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Received: 18 June 2021 Revised: 18 April 2022 Accepted: 28 April 2022

DOI: 10.1002/vrc2.389

CASE REPORT
Companion or pet animals

Treatment of an extrahepatic portosystemic shunt by placement of

a hydraulic occluder followed by a thin film band in a dog: An
eventful story

Margaux Bondel, Victor Morvan Pierre Moissonnier

1
Université de Toulouse, ENVT, Toulouse, France Abstract
2
Campus vétérinaire de Lyon, VetAgro Sup, Marcy A 1-year-old, female, Yorkshire terrier was evaluated for two episodes of disorientation
l’Etoile, Lyon, France and severe depression. A portosystemic shunt was suspected based on clinical signs
and biochemical analysis, and further confirmed by computed tomography angiogra-
Correspondence
Margaux Blondel, Université de Toulouse, ENVT,
phy. After initial stabilisation with medical treatment, the dog underwent surgery. Inva-
Toulouse, France. sive measurement of portal pressure after temporary complete shunt occlusion revealed
Email: margauxblondel05@gmail.com a very high pressure of 40 mmHg, motivating placement of a hydraulic occluder. Sev-
eral complications occurred in the postoperative period, including kinking of the device,
necessitating removal of the hydraulic occluder in emergency; development of signs of
portal hypertension during inflation of the hydraulic occluder, requiring partial bal-
loon deflation; and persistent shunting, which was managed by replacing the hydraulic
occluder by a thin film band.

BACKGROUND episodes of severe depression: the first episode had occurred

Surgery is the recommended treatment for single extrahep-
atic congenital portosystemic shunt (PSS) in dogs and con-
sists of attenuating the shunting vessel to redirect the portal
blood flow to the liver.1–3 Some studies have reported that
approximately 50% of dogs with extrahepatic PSSs can toler-
ate a complete ligation.4 Several methods for gradual attenua-
tion are available, including placement of a cellophane or thin
film band (TFB), an ameroid constrictor (AC), a hydraulic
occluder (HO), or a self-retaining polyacrylic acid-silicone
device.5–10 However, attenuation of an extrahepatic PSS with
an HO has not been reported in the literature.9 The device
used to attenuate the shunt should be carefully selected by tak-
ing into consideration factors related to the patient (clinical
signs, liver size) and to the abnormal vessel (diameter, por-
tal pressure after temporary acute complete occlusion during
surgery). We underline the need for this careful selection by
presenting the complicated but eventually successful surgical
management of an extrahepatic PSS with an HO followed by
a TFB in a dog.
CASE PRESENTATION
A 1-year-old, entire, female Yorkshire terrier presented in an
emergency for disorientation. The dog had presented two
7 days before presentation secondary to ingestion of pork
meat, and the second episode 3 days before, with no obvious
triggering cause. The dog had been treated with corticosteroid
and antibiotic, with only temporary improvement.
At the time of presentation, the dog was severely depressed
and walked in circles. General clinical examination was oth-
erwise normal. Neurological examination revealed decreased
postural reactions in all limbs with intact spinal reflexes and
bilateral absent menace response. Clinical presentation was
suggestive of a diffuse forebrain disorder. Differential diagno-
sis included intracranial hypertension, primary or secondary
encephalopathy and poisoning.
INVESTIGATIONS
Routine blood screening revealed leukocytosis with an
increased neutrophil count and monocytosis (Table 1).
Biochemical abnormalities included hypoglycaemia,
hypouremia, hypoproteinaemia with hypoalbuminemia
and hypoglobulinemia, hyperammonemia, and elevation of
ALT, fasting bile acids and post-prandial bile acids (Table 1).
Abdominal ultrasound (US) showed a small, hypere-
chogenic liver with a poorly developed portal vascular net-
work. An abnormal vessel was visualised, originating from
the right gastric vein and terminating into the caudal vena

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© 2022 The Authors. Veterinary Record Case Reports published by John Wiley & Sons Ltd on behalf of British Veterinary Association.

Vet Rec Case Rep. 2022;10:e389. wileyonlinelibrary.com/journal/vrc2  of 

https://doi.org/10.1002/vrc2.389
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 of  Veterinary Record Case Reports

TA B L E  Blood screening and biochemical abnormalities

Value Reference interval LEARNING POINTS/TAKE HOME MESSAGES

White blood cell count 33.3 × 103 /µl 6 × 103 –17 × 103 /µl ∙ Hydraulic occluders can be used for gradual atten-
Neutrophil count 24.9 × 103 /µl 2.9 × 103 –13.6 × 103 /µl uation of extrahepatic portosystemic shunts in
Monocyte count 4.3 × 103 /µl 0.3 × 103 –1.6 × 103 /µl dogs, but care must be taken with positioning and
Glucose 2.1 mmol/L 3.5–6.5 mmol/L sizing to prevent kinking.
∙ In some instances, different attenuation devices
Urea <2 mmol/L 2–7 mmol/L
may be preferable to others. It is important to con-
Protein 41 g/L 50–69 g/L
sider alternative options if one technique is not
Albumin 20 g/L 23–34 g/L successful.
Globulin 22 g/L 24–39 g/L ∙ Intraoperative portal pressure secondary to tem-
Ammonium 120 µmol/L 0–98 µmol/L porary complete ligation of the shunt can aid in
ALT 191 UI/L 12–80 UI/L choosing the most appropriate attenuating device.
∙ Complete shunt closure may be challenging to
Fasting bile acids 75 µmol/L 0–20 µmol/L
achieve in animals with very underdeveloped
Post-prandial bile acids 163 µmol/L 0–20 µmol/L
intrahepatic vasculature/liver.

F I G U R E  Preoperative transverse computed tomography
angiography (CTA) view of the abdomen. An abnormal vessel (*) rising
from the right gastric vein is visualised (a). It measures 8.5 mm in diameter
as it enters the caudal vena cava (CVC) (b)
cava. Computed tomography angiography (CTA) confirmed
the presence of a single extrahepatic right gastric PSS, mea-
suring approximately 8.5 mm in diameter at its entry in the
caudal vena cava (Figure 1a,b).
TREATMENT
Medical treatment combining oral administration of lev-
etiracetam (10 mg/kg twice daily, Keppra, UCB Pharma),
metronidazole (7.5 mg/kg twice daily, Flagyl, Sanofi-Aventis)
and lactulose (0.5 ml/kg twice daily, Duphalac, Mylan) was
initiated to stabilise the animal, and a low-protein diet was
advised. One month later, all clinical signs had resolved and
surgery was advocated.
The dog was anaesthetised and a midline celiotomy was
performed. The aberrant vessel was identified according to
CTA findings and was isolated with right angle forceps. A
jejunal vein was isolated, catheterised with a 22 gauge catheter
and connected via saline-filled tubing to a TruWave pressure
transducer (Edwards Lifesciences, Guyancourt, France) and
a multiparameter monitor (Carescape B450, GE Healthcare,
Helsinki, Finland) for portal pressure measurement. Baseline
portal pressure was 14 mmHg. Temporary complete occlusion
of the abnormal vessel with a bulldog forceps led to a portal
pressure of 40 mmHg (change in portal pressure of 26 mmHg)
and to discoloration of the pancreas and the small intestines,
increased intestinal peristalsis, increased mesenteric vascular
pulsations and oedema of the pancreas. These signs progres-
sively disappeared when the bulldog forceps was removed.
The caudal vena cava was approached by passing cranially
to the lesser curvature of the stomach in order to place a
10 mm HO (Hepatic Shunt Occluder Port System, Norfolk
Vet Products) (Figure 2) around the aberrant vessel as close
as possible to its terminus on the caudal vena cava. The cuff
of the HO was secured around the shunt by passing two
nonabsorbable sutures (2-0 polypropylene) into the eyelets
intended for this purpose. No change in portal pressure was
identified with the uninflated HO in place. Complete inflation
of the HO was performed to test the device, which led to a
portal pressure of 40 mmHg. The HO was then deflated and
the jejunal catheter was removed after having checked that
portal pressure had returned to its initial value. A stab incision
was made in the paramedian portion of the abdominal wall
to pass the actuating tubing of the HO, and a subcutaneous
port was connected to the tubing. The port was placed 3 cm
lateral to the abdominal midline, and was sutured to the

Veterinary Record Case Reports
F I G U R E  Photograph of a hydraulic occluder. The silicone inflatable
cuff (*) is placed around the shunting vessel, and is connected to a
subcutaneous port (→) by an actuating tubing
body wall using nonabsorbable suture (2-0 polypropylene)
through all four eyelets. Exploration of the remainder of the
abdominal contents revealed no other anomaly. Closure of
the abdominal cavity was performed routinely.
The dog recovered in the intensive care unit. Administra-
tion of levetiracetam and metronidazole was pursued intra-
venously at the same dosage, and analgesia was provided with
methadone (0.2 mg/kg IV every 4 hours, Comfortan, Eurovet
Animal Health). During the night, the dog developed acute
abdominal pain, severe depression, hypovolaemic shock and
moderate abdominal distension, all suggestive of portal hyper-
tension. Peritoneal effusion was confirmed with abdominal
US. Exploratory median celiotomy was hence performed in
emergency, and revealed acute shunt occlusion due to kink-
ing of the HO, thus causing portal hypertension. The sutures
securing the cuff of the HO around the shunt were cut, and
the device was removed, leaving only the subcutaneous port
in place. The abdominal wall was closed routinely. Clinical
improvement was observed the following day, and the dog was
discharged 5 days later under the same medical treatment as
preoperatively.
One month later, the dog was anaesthetised for a further
surgery when an 8 mm HO was placed around the aberrant
vessel within the epiploic foramina. During this third surgery,
portal pressure varied as follows: baseline = 7 mmHg, after
temporary complete shunt occlusion = 25 mmHg (change
in portal pressure = 18 mmHg), with the uninflated HO in
place = 9 mmHg. The dog recovered uneventfully and was
discharged with prescriptions of levetiracetam, metronidazole
and lactulose to be continued at the same dosage as preopera-
tively. Tramadol (4 mg/kg orally twice daily, Topalgic, Sanofi-
Aventis) was also added for 5 days, and a low-protein diet was
pursued.
OUTCOME AND FOLLOW-UP
At follow-up examination 3 weeks later, general clinical and
neurological examinations were normal. Ultrasound exam-
ination showed persistence of shunting through the abnor-
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 of 
F I G U R E  Postoperative transverse computed tomography
angiography (CTA) view of the abdomen after complete inflation of the
hydraulic occluder (HO). The HO (arrow) encircles a persistent shunting
vessel (*) measuring 3 mm in diameter
mal vessel and the HO was visualised encircling it. Inflation
of the HO was performed with 0.5 ml of saline, and the dog
was hospitalised during the day for monitoring. Few hours
after inflation, the dog became abruptly lethargic, and dis-
crete peritoneal effusion was evident on abdominal US con-
trol. The HO was thus partially deflated by re-aspirating 0.2 ml
of saline. The dog progressively improved and peritoneal effu-
sion resolved the next day.
Gradual inflation of the HO was subsequently performed
every 3 weeks (0.3 ml → 0.7 ml → 1.1 ml → 1.5 ml → 2 ml)
under US guidance, with no more adverse events. At the fifth
inflation, the aberrant vessel appeared completely occluded at
US examination. Medical treatment was progressively discon-
tinued and stopped after 1 month.
At the time of follow-up 2 months later, the owner reported
several episodes of disorientation since the last 3 weeks. Clin-
ical and neurological examinations were normal. Biochemi-
cal analysis was repeated, and revealed persistent hypouremia
(<2 mmol/L, RI: 2–7 mmol/L), hypoalbuminemia (18 g/L, RI:
23–34 g/L) and elevated fasting bile acids (111 µmol/L, RI: 0–
20 µmol/L) and post-prandial bile acids (419 µmol/L, RI: 0–
20 µmol/L). CTA was again performed, and showed residual
shunting, with the abnormal vessel encircled by the cuff of the
HO and measuring 3 mm in diameter (Figure 3).
Medical treatment was re-introduced, and revision surgery
was performed 1 week later. The dog was anaesthetised and
a midline celiotomy was performed. The HO was removed
(Figure 4), and the residual shunting vessel was identified.
Portal pressure was initially measured at 10 mmHg, and
increased to 20 mmHg when temporary complete occlu-
sion with bulldog forceps was performed (change in portal
pressure = 10 mmHg). A 1 × 10 cm strip of TFB was folded
longitudinally into thirds, placed around the abnormal vessel
without constricting it and secured with three vascular clips.
The corresponding portal pressure with the band in place was
12 mmHg. The abdominal cavity was closed routinely. The
dog recovered in the intensive care unit and was discharged
3 days later.

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F I G U R E  Intraoperative photograph showing the hydraulic occluder
(HO) (→) in place within the epiploic foramina and completely inflated
before removal. Cranial is to the left of the image
Medical treatment was progressively discontinued and fur-
ther stopped after 2 months. At final follow-up 6 months
after placement of the TFB, the owner reported no relapse of
neurological signs. General clinical and neurological exam-
inations were normal. Although fasting bile acids were still
increased (125 µmol/L, RI: 0–20 µmol/L), post-prandial bile
acids returned to normal (12 µmol/L, RI: 0–20 µmol/L). Per-
sistent shunting was not identified at the final US examination.
DISCUSSION
This case report describes the complicated but eventually suc-
cessful surgical management of a single right gastric extrahep-
atic PSS in a dog by using two different attenuation devices: an
HO and a TFB. The HO enabled complete control over grad-
ual attenuation of the shunt and reduction of its diameter. The
TFB was then used to achieve full closure. Use of an HO has
proven to be an effective method for treating dogs with intra-
hepatic PSSs.9 This is the first clinical case describing attenu-
ation of an extrahepatic PSS with an HO.
Different devices are available for gradual attenuation of
extrahepatic PSSs. The most commonly used techniques
include placement of an AC or a TFB around the abnor-
mal vessel.11 While both devices lead to vascular occlusion
secondary to inflammation and thrombosis, the inner casein
ring of the AC also gradually swells as it absorbs body fluid,
resulting in compression of the vessel.5,8,12,13 Time to com-
plete occlusion can be extremely variable, ranging from 6 to
210 days after placement of an AC14,15 and exceeding 16 weeks
after placement of a TFB.13 As both TFBs and ACs rely on
endogenous factors for gradual occlusion, they might produce
too rapid or insufficient attenuation resulting in persistent
shunting. Unlike these two devices, the HO does not rely on
inflammation to lead to occlusion but rather on compression
of the vessel through inflation of the silicone cuff.5 Complete
control over the attenuation is possible by injecting the desired
volume of sterile saline into the subcutaneous port, and should
be able to result in complete closure. The occlusion can also
be reversed by deflating the cuff through re-aspiration of pre-
viously injected saline. Time to complete occlusion is deter-
mined by the surgeon, and is patient-specific and adjusted
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Veterinary Record Case Reports
on a case-by-case basis. It depends on the residual intrahep-
atic portal vasculature and on the liver size as measured pre-
operatively, and, as per the authors’ opinion, on intraopera-
tive measurement of portal pressure. Indeed, the presence of
a PSS causes blood to be diverted from the portal to the sys-
temic venous circulation, thus shunting the liver and resulting
in its underdevelopment.2 The goal of surgery is to redirect
blood to the liver by progressively closing the shunt. Tempo-
rary complete occlusion of the shunting vessel leads to high
portal pressure because of the limited intrahepatic portal vein
development. Thus, the higher the portal pressure is, the more
progressive closure of the shunting vessel—and the more cuff
inflations with a small volume of saline each time—will be
needed to allow the liver to adapt to increased blood flow.
We believe that complete control over shunt attenuation
was extremely important in this dog given the intraoperative
value of portal pressure during the first surgery. In fact, mea-
suring intraoperative portal pressure is useful to verify that a
vessel has correctly been identified as a shunt and to guide the
degree of attenuation. Normal baseline portal pressure in dogs
vary between 6 and 10 mmHg, and an increase to no more
than 17.6 mmHg with a maximal change in portal pressure of
6.6–7.35 mmHg is recommended after occlusion of the abnor-
mal shunting vessel.2 If portal pressure variation exceeds these
values, acute complete ligation should not be attempted. In
our case, the dog had a high baseline portal pressure during
the first surgery (14 mmHg). This was due to incorrect cali-
bration of the measurement device. Surgical decision-making
was therefore based on portal pressure variation. The varia-
tion of more than 25 and 18 mmHg after temporary occlu-
sion during the first and third surgery, respectively, precluded
definite occlusion. This variation also led us to think that a
rapid occlusion, such as that could have been obtained with
an AC or a TFB, would have been inappropriate for this dog.
We therefore felt that the dog would not have tolerated shunt
attenuation with an AC or a TFB placed as first-line treatment.
This was further supported by the fact that the dog developed
signs of portal hypertension after the first cuff inflation with
0.5 ml of saline (corresponding to one-fourth of complete cuff
inflation) 4 weeks after placement of the HO. The choice of
using a TFB during the fourth and final surgery was justi-
fied by the smaller diameter of the abnormal vessel (3 mm)
and by the less consequent variation in portal pressure follow-
ing temporary occlusion of the shunting vessel (variation of
10 mmHg). This smaller variation reflected the ability of the
dog to tolerate more attenuation, presumably due to the fact
that the liver had developed in response to increased blood
flow.16
We chose to use an HO with a larger internal diameter
(10 mm) than that of the abnormal vessel (8.5 mm) during
the first surgery so as not to cause partial attenuation dur-
ing placement of the cuff. However, this led to kinking of
the device due to its relative mobility, and caused acute shunt
occlusion and portal hypertension. This type of complication
has been reported after placement of an AC,5 but never after
placement of an HO. This device instability was most likely
due to the unusual approach of the aberrant vessel. Indeed, the
10 mm HO used was too large to be placed within the epiploic
foramina to encircle the shunting vessel as it entered the cau-
dal vena cava. Therefore, the caudal vena cava was approached
by passing cranially to the lesser curvature of the stomach.
This more cranial position combined with the larger size of

Veterinary Record Case Reports
the HO relative to the shunt may have been sufficient to cause
kinking of the device.
The rate of vascular occlusion can be adjusted postopera-
tively after placement of an HO because it does not rely on
endogenous factors for gradual shunt occlusion.5,9 In order to
prevent formation of multiple acquired shunts, gradual infla-
tion of the HO is performed every 2–3 weeks at our institution
if no complication occurs, similarly as to what is reported in
the literature for intrahepatic PSS attenuation.9 A US exam-
ination is always performed before HO inflation to rule out
ascites or other signs of portal hypertension and to docu-
ment liver development, and the US exam is repeated 6–
8 hours after inflation to again rule out ascites suggestive of
portal hypertension. As stated earlier, the number of infla-
tions required to completely close the HO, and thus the vol-
ume of saline injected at each inflation, is mainly determined
by the portal pressure value obtained after temporary com-
plete occlusion of the shunting vessel.
This case also illustrates another advantage of placing an
HO rather than an AC or a TFB: the possibility to reverse
occlusion by re-aspirating saline that has been injected. As
a matter of fact, the HO is the sole reversible device that
allows reversal of occlusion in case signs of portal hyper-
tension develop. This was proven useful after the first HO
inflation when the dog developed ascites suggestive of portal
hypertension. Partial deflation of the balloon enabled resolu-
tion of all signs.
Complete occlusion of the abnormal vessel is anticipated
with the use of an AC, a TFB or an HO. However, com-
plete occlusion of congenital PSS has been reported in 30%–
65%8,11,12,17,18 and 0%–80%11,17–19 of dogs following placement
of a TFB and an AC, respectively. Persistent shunting has been
reported more frequently when congenital PSS was treated
with a TFB than with an AC.11,18 In our case, persistent shunt-
ing was most likely due to a mechanical failure of the HO used.
As a matter of fact, when we checked the entire device after its
removal during the last surgery, we evidenced that complete
inflation did not lead to obstruction of the cuff, even if no leak
in the balloon was evidenced. It is therefore very likely that the
device did not fully close the shunt because the inflated cuff
did not fully obstruct it. Even though such mechanical failure
of an HO has not been reported, it could constitute a potential
limitation of using this device.
Resolution of clinical signs, of biochemical anomalies and
disappearance of the abnormal vessel on diagnostic imaging
are diverse methods used to assess outcomes following treat-
ment of PSS.9 Serum bile acids are commonly used as diagnos-
tic tool for congenital PSS and to follow response to surgical
treatment. In fact, the test is relatively easy to perform and is
highly sensitive and specific.20,21 In dogs with complete occlu-
sion, it has been shown that mild increases in serum bile acids
may persist, but should not be interpreted as clinically relevant
if clinical signs have resolved.17 Even though fasting bile acids
were still increased in our case 6 months after TFB placement,
complete resolution of clinical signs and absence of persistent
shunting on US examination suggested a favourable outcome.
CONFLICT OF INTEREST
The authors declare they have no conflicts of interest.
F U N D I N G I N F O R M AT I O N
The authors received no specific funding for this work.
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 of 
E T H I C S S TAT E M E N T
This case was managed in a university teaching hospital with
high standards in ethical practice. Owner’s consent has been
obtained to publish this case report.
AU T H O R C O N T R I B U T I O N S
All authors contributed equally to the acquisition of the data
for this case report. Margaux Bondel and Pierre Moissonnier
wrote the paper.
ORCID
Margaux Bondel https://orcid.org/0000-0001-7473-5075
REFERENCES
1. Tivers MS, Upjohn MM, House AK, Brockman DJ, Lipscomb VJ. Treat-
ment of extrahepatic congenital portosystemic shunts in dogs - what is
the evidence base? J Small Anim Pract. 2012;53(1):3–11.
2. Berent A, Tobias KM. Hepatic vascular anomalies. In: Veterinary
surgery: small animal. 2nd ed. Elsevier; 2018. p. 1852–87.
3. Greenhalgh SN, Reeve JA, Johnstone T, Goodfellow MR, Dunning MD,
O’Neill EJ, et al. Long-term survival and quality of life in dogs with clin-
ical signs associated with a congenital portosystemic shunt after surgical
or medical treatment. J Am Vet Med Assoc. 2014;245(5):527–33.
4. Swalec KM, Smeak DD. Partial versus complete attenuation of single por-
tosystemic shunts. Vet Surg. 1990;19(6):406–11.
5. Sereda CW, Adin CA. Methods of gradual vascular occlusion and their
applications in treatment of congenital portosystemic shunts in dogs: a
review. Vet Surg. 2005;34(1):83–91.
6. Hunt GB, Kummeling A, Tisdall PLC, Marchevsky AM, Liptak JM,
Youmans KR, et al. Outcomes of cellophane banding for congenital por-
tosystemic shunts in 106 dogs and 5 cats. Vet Surg. 2004;33(1):25–31.
7. Mehl ML, Kyles AE, Hardie EM, Kass PH, Adin CA, Flynn AK, et al.
Evaluation of ameroid ring constrictors for treatment for single extra-
hepatic portosystemic shunts in dogs: 168 cases (1995–2001). J Am Vet
Med Assoc. 2005;226(12):2020–30.
8. Nelson NC, Nelson LL. Imaging and clinical outcomes in 20 dogs treated
with thin film banding for extrahepatic portosystemic shunts. Vet Surg.
2016;45(6):736–45.
9. 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 portosystemic shunts. J Am Vet Med
Assoc. 2006;229(11):1749–55.
10. Wallace ML, Ellison GW, Giglio RF, Batich CD, Berry CR, Case JB, et al.
Gradual attenuation of a congenital extrahepatic portosystemic shunt
with a self-retaining polyacrylic acid-silicone device in 6 dogs. Vet Surg.
2018;47(5):722–8.
11. Matiasovic M, Chanoit GPA, Meakin LB, Tivers MS. Outcomes of dogs
treated for extrahepatic congenital portosystemic shunts with thin film
banding or ameroid ring constrictor. Vet Surg. 2020;49(1):160–71.
12. Landon BP, Abraham LA, Charles JA. Use of transcolonic portal scintig-
raphy to evaluate efficacy of cellophane banding of congenital extrahep-
atic portosystemic shunts in 16 dogs. Aust Vet J. 2008;86(5):169–79; quiz
CE1.
13. Youmans KR, Hunt GB. Experimental evaluation of four methods of pro-
gressive venous attenuation in dogs. Vet Surg. 1999;28(1):38–47.
14. Vogt JC, Krahwinkel DJ, Bright RM, Daniel GB, Toal RL, Rohrbach B.
Gradual occlusion of extrahepatic portosystemic shunts in dogs and cats
using the ameroid constrictor. Vet Surg. 1996;25(6):495–502.
15. Besancon MF, Kyles AE, Griffey SM, Gregory CR. Evaluation of the char-
acteristics of venous occlusion after placement of an ameroid constrictor
in dogs. Vet Surg. 2004;33(6):597–605.
16. Tivers MS, Lipscomb VJ, Smith KC, Wheeler-Jones CPD, House AK.
Markers of hepatic regeneration associated with surgical attenuation of
congenital portosystemic shunts in dogs. Vet J. 2014;200(2):305–11.
17. Vallarino N, Pil S, Devriendt N, Or M, Vandermeulen E, Serrano G, et al.
Diagnostic value of blood variables following attenuation of congenital
extrahepatic portosystemic shunt in dogs. Vet Rec. 2020:187(7):e48.
18. Traverson M, Lussier B, Huneault L, Gatineau M. Comparative outcomes
between ameroid ring constrictor and cellophane banding for treatment
of single congenital extrahepatic portosystemic shunts in 49 dogs (1998–
2012). Vet Surg. 2018;47(2):179–87.
 20526121, 2022, 3, Downloaded from https://bvajournals.onlinelibrary.wiley.com/doi/10.1002/vrc2.389 by CAPES, Wiley Online Library on [04/11/2022]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
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19. 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 portosystemic shunts in dogs. Vet How to cite this article: Bondel M, Morvan V,
Surg. 2013;42(8):951–7. Moissonnier P. Treatment of an extrahepatic
20. Ruland K, Fischer A, Hartmann K. Sensitivity and specificity of fasting portosystemic shunt by placement of a hydraulic
ammonia and serum bile acids in the diagnosis of portosystemic shunts occluder followed by a thin film band in a dog: An
in dogs and cats. Vet Clin Pathol. 2010;39(1):57–64.
21. Winkler JT, Bohling MW, Tillson DM, Wright JC, Ballagas AJ. Por-
eventful story. Vet Rec Case Rep. 2022;10:e389.
tosystemic shunts: diagnosis, prognosis, and treatment of 64 cases (1993– https://doi.org/10.1002/vrc2.389
2001). J Am Anim Hosp Assoc. 2003;39(2):169–85.