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CONTRAST-ENHANCED PORTAL MAGNETIC RESONANCE
ANGIOGRAPHY IN DOGS WITH SUSPECTED CONGENITAL PORTAL
VASCULAR ANOMALIES
WILFRIED MAI, CHICK WEISSE
Contrast-enhanced multiphase magnetic resonance angiography (CE-MRA) was used in 17 dogs with a
suspected congenital portal vascular anomaly. Portal vascular anomalies were identified in 16 of the 17 dogs.
Eleven had a single intrahepatic portocaval shunt (two central divisional, three right divisional, and six left
divisional), one dog had a double intrahepatic portocaval shunt, one dog had a hepatic arteriovenous
malformation, one dog had a complex intrahepatic porto-caval shunt. Two dogs had an extrahepatic
portosystemic shunt and no shunt was identified in one dog. Total imaging time waso10min and image quality
was good to excellent in all dogs. Portal CE-MRA is a feasible, fast and non invasive technique to diagnose
portal vascular anomalies in dogs, with a large field-of-view and good anatomic depiction of the abnormal
vessels. Based on these results, CE-MRA is an efficient imaging technique for the diagnosis of portal vascular
anomalies in dogs. r 2010 Veterinary Radiology & Ultrasound, Vol. 52, No. 3, 2011, pp 284–288.
Key words: arteriovenous fistula, dogs, gadolinium, magnetic resonance angiography, portosystemic
shunts.
PORTAL VASCULAR ANOMALIES in the dog and cat include
congenital or acquired porto-systemic shunts, portal
venous hypoplasia (formerly called micro-vascular dyspla-
sia), noncirrhotic portal hypertension with portal vein
atresia and hepatic arteriovenous malformation.1–9
Vascular opacification with contrast medium to identify
abnormal anatomy can be replaced with computed
tomography angiography or magnetic resonance angio-
graphy (MRA), which are noninvasive. In addition, as
interventional procedures are becoming more available to
treat portosystemic shunts, minimally invasive imaging
techniques that provide anatomic depiction and precise
measurements of the abnormal vessels are needed.10–16
Contrast-enhanced magnetic resonance angiography
(CE-MRA) can provide excellent assessment of portal
vascular anatomy in short acquisition times.17,18 CE-MRA
has surpassed noncontrast MRA techniques in many
applications.19–21 Although magnetic resonance imaging
is used frequently in veterinary medicine, there is only
limited information on the use of MRA.17,18,22–30 Our
objective was to evaluate CE-MRA for the diagnosis of
congenital hepatic vascular diseases in dogs.
Materials and Methods
Seventeen dogs suspected of having congenital vascular
liver disease were evaluated. Inclusion criteria were: clinical
signs consistent with hepatic vascular disease and elevated
circulating bile acids. There were eight males and nine
females, with age ranging between 4 and 36 months
(median 7 months). Breeds were: Brittany spaniel (n¼ 2),
Golden Retriever (n¼ 2), Labradoodle (n¼ 2), Bernese
mountain dog (n¼ 2), Labrador mixed dog (n¼ 2), Ger-
man shepherd (n¼ 1), Pomeranian (n¼ 1), Boxer (n¼ 1),
Labrador (n¼ 1), Portuguese water dog (n¼ 1), Maltese
(n¼ 1), Havanese (n¼ 1). Whenever possible, MRA
findings were confirmed at surgery or with invasive
angiography during coil embolization.
Anesthesia and imaging protocols were similar to those
described previously.18 Briefly, a three plane 2D T2�-weighted gradient echo localizer was used to plan the
MRA acquisition. For CE-MRA, a 3D Fast Spoiled
Gradient Recalled Echo (3D FSPGR) sequence with
elliptic centric view ordering of k-space was used with
parallel acquisition (array spatial sensitivity encoding
technique). The 3D volume for MRA was prescribed in
the dorsal plane, and positioned to cover as much of the
liver as possible in the dorsal to ventral direction, and
including at least the confluence of the left hepatic vein
cranially and the splenoportal confluence caudally. In each
dorsal plane, phase encoding was left to right and
This study was funded by a grant from the American Kennel Club/Canine Health Foundation (ACORN No. 1160-A).Partial results from this study were presented at the ACVR AnnualScientific Meeting, San Antonio, TX, August 2008.Address correspondence and reprint requests to Dr. WilfriedMai, at the
above address. E-mail: [email protected] July 23, 2010; accepted for publication October 26, 2010.doi: 10.1111/j.1740-8261.2010.01771.x
From the Rosenthal Imaging and Treatment Center, University ofPennsylvania, School of Veterinary Medicine, Philadelphia, PA 19104(Mai), and The Animal Medical Center, New York, NY 10065 (Weisse).
284
frequency encoding cranial to caudal. Scan parameters
varied slightly depending on patient size and were as
follows: field of view 24� 24–34 � 34 cm; in-plane matrix
256 � 160; 2mm section thickness; 301 flip angle; band-
width 31.25–62.5 kHz; TR 4.1–6.6ms; TE 1.02–1.77ms;
NEX of 0.5–1. Zero filling was performed to obtain an
interpolated matrix of 512 pixels in the frequency encode
direction with additional overlapping interpolated slices
along the z-axis. The number of locations per 3D volume
varied from 34 to 60 depending on the size of the dog.
For image acquisition, apnea was induced by a constant
infusion of cisatracurium and turning the ventilator off
during acquisition.� In some patients, this was later
reversed using atropinew and neostigmine.z A precontrast
mask was acquired for all dogs just before gadolinium
injection. Four consecutive 3D-volumes were acquired
starting immediately after the injection of gadolinium
(0.3mmol/kg, followed by a flush of 5–10ml of saline).y As
reported previously, the contrast medium was injected
manually as rapidly as possible.17,18 A single injection was
used in all dogs.
Images were reviewed on a dedicated work station by a
board-certified radiologist (W.M.).z The phase with overall
best portal vascular enhancement was identified subjec-
tively and the mask was subtracted from this series before
reconstruction. Images were examined using full and
subvolume maximum intensity projections (MIP) in
various planes as well as volume rendering. Single voxel-
thick images in the dorsal, transverse, and sagittal planes
were also reviewed to assess specific vessels.
Results
Acquisition time ranged between 60 and 70 s. Including
the 3-plane localizer, 3D volume planning, mask acquisi-
tion and CE-MRA multiphase acquisition, total imaging
time was o10min. An additional 10–15min was required
for inspection, subtraction, reformatting, and generation of
MIPs and volume rendering.
In all dogs arterial enhancement occurred during the first
phase and the best enhancement of the portal venous
system occurred during the second or third phase after
contrast medium injection. No motion artifact was present,
and adequate suppression of background signal from soft
tissues was observed. At the portal phase, the enhanced
liver parenchyma and kidneys provided useful landmarks
for identification of specific vessels.
Three dogs had a single intrahepatic right divisional
shunt (Fig. 1), two dogs had a single intrahepatic central
divisional shunt (Fig. 2), six dogs had a single intrahepatic
left divisional shunts (Fig. 3), one dog had a combination
of two intrahepatic shunt (right divisional and central
divisional) (Fig. 4), one dog had a complex intrahepatic
shunt with multiple intrahepatic tortuous vessels which
were believed to be secondary intrahepatic communica-
tions, two dogs had an extrahepatic shunt (splenocaval and
splenophrenic), and one dog had a hepatic arteriovenous
Fig. 1. Left panel: 3D volume rendering of a right divisional intrahepaticshunt in a dog. The U shaped shunting vessel can be seen entering the rightside of the caudal vena cava (CVC). Right panel: Corresponding selectiveportal angiography. The shunting vessel (S) is visible.
Fig. 2. Dorsal oblique thick subvolume maximum intensity projectionat the portal phase in a dog with a typical bulbous intrahepatic cen-tral divisional portocaval shunt (CVC, caudal vena cava; LK, left kidney;LGV, left gastric vein, PDV, pancreatico-duodenal vein, GDV, gastro-duodenal vein; SV, splenic vein).
�Nimbex, cisatracurium bensylate 2mg/ml, Abbott Laboratories,North Chicago, IL.wAtroject, atropine 5mg/ml, Butler American Health Supply, St.
Joseph, MO.zReversal Neostigmine, 1mg/ml, American Regent, Shirley, NY.yMagnevist, Berlex Imaging, Wayne, NJ.zGE Signa, 1.5T, 9.1 Software M4, Milwaukee, WI.
285PORTAL MRAVol. 52, No. 3
malformation (Figs. 5 and 6). One dog (Havanese) did not
have a macroscopic shunt.
The abnormal vessels could be identified in all animals
and the origin and termination were clearly visible in all
but one dog, in which there was a complex network of
enlarged tortuous intrahepatic vessels; some communicated
with the portal vein or its intrahepatic branches while
others communicated with the caudal vena cava. During
transjugular retrograde portography, it was apparent that
the primary shunt was central divisional and there had
been development of a complex network of large intra-
hepatic venous collaterals.31
In one dog a complex double intrahepatic shunt was
observed (Fig. 4): there was a combination of a right-
divisional-like vessel that appeared as a U-shaped loop in
the right dorsal liver blending cranially with an aneurismal
dilation of the portal vein, which was communicating
dorsally with the caudal vena cava, suggestive of a central-
divisional anatomy.
Fig. 3. 3D reconstructions in a dog with a left divisional intrahepaticshunt. Left lateral view is on the left and ventral view on the right. Theshunting vessel (S) can be seen merging with a dilated portion of the lefthepatic vein (CVC, caudal vena cava; LK, left kidney; PDV, pancreatico-duodenal vein; GDV, gastro-duodenal vein; SV, splenic vein, Ao, aorta).
Fig. 4. Dorsal subvolume MIPs at six different levels in a dog with a double intrahepatic shunt. The U-shaped right divisional shunt is indicated by the blackarrow and the bulbous central divisional shunt is indicated by � (PDV, pancreaticoduodenal vein; GDV, gastroduodenal vein; SV, splenic vein).
Fig. 5. Volume rendering of the arterial phase of the multiphase magneticresonance angiography study in a dog with a hepatic arteriovenousmalformation. Cranial is to the top. (A) Oblique view from the left side.(B) ventral view. Note the large size of the celiac artery compared with thecranial mesenteric artery. The celiac artery feeds a network of tortuousvessels in the liver around the gallbladder and early filling of dilatedintrahepatic portal vessels is seen. In (B) early retrograde filling of the mainportal vein (�) indicative of hepatofugal flow is seen, due to the high pressuretransmitted through the fistula. Also note the dramatic reduction in size ofthe aorta just caudal to the origin of the celiac artery, also typical of thisanomaly.
286 MAI ANDWEISSE 2011
In the Boxer, a hepatic arteriovenous malformation was
diagnosed and confirmed with selective arteriography. At
the arterial phase of the study (Phase 1) the celiac artery fed
a fine network of tortuous vessels near the gallbladder that
communicated with a large dilated portal venous branch,
in the cranioventral aspect of the liver. There was early
retrograde filling of the portal vein during the arterial
phase consistent with hepatofugal portal flow (Fig. 5). The
aorta decreased in size abruptly caudal to the origin of the
celiac artery, and the celiac artery was dilated compared
with the cranial mesenteric artery (Fig. 5). At the portal
venous phase, a complex network of intrahepatic dilated
vascular structures was seen. Multiple extrahepatic tortu-
ous small vessels were observed in the region of the left
kidney, draining into an enlarged left phrenicoabdominal
vein consistent with gastrophrenic varices (Fig. 6).32
Results of CE-MRA were confirmed with invasive
selective angiography in 13 dogs (Fig. 1) and surgery in
one dog. In the other three dogs, no additional procedures
were performed.
Discussion
CE-MRA allowed accurate characterization of porto-
systemic shunts in 16 dogs. The single intrahepatic and
extrahepatic shunts had the typical expected appear-
ance.33,34 For the complex double intrahepatic shunt, the
anatomy was similar to that described previously.35 Others
have also found excellent depiction of portosystemic shunts
with CE-MRA.17
In one Havanese dog, a portosystemic communication
was not identified. This dog was 2.5 years old and referred
because of mildly elevated ALT values found incidentally.
Post-prandial bile acids were increased moderately. A
biopsy was not obtained but based on the absence of
macroscopic shunt a tentative diagnosis of portal venous
hypoplasia was made.
In other work using CE-MRA for portosystemic shunt
characterization, the majority of the shunts were of the
single extrahepatic type.17 Our population, on the other
hand, contained a majority of dogs with a single in-
trahepatic shunts. This was expected as the majority of
dogs in our study were large breed dogs, whereas in the
other work the population was mostly small and toy-breed
dogs.
In the context of assessing a patient for portal vascular
anomalies, MRA has some limitations. It does not allow
accurate identification of renoliths or cystoliths that are
commonly associated with portosystemic shunts in dogs.
Such lesions are usually readily identified with CT due to
their high attenuation. If a portal anomaly is identified
with MRA, it is warranted to perform an ultrasound to
identify calculi.
Our study complements other recently published in-
formation and illustrates the use of CE-MRA in the
diagnosis of portosystemic communications of various
types. Altogether, these data indicate that CE-MRA is an
efficient tool for the diagnosis of all types of macroscopic
portal vascular anomalies in the dog.
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