CASE REPORT

CT features of extrahepatic
arterioportal fistula in two cats
M. Choi*,†, H. Kim*, J. Yoon† and M. Choi1,†

*Department of Veterinary Medical Imaging, Haemaru Referral Animal Hospital, Seongnam 463-050, Republic of Korea
†
Department of Veterinary Medical Imaging, College of Veterinary Medicine, Seoul National University, Seoul 151-742, Republic of
Korea
1
Corresponding author email: mcchoi@snu.ac.kr

Two cats presented with large volume ascites and the cause was suspected to be portal hypertension.
On contrast CT they both showed enhancement of the main portal vein during the arterial phase and
an anomalous connection between the celiac artery and extrahepatic portal vasculature, prompting a
diagnosis of extrahepatic arterioportal fistula. An extrahepatic arterioportal fistula is a connection
between any artery and the portal vein outside the liver and, to our knowledge, this is the first
report in cats.

Journal of Small Animal Practice (2018)

DOI: 10.1111/jsap.12957
Accepted: 5 July 2018

INTRODUCTION 270 IU/L (RI 28 to 106 IU/L)], elevated aspartate trans-

An arterioportal fistula (APF) occurs when a branch of the arte-
rial circulation communicates directly with the portal system,
resulting in severe portal hypertension (Vauthey et al. 1997, Guz-
man et al. 2006). Portal hypertension results in the formation of
multiple acquired extrahepatic portosystemic shunts and severe
ascites (Vauthey et al. 1997). APF may occur intrahepatically
(IHAPF) or extrahepatically (EHAPF) and may be congenital or
acquired (Vauthey et al. 1997, Guzman et al. 2006). In human
medicine, the most common type is intrahepatic and is caused
by cirrhosis, trauma or as a complication of an abdominal inter-
ventional procedures (Guzman et al. 2006). In veterinary medi-
cine, only four cases of IHAPF have previously been reported in
cats (Legendre et al. 1976, McConnell et al. 2006, Uemura et al.
2016) and, as far as we know, EHAPF has not previously been
described in cats.
CASE HISTORIES
Case 1
A 1-year-old, intact female Turkish angora cat was referred
for evaluation of hyperammonaemia [444 μmol/L reference
interval (RI 0 to 95 μmol/L)]. On physical examination, the
cat demonstrated mild ptyalism. The complete blood count
showed no remarkable findings. Serum biochemistry revealed
a mildly decreased total protein concentration (6.2 g/dL;
RI 6.3 to 8.8 g/dL), elevated alanine transaminase [(ALT)
aminase [(AST) 178 IU/L (RI 12 to 46 IU/L)] and elevated
ammonia [382 μmol/L (RI 0 to 95 μmol/L)]. Abdominal
ultrasound demonstrated a large volume of ascites. Fluid anal-
ysis confirmed the ascites to be a transudate (total protein was
2.2 g/dL; RI <2.5 g/dL, nucleated cell count was 1100/μL;
RI <3000/μL).
One week later, a three-phase CT examination was under-
taken. On CT angiography (CTA), enhancement of the main
portal vein was noted during the arterial phase (Fig. 1A). More-
over, CTA showed an anomalous connection between the celiac
artery and the splenic vein (Fig. 1B) and decreased diameter
of the abdominal aorta caudal to the origin of the celiac artery
(diameter cranial to the celiac artery: 4 mm, diameter caudal to
the celiac artery: 2 mm) (Fig. 1C). There were multiple tortu-
ous vessels near the splenic vein and fluid-attenuating tubu-
lar structures [8.5 ± 6.3 Hounsfield unit (HU)] in the hepatic
parenchyma that were thought to represent dilated hepatic ducts
as they followed the path of the portal veins. The diameters of
the common bile duct, proximal duodenum and hepatic paren-
chyma were normal. The ratio between the diameter of the extra-
hepatic portal vein and aorta was 0.42 and the intrahepatic portal
vein was subjectively small. An abnormal intrahepatic left portal
branch continued to the intrathoracic vein caudal to the xiphoid
process (Fig. 2A). An enlarged left phrenicoabdominal vein was
also noted (Fig. 2B). The owner declined hepatic biopsy.
The cat was treated conservatively with diuretics, antibiotics
and hepatic supporters for 1 month and maintained its preinves-
tigation clinical status. However, the cat died of recurrent hepatic
encephalopathy 1 month after presentation.

Journal of Small Animal Practice • © 2018 British Small Animal Veterinary Association 1
 M. Choi et al.

FIG 1. Transverse CT image of case 1 with an extrahepatic arterioportal fistula (EHAPF), during the arterial phase. (A) At the level of porta hepatis.
Note the enhancement of portal vein (arrow head) in the arterial phase and diameter of the aorta which is larger than at the kidney level (black
arrow). Multiple tubular, hypoattenuating (8.5 ±6.3 HU) structures (*) within the hepatic parenchyma. Normal gall bladder (GB). (B) At the level of the
fistula. An anomalous connection between the celiac artery (black arrow) and splenic vein as well as multiple portosystemic shunts. (C) At the level
of the kidneys (RK: right kidney, LK: left kidney). Caudal to the origin of the EHAPF, the aorta (black arrow) is small. Caudal vena cava (arrow head)
showed no filling of contrast media

FIG 2. (A) Volume rendering reformatted CT image of case 1. An abnormal tortuous vessel from branch of the intrahepatic left portal branch (arrows)
continued to the intrathoracic vein. (B) Dorsal plane reformatted image during the portal phase of the dual-phase CT. There was dilation of the left
phrenicoabdominal vein (arrows)

Case 2 was 1.1 g/dL; RI <2.5 g/dL, nucleated cell count was 300/μL;

A 5-year-old, neutered male domestic short hair cat weighing 5.3 kg
was referred for the investigation of ascites. On physical examina-
tion, the cat had severe abdominal distension. The complete blood
count showed no remarkable findings. Serum biochemistry revealed
a mildly decreased total protein concentration (6.1 g/dL; RI 6.3 to
8.8 g/dL), elevated alkaline phosphatase [ALP 82 IU/L (RI 12 to
59 IU/L)], elevated ammonia [211 μmol/L (RI 0 to 95 μmol/L)] and
elevated total bilirubin [0.4 mg/dL (RI 0 to 0.2 mg/dL)].
Ultrasonographic examination revealed a large volume of
ascites and multiple heterogeneous nodules in the hepatic paren-
chyma. A large tortuous extrahepatic portal vein was also iden-
tified. Abdominocentesis was performed (draining 1 L of fluid)
to obtain diagnostic samples and to relieve the patient’s discom-
fort. Analysis confirmed the fluid as a transudate (total protein
RI <3000/μL). Ultrasound-guided fine needle aspiration of the
hepatic nodules showed mild cytoplasmic rarefaction and accu-
mulation of bile casts in the hepatocytes without evidence of
malignancy. Based on the blood analysis and abdominal ultra-
sound examination, the cause of ascites was suspected to be por-
tal hypertension. The cat was treated with diuretics, and a CT
examination was performed 2 months later.
On precontrast abdominal imaging, the liver was normal in
size. CTA confirmed enhancement of the portal vein during the
arterial phase and confirmed the presence of an abnormally dis-
tended extrahepatic portal vein (Fig. 3A). The abdominal aorta
decreased in diameter caudal to the origin of the celiac artery
(diameter cranial to the celiac artery: 6 mm, diameter caudal to
the celiac artery: 3.3 mm). CT also confirmed the presence of

2 Journal of Small Animal Practice • © 2018 British Small Animal Veterinary Association
 Arterioportal fistula by CT in the cat

FIG 3. Reformatted image of case 2 with the extrahepatic arterioportal fistula (EHAPF), during the arterial phase. (A) Dorsal plane image shows
abnormal aneurysmal change of the extrahepatic portal vein (PV aneurysm) and multiple heterogeneous contrasting nodules throughout the hepatic
parenchyma. (B) Volume rendered image shows multiple abnormal tortuous vessels throughout abdomen. (C) Sagittal plane image shows enlarged
azygos vein (arrows). A: Aorta

FIG 4. Three-phase CT characteristics of hepatic nodules (arrows) in case 2. (A) Dorsal reformatted precontrast CT image showing multiple
hypoattenuating nodules (51 ±4 HU) in the liver parenchyma. (B) The nodules show marked enhancement in the arterial (280 ±73 HU) and (C) portal
venous phase (352 ±27 HU) with wash out in the delayed phase (169 ±16 HU) (D)

acquired portosystemic shunts (Fig. 3B). An enlarged azygos
vein (Fig. 3C) and an abnormally dilated left-sided subcutaneous
vein continuing to the vertebral vein were also noted. There were
multiple hepatic nodules (up to 2 cm) in precontrast images (51
±4 HU, Fig. 4A) and the contrast values of these nodules were
280 ±73 HU in the arterial phase (Fig. 4B), 352 ±27 HU in the
portal venous phase (Fig. 4C), 169 ±16 HU in the delayed phase
(Fig. 4C).
A liver biopsy was obtained through exploratory coeliotomy.
Histopathology of the liver biopsy showed portal vein hypopla-
sia with mild lymphocytic portal hepatitis. The cat was treated
with diuretics and repeated abdominocentesis was performed to

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 M. Choi et al.
maintain the patient’s comfort. After 1 year, the owners elected
euthanasia.
DISCUSSION
In human medicine, APFs are classified by their aetiology, size
and involved vessels (Vauthey et al. 1997, Guzman et al. 2006).
Depending on the location of the anomalous connection with
the portal vein, they are divided into two groups: IHAPF and
EHAPF. In veterinary medicine, EHAPFs are extremely rare
(Legendre et al. 1976, Uemura et al. 2016). There is a single
report of EHAPF in a dog (White et al. 2015) but to our knowl-
edge, there have not been any reports in cats.
For diagnosing APFs, CT is considered the gold standard in
human and veterinary medicine (Vauthey et al. 1997, Zwingen-
berger et al. 2005, McConnell et al. 2006). Although it did not
definitively confirm the diagnosis, Doppler ultrasound can be sug-
gestive of arterialisation of a dilated portal vein (McConnell et al.
2006). On dual-phase CT, APFs are characterised by enhance-
ment of the portal vein during the arterial phase. CT also can
identify an underlying cause such as hepatic neoplasm, chronic
hepatopathy or trauma (Guzman et al. 2006) and detect second-
ary changes such as portal hypertension (Vauthey et al. 1997).
According to previous veterinary reports (Zwingenberger et al.
2005), imaging characteristics of IHAPFs are enhancement of por-
tal veins in the arterial phase, aneurysmal dilation of intrahepatic
portal veins, decrease in size of the aorta caudal to the level of the
fistula, microhepatica and multiple acquired portosystemic shunts.
Compared with IHAPF cases, our cases showed aneurysmal dila-
tion of extrahepatic portal vasculature due to the location of the
fistula. In addition, multiple acquired portosystemic shunt hin-
dered Doppler ultrasound examination and the ability to detect
any alteration of blood flow profile of the extrahepatic portal vein.
Otherwise, imaging characteristics were similar to IHAPF.
The causes of the APFs were not established conclusively,
neither patient had any previous traumatic history nor previous
abdominal surgery, thus a congenital aetiology was considered
most likely.
Case 1 showed prominent dilatation of the biliary tract. In
a previous report (Zwingenberger et al. 2005), IHAPF was fre-
quently accompanied by dilated intrahepatic biliary ducts. It is
possible that development of the hepatic artery is closely related
to that of the bile duct (Van Haeften & Bröker 1984). Because of
this unique developmental relationship, APFs may be associated
with biliary duct abnormalities and this patient’s anomalies were
suspected to result from this relationship. Case 2 also revealed
dilation of the azygos vein. In human cases with elevated por-
tal venous pressure, multiple varices passed through the azygos
system to the superior vena cava (Dudiak et al. 1991, Vilgrain et
al. 2000). Similar results were also mentioned in dogs (Doige &
Furneaux 1975).
4 Journal of Small Animal Practice
The optimal therapy for APFs remains controversial. For cor-
rection of IHAPF, hepatic lobectomy could be chosen (Chanoit
et al. 2007). Otherwise, EHAPF is corrected by direct ligation
of the shunting vessels (White et al. 2015). However, both these
cases had already progressed to portal hypertension and so con-
servative therapy was selected.
In conclusion, three-phase CTA proved to be a useful diag-
nostic tool for EHAPF by providing information regarding the
timing of vessel opacification (such as enhancement of the por-
tal vein during the arterial phase), identification of abnormal
vessel anatomy as well as concurrent hepatic parenchymal and
biliary abnormalities. Also, compared with IHAPF cases, abnor-
mal aneurysmal extrahepatic portal vein dilation and multiple
acquired portosystemic shunt made ultrasound examination
challenging. Thus, CTA may be helpful in cases in which anat-
omy cannot be fully elucidated by ultrasound evaluation alone.
Acknowledgements
We would like to thank the referring veterinarians and the past
and present clinicians at the Haemaru Referral Animal Hospital
and this study was supported by the Research Institute for Veteri-
nary Science at Seoul National University. The authors received
no financial support for the research, authorship and/or publica-
tion of this article.
Conflict of interest
The authors declared no potential conflicts of interest with
respect to the research, authorship and/ or publication of this
article.
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