteria
are the same as for native kidneys, but indirect parameters
should not be used. Instead, stenosis must be demonstrated
directly on the basis of an increased blood ow velocity at
the anastomosis or along the course of the transplant renal
artery. An arteriovenous stula mainly develops aer needle
biopsy and may resolve spontaneously. A persisting stula
is characterized by a mosaic of colors (due to vibration artifacts) and pulsatile ow in the draining vein (see . Fig.6.72
(Atlas) and 7 Chap. 4).
. Fig. 6.16 Infarction of the left kidney. The color duplex image
obtained with a lower PRF and higher receive gains shows no ow
signals in the renal hilum or in the parenchymal region. True absence of
ow in the kidney is conrmed by the fact that, with these instrument
settings, ow signals are depicted from intraparenchymal vessels in the
lower pole of the spleen
6.1.6.1.6 Renal Artery Occlusion
Renal artery occlusion may be suggested by poor visualization of the renal artery on gray-scale ultrasound and a very
small kidney (<8–9cm in length). Duplex imaging shows no
ow at the renal artery origin or in the renal hilum and, at
most, isolated intrarenal ow signals, indicating supply from
capsular veins. Taken together, the results of several studies with small numbers of cases show an accuracy of 93%
(Miralles etal. 1996; Homann etal. 1991; Olin etal. 1995).
For correct interpration of the sonographic ndings, it is
Graft failure may occur immediately aer transplanta-
tion (urine output less than 30mL/h and progressive elevation of retention parameters). e most common cause is
acute tubular necrosis. Perfusion is preserved while most
patients have an excessively high resistive index (RI) of >0.9.
Secondary failure aer primary gra function is chiey
caused by acute rejection, infection, or nephrotoxic drug
eects. Function may be impaired by stenosis of the gra
artery or of the ureter. In addition, late failure may be due to
chronic rejection.
Acute rejection typically occurs within the rst 3months
of transplantation and may be of vascular or interstitial origin.
e vascular form of rejection with intimal and medial thickening, brinoid necrosis, and subsequent thrombus formation in the small vessels can be identied by an early acute RI
increase in the renal artery. In the interstitial form with tubulitis
and interstitial lymphocyte inltration and interstitial edema,
6.1 · Abdominal Aorta, Visceral andRenal Arteries
. Fig. 6.17 Transplant kidney in subfascial location in the left true
pelvis with rejection and a resistive index (RI) of 0.9, calculated from a
peak systolic velocity (PSV) of 137cm/s and an end-diastolic velocity
(EDV) of 13cm/s (RI=(PSV– EDV)/PSV). The sample volume is placed
in the renal artery, and the transplant kidney is located to the left of it
(with blood ow in segmental arteries). The iliac vessels are displayed
posterior to the renal artery
there will be no signicant increase in RI despite incipient dysfunction. In vascular rejection, the RI may increase 1–5days
before the diagnosis is suggested clinically; however, a reliable
diagnosis of rejection in the case of an insidious increase in
the RI can only be made on the basis of serial measurements,
to then establish the indication for biopsy or treatment (Hollenbeck etal. 1994; Kubale 1987; Rigsby etal. 1987).
In the 1980s, the resistive index (RI) of the transplant
renal artery
, calculated as peak systolic velocity (PSV) minus
end-diastolic velocity (EDV) divided by PSV (see . Figs.
1.28
and 6.17), was overrated as a predictor of gra rejection.
While certain forms of rejection are indeed associated with
an increase in RI, it is not a sensitive marker and provides
no clue as to the cause of a failing renal transplant (Tublin
etal. 2003). However, another study found an RI of >0.8 to
be a strong predictor of a poor prognosis (Radermacher etal.
2003). On the other hand, it is known that, in native arteries,
atherosclerotic lesions or subclinical atherosclerosis (increase
in intima-media thickness) can also lead to a higher RI, and
such an increase in RI has been observed in transplant renal
arteries as well.
e RI should be documented at each follow-up and a
change in RI should prompt a search for the underlying cause,
including vascular complications, which may be amenable to
correction. Renal causes of an increased RI in patients with a
kidney gra include acute and chronic rejection, acute tubular necrosis, renal vein thrombosis, pyelonephritis, and glomerulonephritis. Other causes are compression of the artery,
urinary obstruction, and drug-induced dysfunction. A low
heart rate can lead to an articially high RI because the prolonged diastole results in a lower EDV.
Duplex ultrasound is well suited for identifying vascu-
lar complications of the transplant renal vessels
as the
413
underlying mechanism of transplant failure (Osman et al.
2003). e supercial location of a transplant kidney in the
true pelvis oen allows better sonographic evaluation with
fewer artifacts compared to native kidneys. e only potential
source of error in TRAS grading is inaccurate PSV measurement resulting from problems in Doppler angle correction in
an arched transplant artery (see
Renal vein thrombosis typically occurs in the first
. Fig. 1.23).
week after transplant and accounts for one third of all
allograft losses in the early postoperative phase (Orlic
etal. 2003; Giustacchini etal. 2002). The reported incidence is 1–3% (Aschwanden etal. 2006; Renoult et al.
2000). Sonographic findings in thrombosis of the transplant renal vein include dilatation and possibly a higher
intraluminal echogenicity with absence of flow on color
duplex imaging.
When venous drainage is obstructed, ow in the renal
artery becomes more pulsatile with a decrease in the diastolic component or even diastolic backward ow (to-andfro ow), similar to the ow prole in peripheral arteries
(Aschwanden etal. 2006; Voiculescu et al. 2005). Prompt
surgical thrombectomy is the only measure that can salvage the renal allogra in this situation. rombus may
arise from renal vein stenosis, but the cause oen remains
unclear. Renal vein stenosis is suggested by an abrupt
marked increase in venous ow velocity (three- to fourfold;
Frauchiger etal. 1995; Baxter 2002); in the early postoperative phase, however, rather high ow velocities occur in the
vein, particularly more centrally, where it crosses the iliac
artery (alhammer etal. 2006).
Transplant renal artery stenosis (TRAS) becomes clini-
cally apparent in deteriorating gra function and intractable
arterial hypertension. TRAS can occur at the anastomosis,
or it can be caused by kinking or atherosclerosis of the renal
artery; the incidence is up to 10% (Baxter 2002; Bruno etal.
2004). In the color duplex examination, a stenosis along the
course of the artery is revealed by an abrupt increase in ow
velocity. e more common TRAS at the origin, or anastomosis with the iliac artery, is diagnosed by calculating a
renoiliac ratio from PSV at the renal artery origin and PSV
in the iliac artery. A PSV ratio>2 is 80% sensitive and 100%
specic for anastomotic stenosis (De Morais et al. 2003).
e problem with using absolute PSV for grading TRAS is
the same as in the native renal arteries. PSV cuto values
of 200–250cm/s have been proposed in the literature, with
sensitivities of 90–100% (De Morais etal. 2003; Baxter 2002;
Patel etal. 2003).
Intra-arterial digital subtraction angiography (DSA) is
the gold standard for corroborating the diagnosis, while
magnetic resonance imaging is subject to artifacts and
may lead to false-positive results or overestimate stenosis
(Loubyre etal. 1996; Clerbaux etal. 2003).
Arteriovenous stulas are iatrogenic complications
with an incidence of 2–10% following biopsy (Furness etal.
2003; Merkus etal. 1993; Schwarz etal. 2005). If all patients
6
414
F
dysplasia
Celiac trunk
syndrome)
Chapter 6 · Visceral andRetroperitoneal Vessels
. Fig. 6.18 Diagram of dierent types of celiac trunk
stenosis and underlying pathologies (see . Fig.6.54
(Atlas))
ibromuscular
Atherosclerotic
stenosis
External compression
(arcuate ligament
6
were examined by color duplex aer biopsy, the rate would
probably be greater than 10%; however, 95% of all AV stulas close spontaneously (Omoloja etal. 2002). As with all
AV stulas, the site is identied by a mosaic of colors due to
perivascular tissue vibration. e higher ow volume results
in an increase in EDV, and the RI is decreased due to direct
drainage into the low-resistance venous system. Flow in the
vein becomes more pulsatile and arterialized (see
. Fig.6.72
(Atlas)).
6.1.6.2 Visceral Arteries
6.1.6.2.1 Celiac Trunk
Celiac Trunk Stenosis
z
Stenosis of the celiac trunk is rare and may be caused
by atherosclerosis or bromuscular dysplasia. e rare
median arcuate ligament syndrome is caused by intermittent compression of the celiac trunk resulting from downward movement of the median arcuate ligament during
expiration (. Fig. 6.18). Atherosclerotic stenosis does not
become clinically apparent unless several visceral arteries
are obstructed.
In a study using a peak systolic velocity (PSV) cuto of
200cm/s
for identifying angiographically proven celiac trunk
stenosis greater 70%, duplex ultrasound had 87% sensitivity
and 80% specicity (Moneta etal. 1993a, b, c). For 50% celiac
trunk stenosis, Perko etal. (1997, 2001) found 94% sensitivity and specicity for a PSV cuto of 200 cm/s. Note that
these cutos yield valid results only in fasting patients with
normal vascular anatomy.
Overall, published data and clinical experience suggest
that a PSV of greater 220–250 cm/s (measured in fasting
patients) reliably identies hemodynamically relevant stenosis (>50%). However, it is likely that only higher-grade
stenosis (>75%) with intrastenotic PSV of >280–300 cm/s
becomes relevant in terms of compromising intestinal blood
supply (see . Fig.6.22).
Celiac trunk occlusion (see
. Figs.6.24 and 6.54 (Atlas))
can be bridged via collaterals coursing toward the splenic
hilum or via the gastroduodenal artery. Depending on the
collateral pathway, there will be retrograde ow in the splenic
artery or hepatic artery. Blood ow velocity in the celiac territory is modulated by respiration and should therefore be
measured at the resting end-expiratory position.
Median Arcuate Ligament Syndrome
z
Median arcuate ligament (MAL) syndrome or celiac artery
compression syndrome (rst operated on by Dunbar in
1965 and therefore also known as Dunbar’s syndrome) is
the intermittent compression of the celiac trunk near its origin (. Fig.6.19), and very rarely of the superior mesenteric
ar ter y.
It is controversial whether the nonspecic abdominal
symptoms (upper abdominal pain, loss of appetite, vomiting)
are due to hemodynamic disturbances or mechanical irritation of the celiac plexus (proven brosis). A primary vascular
component appears unlikely given the rich collateral pathways (. Fig.6.54 (Atlas)).
Intermittent compression of the celiac trunk can damage
the vessel wall and trigger deposition of thrombotic material, resulting in a so-called xed stenosis and poststenotic
dilatation, as in vascular compression syndromes of other
body regions. Upper abdominal pain is most likely due to the
pressure exerted by the arcuate ligament and diaphragmatic
crura on the vegetative nerves encircling the celiac artery.
As with other compression syndromes that are conrmed
by a function test,
duplex sonography is the method of
choice for diagnosing the median arcuate ligament syndrome.
e examination is performed during both inspiration and
expiration to conrm intermittent compression of the celiac
trunk by the ligament. e intermittent constriction of the
origin of the celiac trunk during expiratory downward movement of the diaphragm (. Fig.6.19) has a characteristic concave appearance on angiograms.