CULP, 2017

Esta é uma pré-visualização de arquivo. Entre para ver o arquivo original

OR I G I N AL ART I C L E
Prospective evaluation of outcome of dogs with intrahepatic
portosystemic shunts treated via percutaneous transvenous coil
embolization
William T. N. Culp VMD, DACVS1 | Allison L. Zwingenberger DVM, MAS, DACVR1 |
Michelle A. Giuffrida VMD, DACVS1 | Erik R. Wisner DVM, DACVR1 |
Geraldine B. Hunt BVSc, PhD1 | Michele A. Steffey DVM, DACVS1 |
Philipp D. Mayhew BVM&S, DACVS1 |
Stanley L. Marks BVSc, PhD, DACVIM (Internal Medicine, Oncology), DACVN2
1Department of Surgical and Radiological
Sciences, University of California-Davis,
School of Veterinary Medicine, Davis,
California
2Department of Medicine and
Epidemiology, University of California-
Davis, School of Veterinary Medicine,
Davis, California
Correspondence
William T. N. Culp, Department of
Surgical and Radiological Sciences,
University of California-Davis, School of
Veterinary Medicine, Davis, CA 95616.
Email: wculp@ucdavis.edu
Funding information
American College of Veterinary
Surgeons (Minimally Invasive Grant);
Center for Companion Animal Health,
School of Veterinary Medicine,
University of California-Davis
Abstract
Objective: To report outcome and complications after percutaneous transvenous coil
embolization (PTCE) and evaluate the clinical, laboratory, and imaging changes in
dogs with intrahepatic portosystemic shunts (IHPSS) pre-PTCE and post-PTCE.
Study design: Prospective clinical trial.
Animals: Twenty-five dogs (15 dogs in imaging subgroup) with IHPSS.
Methods: Clinical signs, hematologic, and biochemical parameters were recorded
before and 3 months after PTCE. All dogs received the same medical treatment and
underwent PTCE. In the imaging subgroup, ultrasonography, hepatic portal scintigraphy,
and computed tomography-angiography were performed pre-PTCE and post-PTCE.
Results: All evaluated bloodwork values improved by at least 50% of their initial
value, by 3 months post-PTCE. Liver volume increased after PTCE (P5 .001), but
remained lower than normal in 11/15 dogs. Hepatic arterial fraction decreased after
PTCE (P5 .029), consistent with increased portal blood flow to the liver. Twenty-
four of 25 dogs were available for reevaluation at 3 months, and all abnormal clinical
signs had resolved in 22/24 dogs.
Conclusion: PTCE appears promising as a treatment for IHPSS, as clinical signs
resolved in most cases, bloodwork abnormalities often normalized, and the procedure
was performed safely with minimal complications. PTCE increased hepatic portal
perfusion and liver volume in most dogs. These promising results justify a future
randomized clinical trial comparing PTCE, other attenuation options, and medical
management alone.
1 | INTRODUCTION
A portosystemic shunt is an anomalous blood vessel between
the portal system and vena cava or azygous vein.1-3 Intrahe-
patic portosystemic shunts (IHPSS) originate from a branch
of the portal vein and are often categorized as left-, right-,
and central-divisional shunts.4 A myriad of clinical signs
occur secondary to IHPSS, but those related to the neuro-
logic, gastrointestinal, and urinary systems are most com-
mon.5-7 Treatment of IHPSS include medical, surgical, and
Veterinary Surgery. 2017;1–12. wileyonlinelibrary.com/journal/vsu VC 2017 The American College of Veterinary Surgeons | 1
Received: 28 June 2016 | Accepted: 22 June 2017
DOI: 10.1111/vsu.12732
http://orcid.org/0000-0002-8982-2558
http://orcid.org/0000-0003-0852-0644
interventional options.2,8-14 The long-term implementation
of medical management as a sole treatment modality for
IHPSS is controversial in cases amenable to surgery or
interventional radiology (IR).8,9,15 Perioperative mortality
rates of 0%-27% have been reported with extravascular sur-
gical occlusion techniques.2,11,13,16-18 IHPSS are generally
considered more challenging to operate on than extrahe-
patic portosystemic shunts (EHPSS) and generally associ-
ated with a worse prognosis.2,12 Survival with resolution of
biochemical abnormalities was significantly less likely to
occur in dogs with IHPSS (50%) versus those with EHPSS
(84%).2
The goal of surgical attenuation of portosystemic
shunts is to divert blood from the shunting vessels to the
liver via the portal vein; liver size consequently increases
through regeneration.19,20 Portal scintigraphy is the method
of choice for detecting ongoing shunting and measuring
shunt fraction.21,22 Several imaging modalities can be used
to measure functional parameters that reflect hepatic regen-
eration and improved portal blood flow. As portal blood
flow increases after shunt attenuation, changes in velocity
can be measured with Doppler ultrasound. Quantitative
computed tomography (CT) imaging can be used to accu-
rately estimate hepatic volume,23 and measure functional
changes in liver perfusion.23-25 In one study, the preopera-
tive fraction of arterial blood delivered to the liver in dogs
with EHPSS was higher than normal but returned to nor-
mal after treatment with ameroid constrictors.25 These
parameters can help veterinarians evaluate the effects of
percutaneous transvenous coil embolization (PTCE) on
liver development in a noninvasive manner.
Minimally invasive techniques, and in particular IR
techniques, are gaining popularity to treat diseases such as
IHPSS. In spite of case reports and case series,10,26-29 the
PTCE procedure is still considered relatively new in vet-
erinary medicine and requires further evaluation. In a
recent retrospective study,10 most dogs with IHPSS treated
with an endovascular stent-supported coil were discharged
from the hospital and the chance for a fair to excellent
long-term outcome was high. Despite these promising
findings, it is important to remember that stent-supported
coil placement is technically challenging and requires spe-
cific training.
The objectives of our study were to evaluate short-term
(3 months) outcome of dogs with IHPSS treated with PTCE,
including changes in selected hematologic, biochemical, and
imaging findings that pertain to liver size and function. We
hypothesized that complications associated with PTCE
would be uncommon, and that most dogs would be dis-
charged from the hospital. We also hypothesized that clinical
signs, blood analyses, and diagnostic imaging biomarkers
would improve after PTCE.
2 | MATERIALS AND METHODS
2.1 | Study population
Dogs diagnosed with an IHPSS at the William R. Pritchard
Veterinary Medical Teaching Hospital at the University of
California-Davis from 2010 to 2015 were prospectively
enrolled in the clinical study and treated with PTCE after
informed owner consent. The study was approved by the
Institutional Animal Care and Use Committee. In this study,
all dogs (n5 25) are included in the prospective evaluation
of clinical outcome (“Clinical Outcome” group) and a sub-
group of dogs (15/25) are included in the assessment of diag-
nostic imaging findings (“Imaging” subgroup).
The medical management of all dogs was prospectively
standardized pre-PTCE and post-PTCE. Before surgery, all
dogs were treated with amoxicillin (22 mg/kg orally twice
daily), lactulose (orally, at a dose to maintain soft but formed
feces), famotidine (0.5 mg/kg orally twice daily), and fed a
prescription diet (Hill’s Prescription Diet l/d Canine, Topeka,
Kansas) for at least 4 weeks. All dogs were weaned from
medications at the same rate over 3 months after PTCE, so
that all medications were discontinued prior to final post-
treatment assessment.
2.2 | PTCE procedure
A contrast-enhanced CT scan was performed prior to PTCE
in all cases as previously described.30,31 The diameter of the
caudal vena cava was measured in 2 perpendicular planes on
several CT images. Measurements were averaged, and a stent
of a diameter approximately 20% greater than this average
was selected.
Dogs were anesthetized with a protocol determined by
the anesthetist. Dogs were placed in dorsal recumbency, and
the ventral neck prepared for aseptic surgery. A stab incision
was made over the right jugular vein with a #11 blade. An
18-gauge
over-the-needle catheter (Becton, Dickinson and
Company, Franklin Lakes, New Jersey) was placed in the
jugular vein, and the needle removed. A 0.035-inch 3
180 cm long hydrophilic guide wire (Weasel Wire, Infiniti
Medical, Menlo Park, California) was introduced into the
over-the-needle catheter and advanced into the caudal vena
cava under fluoroscopic guidance. The catheter was removed
over the guidewire, and a 12 French vascular access sheath
(Introducer Sheath, Infiniti Medical, Menlo Park, California)
was placed into the jugular vein.
The IHPSS was selected with a hook catheter (Cobra
Catheter, Infiniti Medical) that was passed over the guide
wire into the IHPSS. The guide wire and hook catheter com-
bination was then passed into the portal venous system, and
the guide wire removed. The hook catheter hub was attached
to pressure tubing, and the pretreatment portal venous
2 | CULP ET AL.
pressure was measured. The cranial vena cava pressure was
measured from the sidearm of the vascular access sheath. A
second guide wire and a straight marker catheter (Infiniti
Medical) combination were advanced through the vascular
access sheath into the caudal vena cava. A portogram and
caudal vena cavogram were performed simultaneously to
determine the location of the shunt ostium at the level of the
vena cava. When the site intended for placement of the stent
was located, the marker catheter and hook catheter were
removed. A stent of predetermined diameter was placed over
the guide wire and deployed across the opening of the shunt
ostium in the caudal vena cava. The guide wire was then
used to select the IHPSS and portal vein (through the stent
interstices) and a hook catheter was reintroduced into the
IHPSS and portal vein to determine the portal system pres-
sures (after removal of the guide wire). The hook catheter
was left within the portal system, and a second hook catheter
was introduced into the IHPSS over a guide wire to deliver
coils. When the hook catheter was in position, pushable
thrombogenic coils (Cook Medical, Inc, Bloomington, Indi-
ana) were placed into the IHPSS by passing a 0.035 inch 3
180 cm long PTFE guide wire (Bentson Wire, Infiniti Medi-
cal). After delivery of each coil, the portal pressure was
determined. The authors aimed for a pressure gradient
between the portal system and cranial vena cava of 7 mm
Hg. After delivery of all coils, the hook catheters and vascu-
lar access sheath were removed over a guide wire. A 7
French triple lumen catheter (Arrow, Teleflex, Morrisville,
North Carolina) was placed into the jugular vein over the
guide wire. The guide wire was removed when the triple
lumen catheter was appropriately placed. The triple lumen
catheter was removed 1-2 days post-PTCE.
Duration of PTCE procedure, duration of anesthesia, size
of the caval stent, number of coils placed, precoil delivery
portal and caval pressures, postcoil delivery portal and caval
pressures, and procedural complications were recorded.
2.3 | Clinical evaluations
Clinical signs were recorded via questionnaire before and
after PTCE in all dogs. The questionnaire included specific
questions about the presence of clinical signs such as
vomiting, diarrhea, seizures, ataxia, head pressing, “star-
gazing,” lethargy, unresponsiveness, stranguria, hematuria,
pollakiuria, polyuria, and polydipsia as well as the consis-
tency of stool, color of stool, and energy level. A complete
physical examination was performed in all dogs before
treatment. A complete blood count (CBC), chemistry panel,
and preprandial and postprandial bile acids were evaluated.
All dogs were hospitalized for 3 days post-PTCE to moni-
tor for immediate postoperative complications. Each dog
was reevaluated 3 months post-PTCE with a physical
examination and bloodwork consisting of a CBC, chemis-
try panel, and preprandial and postprandial bile acids.
Abnormal clinical signs were recorded.
Improvement in clinical laboratory values was defined as
an increase in hematocrit (Hct), mean corpuscular volume
(MCV), mean corpuscular hemoglobin concentration
(MCHC), blood urea nitrogen (BUN), glucose, total protein,
albumin, and cholesterol. A decrease in the following values
post-PTCE was also considered an improvement: alanine
transaminase (ALT), aspartate transaminase (AST), alkaline
phosphatase (ALP), and gamma-glutamyl transferase (GGT)
post-PTCE.
2.4 | Imaging evaluations
Abdominal ultrasonography was performed on 15 dogs in
dorsal recumbency. Shunt diameter, velocity of flow through
the shunt, portal vein blood flow velocity, and visibility of
intrahepatic portal vein branches were recorded.
Per-rectal portal scintigraphy was performed with a
gamma camera (Technicare Omega 500, Solon Ohio, or IS2,
Ottawa, Canada) and 3-5 mCi (99mTc) technetium pertechne-
tate (99mTcO4; Cardinal Health, Sacramento, California) in
0.2-0.4 mL volume deposited rectally via 5 French soft rub-
ber catheter in fully conscious dogs. A 128 3 128 matrix
with 2 seconds frame rate was acquired for 120 seconds with
dogs positioned in lateral recumbency. Shunt status was
determined by generating time activity curves of the heart
and liver, with positive shunting defined by detection of radi-
onuclide in the heart prior to, or simultaneous with, detection
in the liver. Shunt fractions were calculated for each study
(Mirage, Segami Corporation, Columbia, Maryland).
CT-angiography was performed on anesthetized dogs
with a Lightspeed 16 helical scanner (General Electric Co,
Milwaukee, Wisconsin). All sequences were acquired under
positive pressure breath hold. A dynamic scan was acquired
with a power injector (Vistron CT, Medrad, Inc, Warrendale,
Pennsylvania) and an injection rate of 5 mL/s into the
cephalic vein with 220 mg I/kg of nonionic iodinated con-
trast medium (Isovue 300, Bracco Diagnostics, Inc, Prince-
ton, New Jersey). Image collimation for the dynamic scan
was 5 mm with a 1 second tube rotation and interval, and a
total of 60 images. The dynamic scan was located cranial to
the right kidney near the porta hepatitis. Time attenuation
curves were used to plan the dual phase CT-angiography
scan. The dual phase scan was performed with acquisition
parameters of 880 mg I/kg at 5 mL/s injection rate, 2.5 mm
image collimation in a soft tissue algorithm, 120 kVp, and a
150 mA and 0.625 mm image thickness reformatting as
needed. Images in the arterial phase were obtained from the
porta hepatis to the diaphragm, and in the portal phase from
the caudal thorax to the pelvis.
CULP ET AL. | 3
Liver volume was derived from CT-angiography, imme-
diately before and 3 months after PTCE, using a planimetric
method (GE Advantage Workstation 4.4, General Electric
Co, Milwaukee, Wisconsin).23 Liver volume was normalized
to body size by calculating volume per kg body mass for pre-
procedural and postprocedural volume estimates. The range
of normal liver volume was defined as 24.56 5.6 cm3/kg, as
determined in a previous study.23 Liver perfusion was calcu-
lated using a liver tumor protocol (GE Advantage Worksta-
tion 4.4, General Electric Co). Regions of interest were
placed in the aorta and portal vein, and corrected for respira-
tory motion. Hepatic arterial fraction (arterial blood flow/
total blood flow), blood flow, blood volume, and permeabil-
ity surface area product were measured using regions of
interest on the generated perfusion maps. The presence of
intrahepatic portal vein branches was also recorded.
The anatomy of the origin and termination of the shunt
vessels was determined from the portal phase of the dual
phase CT-angiography scan. Shunts were described as right-,
left-, and central-divisional. The presence of additional intra-
hepatic and extrahepatic anomalous vessels was recorded.
The portal and splenic vein diameters were measured on
transverse images and were normalized to body mass. Exist-
ing and new portal branches were noted pre-PTCE and post-
PTCE.
2.5 | Statistical analysis
CBC and serum biochemical profile values were expressed
as medians
and ranges. The Wilcoxon signed rank test for
paired data was used to compare dogs’ bloodwork values
before and after PTCE. Bloodwork values were also catego-
rized as being within or not within normal reference ranges.
McNemar’s chi-squared statistic was used to make pairwise
comparisons of the proportions of dogs with bloodwork val-
ues within the normal range before and after PTCE, and the
proportions of dogs that experienced clinical signs attribut-
able to IHPSS before and after PTCE. All tests were 2-sided
and P< .05 was considered statistically significant. For the
imaging subgroup, variables were analyzed using paired t
tests, Wilcoxon signed-rank tests, and multinomial logistic
regression. Statistical analysis was performed with the use of
computer software (Stata Statistical Software: Release 12,
College Station, Texas).
3 | RESULTS
3.1 | Enrollment and signalment
Twenty-five dogs were enrolled in the study. The breeds
enrolled in the Clinical Outcome group included Labrador
Retriever (n5 7), Golden Retriever (4), Australian Shepherd
(2), Labradoodle (2), Alaskan Malamute (1), Border Collie
(1), Brittany (1), English Bulldog (1), Siberian Husky (1),
Irish Wolfhound (1), Miniature Schnauzer (1), and Toy Poo-
dle (1), as well as 2 mixed breed dogs. Eleven dogs were
male intact, 4 dogs were male castrated, 7 dogs were female
intact, and 3 dogs were female spayed. The median age of the
dogs at the time of PTCE was 10 months (range, 6-31
months), and median weight was 20.3 kg (range, 1.6-35.4 kg).
Clinical outcomes were assessed in all dogs of the study.
Imaging studies were obtained in 15/25 dogs. This subgroup
consisted of Labrador Retriever (n5 4), Golden Retriever
(4), Labradoodle (1), Alaskan Malamute (1), Australian
Shepherd (1), Border Collie (1), English Bulldog (1), Irish
Wolfhound (1), and mixed breed (1). Seven dogs were male
intact, 3 dogs were male castrated, 3 dogs were female intact,
and 2 dogs were female spayed. The median age of the dogs
at the time of treatment was 9 months (range, 6-31 months),
and median weight was 22.2 kg (range, 16.1-35.4 kg).
3.2 | Physical examination and clinical signs
The physical examination was considered unremarkable in
20 dogs; physical examination abnormalities included der-
matologic disease (alopecia and scaling in 4 dogs) and a
grade 4/6 right apical heart murmur (ventricular septal
defect) in one dog. Subjectively, the investigators considered
20/25 dogs (80%) as small for their age. The median age that
clinical signs were first noted was 4 months old (range, 2-20
months). The following clinical signs were noted before
PTCE and prior to medical management: lethargy (n5 19),
ataxia (18), polydipsia (11), head pressing (9), polyuria (9),
vomiting (8), “star-gazing” (7), poor appetite (6), lack of
responsiveness when called (4), pica (4), ptyalism (4), seiz-
ures (4), aggressiveness (3), circling (3), tremors (2), and
tarry stools (1). Prior to study enrollment and initiation of the
strict pre-PTCE medical management protocol described
above, 25/25 dogs were receiving varying forms of medical
management for a median of 4 months (range, 1-29 months).
After the initiation of medical management alone, clinical
signs improved in 21/25 dogs but did not resolve in any dog.
After treatment, dogs were less likely to show clinical
signs such as vomiting (P5 .005), seizures (P5 .046), ataxia
(P< .001), head pressing (P5 .005), “star-gazing”
(P< .001), lethargy (P< .001), low energy level (as com-
pared to other dogs, P< .001), unresponsiveness (P5 .046),
polyuria (P5 .005), and polydipsia (P5 .007).
3.3 | Clinical laboratory values
Pretreatment clinical laboratory abnormalities included
(Table 1): anemia (13/25; 52%)-microcytic and normochro-
mic in 8 dogs and microcytic and hypochromic in 5 dogs,
4 | CULP ET AL.
decreased BUN (25/25; 100%), hypoproteinemia (21/25;
84%), hypoalbuminemia (23/25; 92%), hypoglobulinemia (8/
25; 32%), hypocholesterolemia (13/25; 52%), and hypoglyce-
mia (8/25; 32%), increased alanine aminotransferase (ALT,
14/25; 56%), increased aspartate aminotransferase (AST,
14/25; 56%), increased alkaline phosphatase (ALP, 20/25;
80%), and increased gamma-glutamyl transpeptidase
(GGT, 5/25; 20%). Preprandial and postprandial bile acids
were increased in 72% and 94% of dogs before PTCE,
respectively.
After treatment, preprandial and postprandial bile acids
values were lower than pre-PTCE values in 52% and 29% of
dogs, respectively, but remained greater than normal in 76%
and 94% of dogs. MCV (P5 .03), BUN (P< .01), total pro-
tein (P< .01), albumin (P< .01), cholesterol (P< .01), ALP
(P5 .04), and GGT (P5 .01) were improved at 3 months
post-PTCE, by a minimum of 50% of their initial value
(Table 1). The proportion of dogs with normal values for
MCV (P5 .03), BUN (P5 .03), and total protein (P5<.01)
was greater after than before treatment.
3.4 | Procedure
Selected stents measured 80 mm in length, and 10 mm
(n5 1), 18 mm (1), 20 mm (2), 22 mm (13), 24 mm (7), and
26 mm (1) in diameter. All stents were caval stents (Infiniti
Medical), except the 10 mm diameter stent which was a ure-
thral stent (Infiniti Medical) and was chosen due to the
patient’s size (Miniature Poodle; 1.6 kg). All deployed coils
were 8 mm diameter and 5 cm long. The median number of
coils deployed per case was 12 coils with a range of 1-18
coils; a single coil was placed in 2 dogs, which were the
smallest 2 dogs in the study (Miniature Poodle: 1.6 kg and
TABLE 1 Comparison of complete blood count and serum biochemical profile values pre-PTCE and post-PTCE among 24 dogs with IHPSS
Value
pre-PTCEa
Value
post-PTCEa P valueb
In normal range
pre-PTCEc
In normal range
post-PTCEc P valued
Value improved
post-PCTEc
Hct 39.6 (26.7-50.5) 41.9 (32.2-52.0) 0.09 12 (50.0) 16 (67.7) 0.21 16 (67.7)
MCV 58.1 (46.0-62.3) 60.3 (48.8-85.0) 0.03 0 (0.0) 5 (20.8) 0.03 18 (75.0)
MCHC 32.1 (29.1-35.1) 32.8 (18.8-37.8) 0.32 8 (33.3) 12 (50.0) 0.25 16 (66.7)
BUN 4 (1-8) 6 (2-35) <0.01 0 (0.0) 5 (20.8) 0.03 18 (75.0)
Glu 90 (42-113) 89 (33-125) 0.75 15 (62.5) 14 (58.3) 0.78 13 (54.2)
TP 4.7 (2.1-6.1) 5.3 (3.8-6.4) <0.01 4 (16.7) 11 (45.8) <0.01 17 (70.8)
Alb 2.8 (0.9-3.7) 3.1 (2.4-3.8) <0.01 2 (8.3) 5 (20.8) 0.18 18 (75.0)
Glob 1.9 (0.9-2.8) 2.1 (1.2-3.3) 0.08 17 (70.8) 20 (83.3) 0.08 16 (67.7)
ALT 93 (24-441) 78 (28-295) 0.41 10 (41.7) 10 (41.7) 1.00 12 (50.0)
ASTe 52 (29-241) 46 (24-173) 0.20 10 (43.5) 12 (52.2) 0.56 13 (56.5)
ALP 147 (52-600) 110 (48-374) 0.04 4 (16.7) 8 (33.3) 0.10 17 (70.8)
GGTe 3 (1-295) 2 (0-88) 0.01 18 (78.3) 21 (91.3) 0.18 16 (69.6)
Chol 128 (3-430) 176 (77-440) <0.01 11 (45.8) 17 (70.8) 0.08 19 (79.2)
BA-pref 95 (4-227) 25 (2-207) 0.21 4 (22.2) 4 (23.5) 1.00 12 (52.2)
BA-posg 125 (1-440) 119 (10-395) 0.71 1 (5.9) 1 (5.9) 1.00 5 (29.4)
Abbreviations: Alb, albumin; ALP, alkaline phosphatase; ALT, alanine transaminase; AST, aspartate transaminase; BA-pos, bile acids-postprandial; BA-pre, bile
acids-preprandial; BUN, blood urea nitrogen; GGT, gamma-glutamyl transferase; Glob, globulins; Glu,; Hct, hematocrit; MCHC, mean corpuscular hemoglobin con-
centration; MCV, mean corpuscular volume; PTCE, percutaneous transvenous coil embolization; TP, total protein.
aMedian (range).
bSigned rank test for matched pairs.
cNumber (percent).
dMcNemar’s chi-square test for matched pairs.
eData only available for 23 dogs.
fData only available for 18 dogs pre-PTCE and 17 dogs post-PTCE.
gData only available for 17 dogs.
CULP ET AL. | 5
T
A
B
L
E
2
C
lin
ic
al
,l
ab
or
at
or
y
va
lu
es
,a
nd
im
ag
in
g
fin
di
ng
s
of
th
e
do
gs
in
th
e
im
ag
in
g
su
bg
ro
up
H
em
at
oc
ri
t
B
U
N
G
lu
co
se
T
ot
al
pr
ot
ei
n
A
lb
um
in
C
ho
le
st
er
ol
Pr
e-
pr
an
di
al
bi
le
ac
id
s
P
os
t-
pr
an
di
al
bi
le
ac
id
s
H
ep
at
ic
vo
lu
m
e
H
ep
at
ic
ar
te
ri
al
fr
ac
tio
n
Sh
un
t
fr
ac
tio
n
Im
pr
ov
ed
N
or
m
al
po
st
-
PT
C
E
Im
pr
ov
ed
N
or
m
al
po
st
-
PT
C
E
Im
pr
ov
ed
N
or
m
al
po
st
-
PT
C
E
Im
pr
ov
ed
N
or
m
al
po
st
-
PT
C
E
Im
pr
ov
ed
N
or
m
al
po
st
-
PT
C
E
Im
pr
ov
ed
N
or
m
al
po
st
-
PT
C
E
Im
pr
ov
ed
po
st
-
PT
C
E
Im
pr
ov
ed
po
st
-
P
T
C
E
R
es
ol
ut
io
n
of
cl
in
ic
al
si
gn
s
po
st
-
P
T
C
E
in
cr
ea
se
d
(im
pr
ov
ed
)
po
st
-
P
T
C
E
de
cr
ea
se
d
(im
pr
ov
ed
)
po
st
-
P
T
C
E
M
ul
tip
le
IH
P
SS
pr
e-
P
T
C
E
M
ul
tip
le
IH
P
SS
po
st
-
P
T
C
E
de
cr
ea
se
d
(im
pr
ov
ed
)
po
st
-
P
T
C
E
1
18
M
O
FS
G
ol
de
n
R
et
ri
ev
er
-
1
1
-
-
-
-
1
-
1
1
1
-
-
-
1
-
-
-
1
2
15
M
O
FS
L
ab
ra
do
r
R
et
ri
ev
er
-
1
-
-
-
-
-
-
-
-
1
1
-
-
-
-
1
-
1
st
at
ic
3
7
M
O
M
A
us
tr
al
ia
n
Sh
ep
he
rd
1
-
1
-
1
1
-
-
-
-
-
1
1
1
-
1
1
-
-
1
4
7
M
O
F
Ir
is
h
W
ol
fh
ou
nd
1
1
-
-
-
-
1
-
1
-
1
1
-
-
-
-
1
-
-
1
5
9
M
O
M
C
G
ol
de
n
R
et
ri
ev
er
1
1
1
-
1
1
1
-
1
-
1
1
-
-
1
1
1
1
1
-
6
31
M
O
M
B
or
di
e
C
ol
lie
-
1
1
-
1
1
1
-
1
-
1
1
-
-
-
1
1
1
1
-
7
11
M
O
M
G
ol
de
n
R
et
ri
ev
er
1
-
1
-
-
-
1
1
1
-
-
1
1
-
-
1
1
-
1
-
8
6
M
O
M
L
ab
ra
do
r
R
et
ri
ev
er
1
-
1
-
1
1
1
-
1
-
1
1
-
-
-
1
1
-
1
1
9
7
M
O
M
L
ab
ra
do
r
R
et
ri
ev
er
1
1
1
-
1
1
1
1
1
-
1
1
1
-
-
-
1
-
-
-
10
18
M
O
M
C
L
ab
ra
do
od
le
1
1
-
-
1
-
1
-
1
-
1
-
-
-
-
st
at
ic
1
-
1
-
11
6
M
O
F
A
la
sk
an
M
al
am
ut
e
1
1
1
-
-
1
1
1
1
1
1
-
-
-
1
1
1
1
1
1
12
9
M
O
M
E
ng
lis
h
B
ul
ld
og
1
1
1
-
1
1
1
1
1
-
-
1
-
-
-
1
1
1
1
-
13
6
M
O
F
G
ol
de
n
R
et
ri
ev
er
1
-
1
-
-
-
1
-
1
-
-
-
1
-
-
-
1
-
-
1
14
10
M
O
M
C
L
ab
ra
do
r
R
et
ri
ev
er
-
1
1
-
1
1
1
-
1
-
1
1
-
-
-
1
1
1
1
1
15
23
M
O
M
m
ix
ed
br
ee
d
do
g
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
1
1
-
-
-
A
bb
re
vi
at
io
ns
:
PT
C
E
,p
er
cu
ta
ne
ou
s
tr
an
sv
en
ou
s
co
il
em
bo
liz
at
io
n;
1
,y
es
;
-,
no
.
6 | CULP ET AL.
Miniature Schnauzer: 6.7 kg). The median caval and portal
pressures before PTCE were 6 and 7.5 mm Hg (range,
4-8 mm Hg and 5-10 mm Hg), respectively. The median
caval and portal pressures after PTCE were 6 and 13 mm Hg
(range, 4-8 mm Hg and 10-15 mm Hg), respectively. The
median PTCE procedure time was 153 minutes (range, 110-
240 minutes), and the median total anesthesia time was 238
minutes (range, 160-355 minutes).
3.5 | Complications
Intraprocedural complications occurred in 2 cases; in both
cases, the portal: caval pressure gradient rose above the goal
of 7 mm Hg after placement of one coil. A hook catheter
was used in both cases to engage the coil and alter the posi-
tion until the pressure gradient decreased. Post-PCTE com-
plications occurring prior to discharge included bleeding
from the jugular catheter site (2 dogs), which eventually
resolved with sustained digital pressure. Complications
occurring by the 3-month post-PTCE time point included
lack of resolution of clinical signs related to the neurologic
system (1 dog) and continued polyuria/polydipsia (1 dog). In
the dog with persistent neurologic-related clinical signs,
medications (amoxicillin and lactulose) had been discontin-
ued without complication until 2 months post-PTCE, when
ataxia, lethargy, and head pressing were noted. Medications
were reinitiated and clinical signs resolved completely. In
both dogs with lack of resolution of signs, CT scan and
potential addition of coils had been recommended but
declined by owners.
3.6 | Portal scintigraphy
All dogs with diagnostic quality scintigraphic studies (pre-
PTCE n5 12, post-PTCE n5 13) had positive scans for
portosystemic shunting. The mean pre-PTCE shunt fraction
was 0.82 (SD 0.15, 0.49-0.96), and the mean post-PTCE
shunt fraction was 0.70 (SD 0.17, 0.45-0.91). Two of 10
dogs with pre-PTCE and post-PTCE shunt fractions avail-
able had an increase in shunt fraction, 1 remained static,
and 7/10 had a decrease in shunt fraction. The decrease in
shunt fraction was not statistically significant (P5 .13),
and no dogs had post-PTCE shunt fractions within the nor-
mal range. All dogs had elevated shunt fractions post-
PTCE.
3.7 | Ultrasonographic evaluation
Abdominal ultrasonographic findings were recorded for all
15 dogs on the pre-PTCE visit, and for 14/15 dogs at the
post-PTCE visit. A single intrahepatic shunt was visualized
in 13/15 dogs (87%) pre-PTCE and in 13/14 dogs (93%)
post-PTCE. The liver size was subjectively described as
small initially in all dogs (100%) and was subjectively small
in 11/14 (79%) and normal in 3/14 (21%) post-PTCE. Intra-
hepatic portal veins were not visualized in 5/15 dogs (33%)
and were small in 10/15 dogs pre-PTCE (67%). Post-PTCE,
intrahepatic portal veins were not seen in 1/14 dogs (7%),
were small in 10/14 dogs (71%), and were normal in 3 dogs
(21%).
Doppler flow measurement of the mean portal vein
velocity was not different prior to (24.73 m/s, SD 18.32) and
after PTCE (25.78 m/s, SD 15.49) (P5 .84). Doppler flow
velocity within the shunt seemed to decrease (pre-PTCE
24.60 m/s, SD 30.40, post-PTCE 14.90 m/s, SD 12.25), but
values did not differ statistically (P5 .34).
3.8 | Computed tomography-angiography
3.8.1 | Shunt morphology
There were 4/15 (27%) central divisional shunts, 9/15 (60%)
left divisional shunts, and 2/15 (13%) right divisional shunts
as assessed by CT-angiography. In 5/15 (33%) dogs, multiple
small vascular connections between the portal system and
the hepatic veins or caudal vena cava were noted on pre-
PTCE images. The vessels were often small and tortuous
with a maximum size similar to the adjacent hepatic veins.
Smaller groups of vessels were very fine and interwoven,
causing a blush of contrast enhancement regionally. Post-
PTCE, these multiple IHPSS tended to increase in size and
conspicuity. An additional 4 dogs had multiple IHPSS post-
PTCE for a total of 9/15 (69%) dogs (Figure 1). All of the
dogs with multiple IHPSS pre-PTCE had left divisional con-
formation. Two dogs with central divisional, 1 dog with left
divisional, and 1 dog with right divisional shunts developed
post-PTCE multiple IHPSS.
3.8.2 | Vascular size
Visible right intrahepatic portal branches were present in 7/
15 (47%) dogs pre-PTCE and in 10/15 (67%) dogs post-
PTCE, 3 of which had increased in size (Figure 2). Vessels
branching from the shunt were present in 9/15 (60%) dogs at
both time points. In 6/15 (40%) dogs, new portal branches
developed post-PTCE.
The hepatic veins were tortuous in 6/15 dogs (40%) on
the pre-PTCE images and in 11/15 dogs (73%) post-PTCE.
Periportal edema was noted in 4/15 (27%) dogs and periarte-
rial edema was seen in 1/15 dogs (7%) post-PTCE.
The mean portal vein diameter was 1.40 cm (SD 0.27)
pre-PTCE and increased to 1.49 cm (SD 0.27) post-PTCE.
After correcting for body mass, this was not statistically sig-
nificant (P5 .10). The maximum shunt diameter increased
CULP ET AL. | 7
from 1.75 cm (SD 0.32) to 2.04 cm (SD 0.40) (P5 .01). The
hepatic artery diameter (pre-PTCE 2.77 mm, SD 2.23, post-
PTCE 3.01 mm, SD 2.48, P5 .23) and splenic vein diameter
(pre-PTCE 3.88 mm, SD 3.15, post-PTCE 4.36, SD 3.58,
P5 .95) did not change in size significantly after correcting
for body weight.
FIGURE 1 Pre-PTCE (A) and post-PTCE (B) MIP thick slab CT angiographic images of a dog with a left divisional intrahepatic portosystemic shunt.
Note the fine, tortuous vessels in the cranial and right side of the liver connecting the shunt (*) and hepatic veins (V) to the caudal vena cava (C). On post-
PTCE images, the size of these tortuous vessels is increased. The stent and coils are visible in the shunt and caudal vena cava; one coil position is away from
the shunt ostium. Abbreviations: CT, computed tomography;MIP, maximum intensity projection; PTCE, percutaneous transvenous coil embolization
FIGURE 2 Pre-PTCE (A, C) and post-PTCE (B, D) CT angiographic images of dogs with portosystemic shunts. Small right portal branches (A)
were capable of enlargement (*) post-PTCE (B). Periportal edema (B) was visible in 4/15 dogs
after surgery. In some dogs with no visible portal branch
pre-PTCE (C), branches did not develop post-PTCE (D). Hepatic hypertrophy of the right caudal lobe was noted in both cases (B, D). Abbreviations: CT,
computed tomography; PTCE, percutaneous transvenous coil embolization
8 | CULP ET AL.
At the junction of the shunt with the caudal vena cava,
the mean length of the shunt was 66.87 mm (SD 10.53) and
the mean width was 23.07 mm (SD 5.84). The size of the
caudal vena cava increased significantly at each level after
placement of the stent.
3.8.3 | Liver volume and perfusion
Liver volume was below the normal range (24.56
5.6 cm3/kg) in 14/15 dogs pre-PTCE with a mean of
12.80 mL/kg (SD 3.15, 8.22-18.98).23 Post-PTCE, mean
liver volume increased to 16.13 mL/kg (SD 4.49, 8.21-
25.10, P5 .001) (Figure 3). Two of 15 dogs had liver vol-
ume per kg in the normal range post-PTCE (22.93 and
25.1 mL/kg). Four of 15 dogs had a slight decrease in liver
volume per kg post-PTCE, and 1 stayed static in size.
Dogs with the largest post-PTCE liver volume per kg had
smaller initial liver volumes and had larger increases in
liver volume compared to those with higher initial liver
volume per kg (P5 .013) (Figure 3). There was a trend to
decreased liver volume per kg post-PTCE in dogs with
multiple IHPSS; however, this was not statistically signifi-
cant (P5 .11).
The hepatic arterial fraction was elevated in 14/15 dogs
pre-PTCE (>31%). There was a significant decrease in
hepatic arterial fraction post-PTCE (P5 .029), and 3 dogs
had a hepatic arterial fraction in the normal range. The per-
meability surface, blood flow, and blood volume did not
change significantly after shunt attenuation (P> .05).
There was a negative correlation between pre-PTCE
hepatic arterial fraction and post-PTCE liver volume
(P5 .015) (Figure 4). One dog had a hepatic arterial fraction
in the normal range pre-PTCE (27%), which improved
slightly post-PTCE (21%). The initial liver volume was high
in this dog (18.98 mL/kg) and decreased slightly after shunt
attenuation (18.35 mL/kg). The dog with the lowest post-
PTCE hepatic arterial fraction (3%) had one of the lower pre-
PTCE hepatic arterial fractions (59%) and the largest increase
in liver volume (12.39 mL/kg pre-PTCE, 25.10 mL/kg post-
PTCE). Hepatic arterial fraction had a trend to correlate with
shunt fraction pre-PTCE (P5 .053), but was not correlated
with post-PTCE (P5 .94).
3.9 | Outcome
All dogs were discharged from the hospital. Twenty-four
of 25 dogs were available for reevaluation at 3 months; 1
dog was hit by a car approximately 1 week after PTCE and
was euthanatized due to a poor prognosis secondary to the
severity of the trauma. All clinical signs had resolved in
22/24 dogs (92%). In the 2 dogs with clinical signs, 1 dog
was ataxic, lethargic, and demonstrated head pressing, and
1 dog had polyuria/polydipsia as well as urate crystalluria.
4 | DISCUSSION
The 25 dogs with IHPSS treated via PTCE in this study were
discharged from the hospital and 22 of 24 that were eval-
uated 3 months after treatment were free of clinical signs.
PTCE was associated with uncommon and minor complica-
tions, and led to an improvement in bloodwork abnormalities
and liver perfusion in most dogs. Portal blood flow to the
liver and liver volume increased in most of the 15 dogs
imaged after PTCE. These findings are consistent with
FIGURE 3 Pre-PTCE and post-PTCE liver volumes in dogs treated
with PTCE. Dogs with smaller pre-PTCE volumes had the largest
increases post-PTCE. Most dogs remained below the normal range (refer-
ence lines) for liver volume. Abbreviation: PTCE, percutaneous transve-
nous coil embolization
FIGURE 4 High pre-PTCE hepatic arterial fraction correlated nega-
tively with post-PTCE liver volume. Hepatic arterial fraction and liver vol-
ume remained out of normal range post-PTCE. Reference lines indicate
normal hepatic arterial fraction and liver volume. Abbreviations: HAF,
hepatic arterial fraction; PTCE, percutaneous transvenous coil
embolization
CULP ET AL. | 9
hepatic hypertrophy in response to shunt attenuation, which
is a goal of this therapy.
The initial clinical signs in this cohort of dogs were
mainly related to the neurologic, gastrointestinal, and urinary
systems with signs such as lethargy, exercise intolerance,
head pressing, polyuria/polydipsia, “star-gazing”, ataxia, and
vomiting predominating. The pretreatment medical manage-
ment of dogs with IHPSS generally consists of medications
and protein-restricted prescription diets aimed at controlling
the clinical signs often associated with IHPSS. It is important
to note that medical management improved clinical signs in
all dogs of the study but did not lead to resolution of signs.
The authors standardized pretreatment and posttreatment
medical management to allow close monitoring of the
response to treatment. Dogs were weaned off medications
over 3 months, although the time required for sufficient
attenuation of the shunt secondary to coil placement is
unclear. Similarly, the time required for blood flow to
become sufficient enough to enhance liver function and
allow cessation of clinical signs is unknown. In this study,
22/24 dogs were clinically normal and did not require medi-
cation to control IHPSS-related signs.
Treatment of IHPSS aims at altering the flow of blood
away from the shunt and toward the liver, subsequently
increasing liver perfusion and filtration, thereby enhancing
hepatic function. Parameters of hepatocellular function were
improved in most dogs by 3 months, glucose and cholesterol
increasing in over 50% dogs, and BUN, total protein, and
albumin values increasing in approximately 70%-80% dogs.
Such changes have been associated with a greater likelihood
of excellent outcome in dogs undergoing endovascular treat-
ment of IHPSS.10
Liver volume increased after PTCE but remained lower
than normal, based on CT imaging. Ultrasonographic assess-
ment of portal vascularity and liver volume was not found to
be sensitive. The relative change in liver volume is techni-
cally much more difficult to quantify via ultrasonography,
and evaluation of liver volume and vascularity was more
subjective than via CT.
Five dogs had multiple IHPSS identified prior to PTCE,
all consisting of left divisional shunts. These small, tortuous
vessels tended to connect the portal system with intrahepatic
veins or the caudal vena cava in the cranial portion of the
liver. Others were present in the caudal portion of the liver,
or had multiple connections cranially and caudally. Pre-
PTCE, they were very small and difficult to follow on CT
imaging. Post-PTCE, the vessels became larger in diameter
with increased conspicuity, and may explain the post-PTCE
detection of multiple IHPSS that were not detected before
treatment in 4 dogs. Alternatively, these vessels may have
developed de novo, due to increased intrahepatic portal
resistance and pressures postattenuation. The clinical
importance of these vessels still remains to be elucidated.
Depending on the individual anatomy and underlying pathol-
ogy of these vessels, knowledge of these vessels pretreatment
may allow treatment during the same initial PTCE or prepa-
ration for treatment during a future PTCE.
Shunt fractions were initially elevated in all dogs and
hepatic arterial fraction was elevated in all but one case.
Scintigraphic measurement of shunt fraction represents the
proportion of blood bypassing the liver, and hepatic arterial
fraction measures the proportion of portal and arterial blood
supply to the liver parenchyma.32 Both of these methods
quantify the portal blood supply to the liver in different but
related ways. A significant decrease in hepatic arterial frac-
tion and shunt fraction confirm that portal blood supply to
the liver has increased post-PTCE. All dogs remained with a
shunt fraction above the normal range, which is expected
with a method of partial attenuation. The presence of multi-
ple IHPSS in many dogs would also contribute to a persis-
tently high shunt fraction. Hepatic arterial fraction decreased
in most dogs in response to shunt attenuation.
Posttreatment changes in liver volume correlates inverse-
ly with post-PTCE hepatic arterial fraction, supporting the
concept of regeneration secondary to an improvement in por-
tal blood flow to the liver.25,30 Liver volume increased post-
PTCE in most of the dogs in this cohort. This surrogate mea-
sure of hepatic hypertrophy encompasses increased blood
supply as well as increased cellular and interstitial compo-
nents.20 Similar to a study in dogs undergoing treatment for
extrahepatic shunts, those with IHPSS starting with smaller
liver volumes had the largest increases post-PTCE.25 Only 2
dogs in our cohort had liver volumes in the normal range
post-PTCE, contrasting with the response to shunt attenua-
tion of previously reported dogs with EHPSS.25 Dogs with
IHPSS may be less capable of liver regeneration than those
with EHPSS; however, this could also be due to a variety of
factors including the initial partial attenuation accomplished
by PTCE. These patients were only evaluated 3 months post-
PTCE, and it is possible that liver volume would continue to
increase if blood flow through the shunt were progressively
attenuated over a greater amount of time.
Peri-procedural complications were uncommon and
minor in our cohort of IHPSS dogs undergoing PTCE. The
study investigators required a mandatory 3-day hospitaliza-
tion postprocedure, although most dogs were fully recovered
within 24 hours of the procedure. While complications such
as portal hypertension and seizures after treatment were not
noted in this cohort, these complications should still be con-
sidered with PTCE. As the number of reported PTCE proce-
dures increases, the true occurrence of these life-threatening
complications will be more accurately determined.
The stents used in this study were large, matching the
size of dogs enrolled. The authors tend to measure the vena
10 | CULP ET AL.
cava size from a preprocedure CT-angiography scan and
oversize the stent by at least 10%-20%. In this group of dogs,
this selection process was effective as no stents migrated and
placement was successful in the appropriate location. The
number of coils deployed into the shunt depended on portal
pressure changes during the procedure, as well as fluoro-
scopic evaluation of shunt filling. Coils act as a scaffold for
clot formation within the shunt, leading to gradual occlusion
of the shunt. The coils used in all cases were 8 mm in size,
which is the authors’ preference. However, in the smallest
dog (1.6 kg), placement of an 8 mm coil led to a dramatic
increase in pressure. In the future, the authors will consider
placement of smaller coils in small dogs to prevent sudden
increases in portal pressures.
The main limitation of this study is the absence of con-
trol groups. A negative control group could have included
dogs maintained on medical management, while a reference
group could have included dogs treated with traditional sur-
gical attenuation options (eg, suture ligation, ameroid ring
constrictors, cellophane banding). As a result, we cannot
eliminate the possible influence of the medical management
received by dogs in this study of their short-term success.
Future prospective studies comparing these different treat-
ment regimens should be considered. Further, as the record-
ing of clinical signs was based on questionnaires, it is
possible that bias may have occurred; the lack of “placebo”
group may result in an under-reporting of the presence or the
severity of clinical signs. Additionally, the scope of this
study is limited to short-term outcome (3 months after
PTCE) of dogs with IHPSS, and additional investigations
would be warranted to determine the long-term effects of
this treatment modality. Lastly, while this is the first prospec-
tive study evaluating PTCE in dogs, sample size is limited
and may not represent the entire population of dogs with
IHPSS. The data generated in this study provide a foundation
to calculate sample size in future confirmatory studies.
In conclusion, PTCE appears promising as a treatment
modality for IHPSS, based on a low morbidity, resolution of
clinical signs in all dogs (with medical treatment in 2 of
those), and normalization or improvement in serum biochem-
ical profiles. Increased portal blood supply and arterial vol-
ume were consistent with hepatic regeneration post-PTCE.
CONFLICT OF INTEREST
The authors declare no conflict of interest related to this
report.
ORCID
Allison L. Zwingenberger DVM, MAS, DACVR http://
orcid.org/0000-0002-8982-2558
Michele A. Steffey DVM, DACVS http://orcid.org/0000-
0003-0852-0644
REFERENCES
[1] Hottinger HA, Walshaw R, Hauptman JG. Long-term results of
complete and partial ligation of congenital portosystemic shunts
in dogs. Vet Surg. 1995;24:331-336.
[2] Hunt GB, Kummeling A, Tisdall PL, et al. Outcomes of cello-
phane banding for congenital portosystemic shunts in 106 dogs
and 5 cats. Vet Surg. 2004;33:25-31.
[3] Falls EL, Milovancev M, Hunt GB, Daniel L, Mehl ML,
Schmiedt CW. Long-term outcome after surgical ameroid ring
constrictor placement for treatment of single extrahepatic porto-
systemic shunts in dogs. Vet Surg. 2013;42:951-957.
[4] Krotscheck U, Adin CA, Hunt GB, Kyles AE, Erb HN. Epide-
miologic factors associated with the anatomic location of intra-
hepatic portosystemic shunts in dogs. Vet Surg. 2007;36:31-36.
[5] Frankel D, Seim H, MacPhail C, Monnet E. Evaluation of cello-
phane banding with and without intraoperative attenuation for
treatment of congenital extrahepatic portosystemic shunts in
dogs. J Am Vet Med Assoc. 2006;228:1355-1360.
[6] Hurn SD, Edwards GA. Perioperative outcomes after three dif-
ferent single extrahepatic portosystemic shunt attenuation techni-
ques in dogs: partial ligation, complete ligation and ameroid
constrictor placement. Aust Vet J. 2003;81:666-670.
[7] Winkler JT, Bohling MW, Tillson DM, Wright JC, Ballagas AJ.
Portosystemic shunts: diagnosis, prognosis, and treatment of 64
cases (1993-2001). J Am Anim Hosp Assoc. 2003;39:169-185.
[8] Greenhalgh SN, Dunning MD, McKinley TJ, et al. Comparison
of survival after surgical or medical treatment in dogs with a
congenital portosystemic shunt. J Am Vet Med Assoc. 2010;236:
1215-1220.
[9] Watson PJ, Herrtage ME. Medical management of congenital
portosystemic shunts in 27 dogs—a retrospective study. J Small
Anim Pract. 1998;39:62-68.
[10] Weisse C, Berent AC, Todd K, Solomon JA, Cope C. Endovas-
cular evaluation and treatment of intrahepatic portosystemic
shunts in dogs: 100 cases (2001-2011). J Am Vet Med Assoc.
2014;244:78-94.
[11] White RN, Burton CA, McEvoy FJ. Surgical treatment of intrahe-
patic portosystemic shunts in 45 dogs. Vet Rec. 1998;142:358-365.
[12] Wolschrijn CF, Mahapokai W, Rothuizen J, Rothuizen J, Meyer
HP, van Sluijs FJ. Gauged attenuation of congenital portosyste-
mic shunts: results in 160 dogs and 15 cats. Vet Q. 2000;22:94-
98.
[13] Bright SR, Williams JM, Niles JD. Outcomes of intrahepatic
portosystemic shunts occluded with ameroid constrictors in nine
dogs and one cat. Vet Surg. 2006;35:300-309.
[14] Knapp T, Navalon I, Medda M, et al. A multimodality imaging
approach for guiding a modified endovascular coil embolization
of a single intrahepatic portosystemic shunt in dogs. Res Vet Sci.
2015;103:156-163.
[15] Greenhalgh SN, Reeve JA, Johnstone T, et al. Long-term sur-
vival and quality of life in dogs with clinical signs associated
with a congenital portosystemic shunt after surgical or medical
treatment. J Am Vet Med Assoc. 2014;245:527-533.
[16] Komtebedde J, Forsyth SF, Breznock EM, Koblik PD. Intrahe-
patic portosystemic venous anomaly in the dog. Perioperative
management and complications. Vet Surg. 1991;20:37-42.
CULP ET AL. | 11
http://orcid.org/0000-0002-8982-2558
http://orcid.org/0000-0002-8982-2558
http://orcid.org/0000-0003-0852-0644
http://orcid.org/0000-0003-0852-0644
[17] Parker JS, Monnet E, Powers BE,
Twedt DC. Histologic exami-
nation of hepatic biopsy samples as a prognostic indicator in
dogs undergoing surgical correction of congenital portosystemic
shunts: 64 cases (1997-2005). J Am Vet Med Assoc. 2008;232:
1511-1514.
[18] Adin CA, Sereda CW, Thompson MS, Wheeler JL, Archer LL.
Outcome associated with use of a percutaneously controlled
hydraulic occluder for treatment of dogs with intrahepatic porto-
systemic shunts. J Am Vet Med Assoc. 2006;229:1749-1755.
[19] Hunt GB, Culp WT, Mayhew KN, et al. Evaluation of in vivo
behavior of ameroid ring constrictors in dogs with congenital
extrahepatic portosystemic shunts using computed tomography.
Vet Surg. 2014;43:834-842.
[20] Tivers MS, Lipscomb VJ, Smith KC, Wheeler-Jones CP, House
AK. Markers of hepatic regeneration associated with surgical
attenuation of congenital portosystemic shunts in dogs. Vet J.
2014;200:305-311.
[21] Landon BP, Abraham LA, Charles JA. Use of transcolonic por-
tal scintigraphy to evaluate efficacy of cellophane banding of
congenital extrahepatic portosystemic shunts in 16 dogs. Aust
Vet J. 2008;86:169-179.
[22] Sura PA, Tobias KM, Morandi F, Daniel GB, Echandi RL.
Comparison of 99mTcO4(-) trans-splenic portal scintigraphy
with per-rectal portal scintigraphy for diagnosis of portosystemic
shunts in dogs. Vet Surg. 2007;36:654-660.
[23] Stieger SM, Zwingenberger A, Pollard RE, Pollard RE, Kyles
AE, Wisner ER. Hepatic volume estimation using quantitative
computed tomography in dogs with portosystemic shunts. Vet
Radiol Ultrasound. 2007;48:409-413.
[24] Kummeling A, Vrakking DJ, Rothuizen J, Gerritsen KM, van
Sluijs FJ. Hepatic volume measurements in dogs with extrahe-
patic congenital portosystemic shunts before and after surgical
attenuation. J Vet Intern Med. 2010;24:114-119.
[25] Zwingenberger AL, Daniel L, Steffey MA, et al. Correlation
between liver volume, portal vascular anatomy, and hepatic per-
fusion in dogs with congenital portosystemic shunt before and
after placement of ameroid constrictors. Vet Surg. 2014;43:926-
934.
[26] Asano K, Watari T, Kuwabara M, et al. Successful treatment by
percutaneous transvenous coil embolization in a small-breed dog
with intrahepatic portosystemic shunt. J Vet Med Sci. 2003;65:
1269-1272.
[27] Bussadori R, Bussadori C, Millan L, et al. Transvenous coil
embolisation for the treatment of single congenital portosystemic
shunts in six dogs. Vet J. 2008;176:221-226.
[28] Gonzalo-Orden JM, Altonaga JR, Costilla S, Gonzalo Cordero
JM, Mill�an L, Recio AO. Transvenous coil embolization of an
intrahepatic portosystemic shunt in a dog. Vet Radiol Ultra-
sound. 2000;41:516-518.
[29] Leveille R, Pibarot P, Soulez G, Wisner ER. Transvenous coil
embolization of an extrahepatic portosystemic shunt in a dog: a
naturally occurring model of portosystemic malformations in
humans. Pediatr Radiol. 2000;30:607-609.
[30] Zwingenberger AL, Schwarz T, Saunders HM. Helical computed
tomographic angiography of canine portosystemic shunts. Vet
Radiol Ultrasound. 2005;46:27-32.
[31] Zwingenberger AL, Schwarz T. Dual-phase CT-angiography of
the normal canine portal and hepatic vasculature. Vet Radiol
Ultrasound. 2004;45:117-124.
[32] Zwingenberger AL, Shofer FS. Dynamic computed tomographic
quantitation of hepatic perfusion in dogs with and without portal
vascular anomalies. Am J Vet Res. 2007;68:970-974.
How to cite this article: Culp WTN, Zwingenberger
AL, Giuffrida MA, et al. Prospective evaluation of out-
come of dogs with intrahepatic portosystemic shunts
treated via percutaneous transvenous coil embolization.
Veterinary Surgery. 2017;00:000-000. https://doi.org/
10.1111/vsu.12732
12 | CULP ET AL.
https://doi.org/10.1111/vsu.12732
https://doi.org/10.1111/vsu.12732