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6.2 · Visceral andRetroperitoneal Veins
445
6
. Table 6.10 Ultrasound ndings in portal hypertension
Ultrasound
technique
B-mode Ascites, splenomegaly (sensitive but not very
Duplex Slower blood ow/reduced ow volume (highly
Color
duplex
Findings
specic)
Possibly cirrhotic changes of hepatic vessel
architecture and parenchymal structure
Signs of congestion of the gallbladder and
stomach walls
Dilated portal vein (rounded rather than oval
cross section)
Portocaval collaterals
Portal vein thrombus (echogenic)
sensitive)
Hepatofugal blood ow (100% specicity)
Loss of respiratory phasicity
Reduced increase in ow velocity after a test meal
Portosystemic collaterals (in 60–90%): left gastric
vein, gastroesophageal varices, azygos vein,
epigastric veins, paraumbilical veins (CruveilhierBaumgarten syndrome)
Splenorenal shunts (100% specicity)
Abnormal hepatic vein waveform (triphasic →
monophasic)
Additional parameters:
– Increased resistance → reduced resistive
index of hepatic artery
– Increased damping index
– Increased intrarenal resistive index >0.7
(highly specic for hepatorenal syndrome)
Portocaval collaterals
Stagnating/reversed blood ow
Portal vein thrombosis
inferior vena cava, and hypertension is dened as a pressure gradient of more than 11 mmHg that persists for an
extended period.
Ultrasound Diagnosis
z
Duplex ultrasound performed for portal hypertension provides valid information on portal venous ow in 93–95%
of patients (Patriquin etal. 1987; Yeh etal. 1996; Seitz and
Kubale 1988). e main criteria are:
5 Portal vein diameter measured by gray-scale ultrasound
5 Hemodynamic information: ow direction, ow charac-
ter, and blood ow velocity in the portal vein
5 Identication of portocaval shunts/collateral pathways
e increased pressure in portal hypertension secondary to liver cirrhosis leads to widening of the portal vein
(. Fig.6.47b–d), its distal tributaries, and the veins recruited
as collaterals (portocaval, gastroesophageal, splenorenal,
umbilical), which may already be noted on B-mode ultrasound (. Table 6.10). Additionally, the normal respiratory
diameter variation of the portal vein is lost (see . Fig.6.101
(Atlas)) or reduced (nicely seen in time-motion mode).
Aportal vein diameter of more than 13mm indicates portal
hypertension with a high sensitivity of 95–100% but a low
specicity of only 45–50% (Bolondi et al. 1982), which is
attributable to the wide variation in the normal portal vein
diameter.
Dilatation and loss of respiratory diameter variation are
observed not only in the portal vein but also in the mesenteric and splenic veins. An important supplementary
sonographic criterion, also attributable to the increased
intravascular pressure, is rounding of the normal oval cross
section of these veins. Other supplementary ndings include
widening of the le gastric vein (diameter>4mm) and high
ow in the reopened umbilical vein (
. Fig.6.47).
e spectral waveform in portal hypertension is characterized by a reduced mean ow velocity and loss of respiratory phasicity (. Table6.10; . Figs.6.97, 6.100, and 6.101
(Atlas)).
e main diagnostic role of color duplex ultrasonography is to follow up patients with portal hypertension
and to timely identify complications such as thrombosis.
Moreover, it provides useful diagnostic information in
presinusoidal, extrahepatic portal hypertension. e most
common causes are primary or secondary tumor thrombosis, inammatory diseases like pancreatitis, and slow ow
due to cirrhosis. e presentation of portal vein thrombosis
varies with the temporal course and collateralization, ranging from unspecic abdominal symptoms to an acute abdomen in rare cases.
Depending on the severity of portal hypertension, spectral Doppler will demonstrate
velocity
, to-and-fro ow, or ow reversal when pressure
antegrade ow with reduced
exceeds 30 mmHg. Normal cardiac pulsatility of the liver
veins is lost in cirrhosis.
e ow direction in the portal vein is determined not
only by the severity of cirrhosis and the magnitude of intraportal blood pressure but also by the direction of collateral
drainage
(. Fig.6.47a). Basically, portocaval collateral circulation may drain toward the center or toward the periphery
and involves a variety of vessels:
1. Shunts draining toward the center:
5 Esophageal varices, gastric corpus and fundus varices
(le gastric vein– azygos vein, short gastric veins–
azygos vein)
5 Gastrosplenic shunts
5 Portorenal and splenorenal collaterals
5 Capsular veins of liver and spleen, diaphragmatic
veins
2. Shunts draining toward the periphery:
5 Paraumbilical veins (Cruveilhier–Baumgarten
syndrome)
5 Splenolumbar shunts
5 Mesenteric veins (superior and inferior mesenteric
veins, ovarian vein, spermatic vein, rectal plexus)
446
Chapter 6 · Visceral andRetroperitoneal Vessels
e demonstration of collateral pathways is a highly sensi-
tive direct sign of portal hypertension and is seen either as
widening of the short gastric veins or le gastric vein with
venous drainage to the esophageal plexus or as a patent
umbilical vein (Cruveilhier–Baumgarten syndrome). Other
collaterals including gastrorenal and splenorenal anastomoses and peripancreatic veins are less amenable to sonographic
evaluation. When a systematic search is performed, 65–90%
of the relevant portocaval collaterals can be identied by
duplex imaging (Lafortune etal. 1987; Takayasu etal. 1984;
Subramanyam etal. 1983).
e le gastric vein with a normal diameter of less than
4mm is usually well visualized, making it of great diagnostic
6
importance in duplex ultrasound. A diameter of over 7mm
and hepatofugal ow indicate portal hypertension (Lafortune et al. 1984; Morin et al. 1992). e demonstration of
hepatofugal ow in the reopened umbilical vein, beginning
in the round ligament, was found to have sensitivities and
intraindividual and interindividual comparison, signicant dierences are identied between healthy subjects and
patients with portal hypertension when mean blood ow
velocities (V
) determined in larger study populations
mean
are compared. Several such studies demonstrated a statistically signicant decrease from 15cm/s in healthy subjects
to half that value in patients with cirrhosis (Seitz and Kubale
1988). ough maximum venous ow velocity is decreased
to 7–15cm/s (mean of 10cm/s) in patients with cirrhosis,
there is wide interindividual variation and overlap with the
ow velocities in normal subjects, which may lead to misinterpretation in individual cases.
In summary, however, portal vein ow velocities allow
the following conclusions to be drawn:
5 Portal hypertension is unlikely if maximum ow velocity
) in the portal vein is >30cm/s
(V
max
5 Portal hypertension may be present if V
5 Portal hypertension is likely if V
is <10cm/s.
max
is 10–30cm/s
max
specicities of up to 100% (Gibson etal. 1989; Mostbeck etal.
1989). Occasionally, ow can be detected in the round ligament in individuals without portal hypertension; however,
in these cases, blood ow velocity does not exceed 5 cm/s
(Casarella 1995; Lafortune etal. 1984, 1987). It is also helpful
to look for collaterals at the esophagogastric junction; these
varices can be dierentiated from enlarged lymph nodes by
the demonstration of ow in the color duplex mode. Sonographic follow-up evaluation of the collateral pathways can
also help in evaluating the outcome of treatment.
When the blood is chiey drained through splenorenal or
esophagogastric shunts and the pressure gradient is markedly
increased, ow in the portal vein is backward (hepatofugal),
while normal, hepatopetal ow may be preserved in patients
with a patent umbilical vein (Cruveilhier–Baumgarten syndrome) (see collateral pathways in
. Fig. 6.47a). In these
patients, there may even be retrograde ow in the right portal vein branch with normal ow direction in the le portal
branch, which feeds the recanalized umbilical vein.
Venous blood ow is dicult to measure, mainly
because the wide variation in vein diameter is dicult to
quantify. is applies especially to the portal vein with its
extreme variation in diameter between inspiration and expiration. erefore,
vein
is a more suitable quantitative parameter for discrimi-
mean blood ow velocity in the portal
nating between healthy individuals and patients with portal
hypertension. Note, however, that mean ow velocity is inuenced by the magnitude of collateralization and the veins
recruited as collaterals. Most importantly, high ow in the
patent and widened umbilical vein (Cruveilhier–Baumgarten syndrome) may mimic normal perfusion of the liver with
a fairly normal ow velocity in the portal vein because the
blood drains through the umbilical vein, circumventing the
sinusoids (see . Fig.6.47).
Although the variable collateralization leads to a
wide variation in mean portal ow velocities, both in
Duplex imaging also allows evaluation of the decrease in
portal blood ow in response to beta-blocker or somatostatin
intake and of the increase aer eating or aer glucagon challenge. Cirrhotic patients show a less pronounced increase in
portal blood ow velocity aer a test meal.
Various tests were proposed to improve the dierentiation of cirrhosis-induced portal hypertension from normal
portal blood ow. Apart from the less marked increase in
postprandial ow, drugs like beta-blockers or nifedipine
also have a less pronounced eect on portal vein blood ow
velocity in cirrhosis. Gaiani etal. (1989) compared 11 cirrhotic patients and healthy controls 60min aer a test meal
and found a markedly lower increase in diameter of 3% in
patients compared with 14% in controls, while the increase
in ow velocity was 3.2% versus 24%. e ow volume aer
the test meal increased by only 8.5% in patients as opposed
to 59% in controls. Such clearcut results were not always conrmed by other study groups.
Another parameter is the congestion index, which is the
ratio between the cross-sectional area of the vein and blood
ow velocity (cm
2
/cm/s=cm×s). e index is <0.07cm×s
in healthy individuals and increases to >0.1cm×s in portal
hypertension secondary to cirrhosis (Moriyasu et al. 1985;
Siringo etal. 1994) (see . Fig.6.101 (Atlas)). Further studies
are necessary to show whether glucagon-induced changes in
portal venous ow can be used to estimate the hemodynamic
reserve and whether measurement of portal ow velocity
aer propanolol administration, despite wide interindividual variation, may enable reliable identication of patients
requiring treatment for portal hypertension.
Quantitative determination of blood ow is not necessary in the routine diagnostic workup of portal hypertension
since there is no close correlation between portal blood ow
and portal hypertension due to the highly variable and ramied collateral system.
6.2 · Visceral andRetroperitoneal Veins
447
. Fig. 6.48a–c Transjugular intrahepatic portosystemic stent shunt (TIPSS). a Color ow image showing reversed ow in the intrahepatic por-
tal vein branch near the hilum after TIPPS. b The shunt is patent, ow direction is toward the heart (blue), and there is a normal ow velocity of
83cm/s. c Nevertheless, continuous mapping of the shunt reveals a focal increase in ow velocity to 228cm/s, which corresponds to 60% luminal
narrowing (continuity equation, calculation of PSV ratio analogous to the method used for grading arterial stenosis)
6
e decreased portal blood ow in portal hypertension
due to cirrhosis can lead to a compensatory increase in
arterial perfusion, which is detectable sonographically. e
higher perfusion can result in an enlargement of the crosssectional areas of the hepatic arteries both within and outside
the liver. Furthermore, progressive cirrhosis is associated
with an increased resistance in the peripheral hepatic artery
branches, resulting in a more pulsatile ow prole with
increased resistive indices of 0.8 to 0.9.
Follow-Up After Treatment (TIPSS)
z
Endoscopic obliteration of esophageal varices and transjugular intrahepatic portosystemic stent shunt (TIPSS) procedures have led to a decrease in portocaval and splenorenal
shunt operations. An important question to be answered
before treatment is whether the portal, mesenteric, and
splenic veins are patent. ere is good evaluability of these
veins by ultrasonography, which is why color duplex imaging has evolved into the method of choice. In the postoperative follow-up, ultrasound enables direct evaluation of shunt
patency. e cardiac uctuation of blood ow in the vena
cava is transmitted to the anastomosed portal vein through
the shunt.
When a distal splenorenal shunt (Warren shunt) is created, the relief of the portal vein leads to ow reversal in the
splenic vein (hepatofugal ow). In the TIPSS procedure, a
short circuit is established between the hepatic vein and portal vein under ultrasound guidance. Color duplex ultrasound
can help in identifying a short puncture tract and is also useful for postinterventional surveillance of stent patency.
In-stent stenosis and shunt thrombosis are common,
resulting in poor 1-year patency rates of 35–66% (Nazarian etal. 1994; Sterling and Darcy 1997; Kerlan etal. 1995).
Patency can be improved by sonographic surveillance with
timely revision. A sonographic examination should be performed within 24 h of stent placement to determine stent
location and ow velocity and to conrm the technical success of the procedure, especially at the junctions between the
stent ends and the native vein. Further examinations should
follow at 3-month intervals with the following ndings suggesting normalization and TIPSS adequacy (
. Fig.6.48):
5 Blood ow velocity in the shunt should be at least
50–60cm/s (Chong etal. 1993; Foshager etal. 1995;
Dodd etal. 1995; Feldstein etal. 1996). Normal peak
shunt velocity ranges between 80 and 120cm/s (Kanterman etal. 1997).
5 Continuous color duplex imaging of the shunt (with an
adequate pulse repetition frequency) should not reveal
any mural thrombus: color-coded ow throughout the
shunt lumen without gaps and without aliasing.
5 Stent ends should extend just as far as necessary into the
vena cava and portal vein.
5 Doppler waveform should reveal largely continuous ow
and at most slight cardiac pulsatility.
5 Hepatopedal ow in the portal vein with a return to nor-
mal ow velocity.
Shunt stenosis is suggested by an abrupt doubling of
shunt ow velocity (. Fig. 6.48). A velocity of less than
50cm/s within the shunt indicates inadequate shunt ow
and should prompt a thorough search for shunt stenosis
or other causes (Bodner et al. 2000; Murphy etal. 1998;
Kanterman etal. 1997; Dodd etal. 1995). Stenosis is common at the stent ends but may occur anywhere along the
course of the shunt. A drop in intrashunt blood ow also
reduces ow velocity in the portal vein, and severe stenosis
is associated with sonographic and clinical signs of portal
hypertension.
When the
shunt is occluded, there is no ow in color
duplex imaging or in the Doppler waveform; the ndings in
the portal vein correspond to those of portal hypertension
obtained before creation of the shunt.
6.2.6.4.3 Hepatic Veins
Like the vena cava, the hepatic veins are subject to both
respiratory phasicity and cardiac pulsatility, giving rise to
a triphasic waveform (. Fig.6.97 (Atlas)). Besides prandial
uctuations in blood ow volume, ow velocity varies with
448
Chapter 6 · Visceral andRetroperitoneal Vessels
changing pressures in the chest cavity, right atrium, and
abdomen. e triphasic, W-shaped waveform reects the
venous pressure variations during the cardiac cycle. e
rst velocity peak directed toward the vena cava occurs
during systole and atrial lling. As the intra-atrial pressure
increases, hepatofugal ow decreases in the hepatic veins
and in the vena cava. Opening of the tricuspid valve leads
to increased ow into the right ventricle and a second ow
velocity peak in the hepatic veins and vena cava. During
atrial contraction, there may be zero ow or retrograde,
hepatopedal ow.
Another factor aecting the Doppler waveform shape of
the hepatic veins is the stiness of the liver parenchyma. As
6
elasticity is lost and the parenchyma stiens with progressive
cirrhotic transformation, the waveform of the hepatic veins is
increasingly attened, changing from a triphasic to biphasic
(loss of early diastolic backward ow) and, ultimately, monophasic appearance. In a population of 60 patients with portal
hypertension conrmed by invasive measurement, 31.6%
had a triphasic waveform, 46.7% a biphasic waveform, and
13% a monphasic waveform. In the healthy control group,
86.7% of subjects had a triphasic waveform, while 3% (1 subject) had a monophasic waveform and 10% a biphasic waveform (Hang etal. 2011).
e amount of attening of the waveform correlates well
with the severity of portal hypertension. Flattening of the
waveform reects increasing liver stiness in progressive cirrhosis (see
. Fig.6.97d,e (Atlas)). is is an important diag-
nostic criterion and also a prognostic factor (Bolondi etal.
1991; Ohta etal. 1994); for instance, a completely at waveform from the the hepatic veins was reported to predict a life
expectancy of less than 2years. In a study of 52 patients with
chronic hepatitis C, a markedly abnormal ow pattern in the
hepatic veins was found to have a diagnostic accuracy of 77%
and specicity of 78% for Child A cirrhosis (Colli etal. 1994).
Since blood ow in the hepatic veins is highly sensitive to
parenchymal changes, which also occur in other liver conditions associated with severe fatty degeneration, attening of
the ow prole in the hepatic veins is not a specic indicator
of cirrhosis. Moreover, there may be physiologic attening of
the waveform in advanced pregnancy.
Blood ow in the hepatic veins and the portal vein is also
inuenced by cardiac activity, and various cardiac diseases
lead to a larger reux component and increased pulsatility
in these veins.
Budd–Chiari syndrome results from compromised
hepatic venous outow due to postsinusoidal obstruction.
e obstruction may be caused by a mass (tumor, cyst,
abscess), hepatic vein thrombosis, or a congenital anomaly
with a connective tissue membrane in the termination of
the middle and/or le hepatic veins. In acute hepatic vein
thrombosis, color duplex ultrasound will show a dilated vein
with intraluminal areas of higher echogenicity and absence
of ow. In chronic thrombosis, there may be recanalization of
an obstructed vein with sonographic identication of membranes and demonstration of venovenous and portosystemic
shunts in the color duplex mode.
Duplex imaging is a valid modality for the routine
diagnostic evaluation of portal hypertension including initial diagnosis, hemodynamic evaluation of the portal vein,
and follow-up. Other imaging modalities are only needed
to examine patients with poor insonation conditions (massive ascites, meteorism) and to answer specic diagnostic
questions. e exibility in choosing sonographic imaging
planes enables hemodynamic assessment as well as precise determination of topographic relationships. is is an
advantage of ultrasound over angiographic procedures as
well as over magnetic resonance imaging, especially with
regard to the determination of blood ow volumes and ow
directions.
6.3 · Atlas: Visceral andRetroperitoneal Vessels
449
6.3 Atlas: Visceral andRetroperitoneal Vessels
. Table6.11 lists the gures presented in the Atlas. e gures illustrate normal ndings, methodology, and diseases of the
visceral and retroperitoneal vessels.
. Table 6.11 Visceral and Retroperitoneal Vessels– Figures
Entity/Pathology Figure
6
Flow prole in the aorta
Celiac trunk
Hepatic artery in liver cirrhosis
Mesenteric blood ow
Waveform patterns of anatomic variants
Inferior mesenteric artery
Median arcuate ligament syndrome
Celiac trunk occlusion– changes in superior mesenteric artery waveform
High-grade mesenteric artery stenosis
Acute mesenteric artery occlusion
Acute mesenteric artery occlusion
Mesenteric artery occlusion– acute versus chronic
Chronic mesenteric artery occlusion
Inammatory bowel disease
Hepatic artery aneurysm
Splenic artery aneurysm
Course of the renal arteries
Sonoanatomy of the renal arteries
Horseshoe kidney
Pelvic kidney
Renal artery stenosis– PTA
Renal artery stenosis– indirect criteria
High-grade renal artery stenosis– PTA
Renal artery stenosis in diabetes mellitus– indication for PTA?
Renal artery stenosis in diabetes mellitus– indirect criteria
Suprarenal aortic aneurysm with renal artery stenosis
Vessel compression by tumor
Transplant kidney
Transplant kidney– rejection– stula
Abdominal aortic and iliac artery aneurysm
. Fig.6.49 (Atlas), page 451
. Fig.6.50 (Atlas), page 452
. Fig.6.50 (Atlas), page 452
. Fig.6.51 (Atlas), page 452
. Fig.6.52 (Atlas), page 453
. Fig.6.53 (Atlas), page 453
. Fig.6.54 (Atlas), page 454
. Fig.6.54 (Atlas), page 454
. Fig.6.55 (Atlas), page 455
. Fig.6.56 (Atlas), page 455
. Fig.6.57 (Atlas), page 456
. Fig.6.57 (Atlas), page 456
. Fig.6.58 (Atlas), page 457
. Fig.6.59 (Atlas), page 457
. Fig.6.60 (Atlas), page 458
. Fig.6.61 (Atlas), page 458
. Fig.6.62 (Atlas), page 459
. Fig.6.63 (Atlas), page 460
. Fig.6.64 (Atlas), page 460
. Fig.6.65 (Atlas), page 461
. Fig.6.66 (Atlas), page 461
. Fig.6.67 (Atlas), page 462
. Fig.6.67 (Atlas), page 462
. Fig.6.67 (Atlas), page 462
. Fig.6.68 (Atlas), page 463
. Fig.6.69 (Atlas), page 463
. Fig.6.70 (Atlas), page 464
. Fig.6.71 (Atlas), page 464
. Fig.6.72 (Atlas), page 465
. Fig.6.73 (Atlas), page 465
(continued)
Chapter 6 · Visceral andRetroperitoneal Vessels
450
. Table 6.11 (continued)
Entity/Pathology Figure
Abdominal aortic aneurysm with arterial embolism
Abdominal aortic aneurysm
Contained perforation of abdominal aortic aneurysm
Abdominal aortic aneurysm due to nonatherosclerotic cause
Follow-up after endovascular aneurysm repair (EVAR)
Type Ib endoleak
6
Type I endoleak after endovascular aneurysm repair (EVAR)
Type II endoleak– high-ow
Type II endoleak– when to treat
Endoleak requiring repair– pulsation in time-mode mode
Small type II endoleak
Type II endoleak– high-ow versus low-ow (comparison with CT ndings)
Patent inferior mesenteric artery, not classied as a relevant endoleak
Endoleak– stepwise diagnostic workup by CDUS, CEUS, CTA
Type II endoleak missed by CDUS but detected with CEUS
Stent graft rupture after EVAR
Follow-up after EVAR– complication versus retroperitoneal brosis
Retroperitoneal brosis– dierential diagnosis: perforated abdominal aortic aneurysm
Inammatory abdominal aortic aneurysm
Abdominal aortic aneurysm in a patient with horseshoe kidney
Aortic dissection– dynamic versus static blood ow reduction
Infrarenal dissection
Aortic dissection
Aortic dissection after intervention
Aortic perforation
Dierential diagnosis: aortic perforation– lumbar artery
Mycotic aortic perforation
Suture aneurysm after placement of a straight stent graft
Suture aneurysm after placement of a straight stent graft
Aortic thrombus (thrombolytic treatment)– aortic stenosis
Vena cava
Situs inversus
Right renal vein
Left renal vein
. Fig.6.74 (Atlas), page 466
. Fig.6.75 (Atlas), page 466
. Fig.6.75 (Atlas), page 466
. Fig.6.76 (Atlas), page 467
. Fig.6.77 (Atlas), page 467
. Fig.6.78 (Atlas), page 468
. Fig.6.79 (Atlas), page 469
. Fig.6.80 (Atlas), page 469
. Fig.6.81 (Atlas), page 470
. Fig.6.81 (Atlas), page 470
. Fig.6.81 (Atlas), page 470
. Fig.6.82 (Atlas), page 471
. Fig.6.82 (Atlas), page 471
. Fig.6.83 (Atlas), page 472
. Fig.6.83 (Atlas), page 472
. Fig.6.84 (Atlas), page 473
. Fig.6.84 (Atlas), page 473
. Fig.6.85 (Atlas), page 474
. Fig.6.86 (Atlas), page 474
. Fig.6.87 (Atlas), page 475
. Fig.6.88 (Atlas), page 475, 476
. Fig.6.89 (Atlas), page 476
. Fig.6.90 (Atlas), page 477
. Fig.6.90 (Atlas), page 477
. Fig.6.91 (Atlas), page 478
. Fig.6.91 (Atlas), page 478
. Fig.6.91 (Atlas), page 478
. Fig.6.92 (Atlas), page 479
. Fig.6.93 (Atlas), page 479
. Fig.6.94 (Atlas), page 480, 481
. Fig.6.95 (Atlas), page 481
. Fig.6.95 (Atlas), page 481
. Fig.6.96 (Atlas), page 482
. Fig.6.96 (Atlas), page 482
6.3 · Atlas: Visceral andRetroperitoneal Vessels
. Table 6.11 (continued)
Entity/Pathology Figure
451
6
Retroaortic left renal vein
Normal and abnormal Doppler waveforms of hepatic veins
Abnormal waveform of hepatic veins in liver cirrhosis
Waveform of hepatic vein in liver cirrhosis
Portal vein and its tributaries
Mesenteric vein thrombosis– surrounded by owing blood
Superior mesenteric vein thrombosis
Portal vein thrombosis
Portal hypertension
Portal vein aneurysm
Portal vein thrombosis
Cavernous transformation of the portal vein
Tumor compression
Vena cava thrombosis
Renal vein thrombus
Tumor thrombus ascending in vena cava
Varicose ovarian vein in nutcracker syndrome
Vena cava umbrella
. Fig.6.96 (Atlas), page 482
. Fig.6.97 (Atlas), page 482
. Fig.6.97 (Atlas), apge 482
. Fig.6.97 (Atlas), page 482
. Fig.6.98 (Atlas), page 482
. Fig.6.99 (Atlas), page 483
. Fig.6.100 (Atlas), page 483, 484
. Fig.6.100 (Atlas), page 483, 484
. Fig.6.101 (Atlas), page 484
. Fig.6.102 (Atlas), page 484
. Fig.6.103 (Atlas), page 485
. Fig.6.104 (Atlas), page 485
. Fig.6.105 (Atlas), page 485
. Fig.6.106 (Atlas), page 486
. Fig.6.107 (Atlas), page 487
. Fig.6.107 (Atlas), page 487
. Fig.6.108 (Atlas), page 488
. Fig.6.109 (Atlas), page 489
. Fig. 6.49a, b (Atlas) Flow prole in the aorta.
a Proximal to the origins of the visceral arteries (T.C, celiac trunk; A.M.S., superior mesenteric artery), the ow prole in the abdominal aorta is predominantly determined by the supply to parenchymal organs: a dip in early diastole is followed by constant diastolic ow. Flow in the aorta is of
a mixed type because it gives o arteries that supply parenchymal organs (monophasic ow prole– low peripheral resistance) and arteries that
supply the extremities (triphasic prole– high peripheral resistance).
b Distal to the origins of the visceral and renal arteries, the aorta has a triphasic ow prole (supply to limbs)
Chapter 6 · Visceral andRetroperitoneal Vessels
452
6
. Fig. 6.50a–d (Atlas) Celiac trunk.
a Transverse view of the celiac trunk showing its origin from the abdominal aorta (AO) and division into the hepatic artery (A.H) and splenic artery
(A.L). The bifurcation is said to resemble a palm leaf or gull’s wings. Supplying parenchymal organs (spleen, liver), the celiac trunk, hepatic artery,
and splenic artery show monophasic ow with a relatively large diastolic component, comparable to ow in the internal carotid artery. The aorta
displayed in red gives o the celiac trunk anteriorly, likewise with ow depicted in red. The lighter color coding is not due to stenosis but to the angle
of insonation. This is conrmed by the normal Doppler waveform with a peak systolic velocity (PSV) of 165cm/s and an end-diastolic velocity (EDV)
of 45cm/s. Flow is synchronous with the cardiac cycle, exhibiting a low-frequency signal with a high amplitude due to wall motion in early systole.
b The hepatic artery courses to the liver hilum along the posterior aspect of the lower liver margin. The artery is coded in blue, indicating ow
away from the transducer. The high diastolic ow is due to the low peripheral resistance of the liver. The splenic artery (A.L) rst appears coursing
in an anterior direction (toward transducer, coded red) and then turns posteriorly (blue) toward the splenic hilum.
c Splenic artery with typical Doppler waveform.
Hepatic artery in liver cirrhosis.
d Liver cirrhosis is associated with parenchymal transformation, resulting in an increase in ow resistance in the hepatic artery. This is reected in an
increased Pourcelot index, which correlates with the severity of parenchymal damage. In the case presented, the index is markedly increased to 0.83
(same patient as in . Fig.6.101a–c (Atlas)). There is marked enlargement and hypoechogenicity of the caudate lobe (LC) as a sign of severe cirrhosis
. Fig. 6.51a–c (Atlas) Mesenteric blood ow.
a Superior mesenteric artery with typical Doppler waveform of the mixed type. The end-diastolic ow component is intermediate between that of
a peripheral artery and that of an artery supplying a parenchymal organ. 24-year-old fasting subject: normal blood ow in the superior mesenteric
artery shortly after its origin with a peak systolic velocity (PSV) of 128cm/s, an end-diastolic velocity (EDV) of 21cm/s, and pulsatile ow. The grayscale image depicts the superior mesenteric artery (MS) arising from the aorta (A) at an acute angle.
b Same subject as in a. Following administration of 20mg of nifedipine, PSV increases to 201cm/s, EDV to 35cm/s.
c Postprandial increase in mesenteric blood ow (PSV of 227cm/s, EDV of 73cm/s). Assuming a threshold of 200cm/s for >50% stenosis, the
increased ow velocity observed after nifedipine administration and after eating would indicate a 50–60% stenosis in a fasting patient
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c
. Fig. 6.52a–c (Atlas) Waveform patterns of anatomic variants.
a Flow in a vessel as reected in the Doppler waveform is determined by the organs it supplies. If the hepatic artery arises from the superior
mesenteric artery (see . Fig.6.3), peak systolic velocity (PSV) is high even in the absence of stenosis (fasting velocity of 214cm/s in the case presented). The patient has chronic pancreatitis with a pancreatic pseudocyst (PPZ) between the aorta and the superior mesenteric artery. The cyst is
hypoechoic in the B-mode image and can be dierentiated from an aneurysm in the color duplex mode.
b Distal to the origin of the replaced hepatic artery (at the level of the pancreatic pseudocyst, where a second hepatic artery arises), the superior
mesenteric artery shows ow with a smaller diastolic component and a reduced PSV.Proximal to the hepatic artery origin, ow is of the mixed
type due to supply of two organs (liver and bowel). The examiner must be aware of these anatomic variants and their hemodynamic eects on
Doppler waveforms obtained in this vascular territory.
c In individuals with pelvic kidneys, as shown here (or in a transplant kidney anastomosed to the iliac artery), the normal Doppler waveform of the
iliac artery proximal to the renal artery origin is monophasic rather than triphasic. The image shows part of the pelvic kidney above the common iliac
artery. The monophasic waveform is due to blood supply to both the peripheral arteries and the renal artery and does not suggest postocclusive
ow despite the presence of plaque proximal to the sample volume. Distal to the renal artery origin, the external iliac artery exhibits triphasic ow
. Fig. 6.53 (Atlas) Inferior mesenteric artery.
Origin of the inferior mesenteric artery from the aorta. The Doppler
waveform resembles that of the superior mesenteric artery but may
occasionally show a smaller diastolic ow component or even enddiastolic zero ow. Anteriorly, a jejunal branch is depicted (blue, away
from transducer) distal to the division of the superior mesenteric
artery. The superior mesenteric artery dividing into the ileocolic and
right colic arteries is seen anterior to the aorta with ow in the same
direction coded in red. Directly anterior to the origin of the jejunal
artery (displayed in blue), the jejunal vein with ow in the opposite
direction (red) courses parallel to the artery and empties into the superior mesenteric vein (V.M.S)
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. Fig. 6.54a–e (Atlas) Median arcuate ligament syndrome.
a, b There is aliasing at the origin of the celiac trunk (T.C) from the aorta (A), which is above the origin of the superior mesenteric artery (A.M.S).
With the sample volume placed just anterior to the origin, the spectral Doppler measurement yields a peak systolic velocity (PSV) of 215cm/s and
an end-diastolic velocity (EDV) of 90cm/s. Respiratory downward movement of the diaphragm displaces and compresses the celiac trunk, visible
as a sharp bend in the proximal celiac segment in the color duplex image (in b). The corresponding spectral Doppler measurement (right) reveals
a PSV of 6m/s and EDV of 150cm/s, consistent with marked compression of the celiac trunk. PSV is dicult to measure in the proximal portions
of aortic branches because of superimposed high amplitudes from pulsatile wall motion in early diastole, which cannot be eliminated from the
waveform by any wall lter.
c Angiogram conrming downward displacement and compression of the proximal celiac trunk by the median arcuate ligament.
Celiac trunk occlusion– changes in superior mesenteric artery waveform.
d Occlusion of the celiac trunk (T.C) is associated with retrograde blood ow in the hepatic artery (A.H) (red, ow toward transducer). The hepatic
artery is relled by the gastroduodenal artery and also supplies the splenic artery (A.L). The Doppler waveform is characteristic of an artery supplying a parenchymal organ and conrms retrograde ow in the hepatic artery. Blood ow direction in the splenic artery is normal.
e In occlusion of the celiac trunk, the liver and spleen are supplied by collaterals such as the pancreaticoduodenal and gastroduodenal arteries.
The superior mesenteric artery (no stenosis) supplying these collaterals shows high blood ow velocity at its origin (average PSV of up to 4m/s
and EDV of 150cm/s) with a ow prole similar to that of arteries supplying parenchymal organs. Chronic celiac trunk occlusion due to stenosis,
as in this case, is associated with poststenotic dilatation (seen here above the superior mesenteric artery)