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12 Veterinary Times
THE liver has many essen-tial functions within the body, including nutrient metabo-lism, removal of toxins and ammonia, protein synthesis (including coagulation factors), bile acid synthesis, vitamin storage, immunoregulation and bilirubin excretion.
To achieve this, blood flow
to the liver is vast, averaging
30ml/min/kg to 45ml/min/kg
(Witte, 1976). The majority of
this (80 per cent of the blood
flow and 50 per cent of the
oxygen requirements) is sup-
plied by the portal vein and the
remainder by the hepatic artery.
Portosystemic shunts (PSS)
are vascular anomalies that con-
nect the portal circulation to the
systemic circulation, bypassing
some or all of the hepatic tissue.
They can form as a result of
a congenital abnormality, either
as persistence after birth of the
ductus venosus, or because of
anomalous, functional com-
munications between the foetal
hepatic vessels (vitelline system)
and non-hepatic abdominal ves-
sels (cardinal system, which
later develops into the caudal
vena cava and azygos vein).The
former abnormality leads to an
intrahepatic shunt and the latter
to an extrahepatic shunt.
Alternatively, shunts may be
acquired, usually secondary
to portal hypertension. This
article will focus on congenital
PSS (Table 1).
DiagnosisPresenting complaints include:
� Poor growth/weight gain. � Drug (such as anaesthetic)
intolerance due to reduced
liver metabolism. � In cats, copper-coloured
irises (Figure 1) are reported.
Controversy exists, however,
as to whether this is truly a dis-
ease association. � Neurological abnormalities,
including behavioural changes,
lethargy, ataxia, circling, head
pressing, blindness or seizures.
These abnormalities may have
gone unnoticed by owners,
either because the changes are
very subtle, or because they
believe this behaviour to be
normal for their new puppy/
kitten. Hepatic encephalopathy
is seen not uncommonly in ani-
mals with PSS, and the cause is
likely to be multifactorial.
Theories include increases in
blood ammonia (with or with-
out other synergistic toxins),
alterations in monoamine or
amino acid neurotransmitters,
or increased cerebral con-
centration of an endogenous
benzodiazepine-like substance.
Experimentally, none of these
factors alone consistently initiates
encephalopathic coma. � Increased incidence of uri-
nary tract infection due to
decreased urea production
and increased ammonia excre-
tion (which may also cause the
development of urinary calculi).
Polyuria and polydipsia (PUPD)
may also be evident. � Gastrointestinal signs, includ-
ing vomiting. � Hypersalivation, particularly
in cats (Figure 2).
Cryptorchidism is recognised
in some dogs with PSS.
Occasionally, other anomalies
are found, such as heart mur-
murs. It is important to evaluate
whether this is a fl ow murmur
secondary to the shunt or rep-
resents a cardiac anomaly.
On routine serum biochem-
istry and haematology, changes
are often subtle and may be
diffi cult to interpret in a young,
growing animal.
Abnormalities may include
microcytosis, with or without
anaemia (Figure 3), and variable
leukocytosis. Microcytosis may
be underestimated on postal
samples due to red cells swell-
ing in transit. Low cholesterol,
low glucose and low blood
urea nitrogen (BUN) may be
seen and, in dogs, low albumin
and low total protein may also
be evident.
Elevated liver enzymes are
uncommon because the hepa-
tocytes themselves are usu-
ally either undamaged or are
affected gradually, as the process
is an atrophic one. However,
mild-to-moderate increases
in liver enzymes are seen in
some patients without additional
hepatic pathology.
Routine urinalysis may dem-
onstrate features consistent with
cystitis (such as haematuria,
pyuria or proteinuria) and PUPD
(low specific gravity of urine).
Ammonium biurate crystals may
be detected (Figure 4), but
the absence of the distinctive
CLINICAL SMALL ANIMAL
TABLE 1. Comparison of extrahepatic PSS and intrahepatic PSS (Tobias, 2003)
Extrahepatic shunt Intrahepatic shunts
More common: 66 per cent to 75 per cent of PSS seen
25 per cent to 33 per cent of PSS seen
Usually small breed dogs (particularly terriers)
Usually large breed dogs
Most common form in cats Less common in cats
Most commonly seen form is portocaval
Causes most severe clinical signs due to larger amount of diverted blood fl ow
PORTOSYSTEMIC SHUNTS IN CATS AND DOGS: SIGNS AND DIAGNOSIS
KELLY BOWLTBVMS, MRCVS
ED FRIENDBVetMed, CertSAS, MRCVS
KATE MURPHYBVSc (Hons), DSAM, Dip ECVIM-CA, MRCVS
consider the presentation of hepatic shunts in dogs and cats, when the circulatory system bypasses the liver, causing toxins to accumulate
Figure 1. Cats with PSS may show copper coloured irises, which resolve on surgical occlusion of the shunt.
Pho
to:
KAT
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PH
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VT40.45 master.indd 12 04/11/2010 16:58
13November 15, 2010
“thorn apple” crystals may be
a false negative and so multiple
samples may be required before
they are detected.
Additional tests are usually
required to assess liver function
in cases with PSS. Plasma ammo-
nia can be assessed, but the
sample should be transported on
ice and analysed without delay
since in-house analysers can
be unreliable.
Elevated ammonia typically
demonstrates abnormal hepatic
function, but a normal level does
not rule out PSS and is seen in
seven per cent to 21 per cent
of dogs with PSS, particularly
after fasting or with effective
medical treatment (Center,
1990). Postprandial ammonia
can be evaluated, but measure-
ment of bile acids is more com-
monly performed.
Bi le ac ids measurement
requires no special sample han-
dling, and their elevation in ani-
mals with PSS is the result of
bile acids shunting away from
the liver to the systemic circula-
tion, avoiding re-uptake by the
hepatocytes. Usually, bile acids
are measured preprandially and
then two hours after a fatty meal.
In animals with PSS or poor liver
function, postprandial bile acids
will be markedly elevated com-
pared to normal animals. Occa-
sionally, preprandial bile acid
levels are signifi cantly elevated
and, therefore, postprandial test-
ing is not required.
Finally, because the liver is
responsible for the synthesis of
many clotting factors, the coagu-
lation profi le should be assessed
where surgery is considered.
Often, this is normal. How-
ever, given the limitations of
conventional coagulation test-
ing, it is still possible bleeding
will be seen.
ImagingDefinitive diagnosis of a PSS
requires visualisation, either
directly at surgery or indirectly
using a variety of diagnostic imag-
ing modalities.
At the authors’ hospital,
ultrasonographic examination
is the modality of choice, and
changes include microhepatica,
decreased number of hepatic
and portal veins in the paren-
chyma, detection of the anoma-
lous vessel and abnormal fl ow
using Doppler (Figures 5 to 7).
Mesenteric portovenography
can also be useful and involves
catheterisation of a jejunal vein
and injection of a water-soluble,
radio-opaque, contrast agent
observed under fluoroscopy
(Figures 8 and 9). The disadvan-
tage of this is the requirement
for a laparotomy and the risk
of thrombus formation in the
catheterised vein. The authors
reserve this technique for cases
in which intraoperative loca-
tion of the shunting vessel is
challenging. Other techniques
described, but less commonly
used, include scintigraphy, com-
puted tomography or magnetic
resonance angiography.
Non-specific changes can
also be seen, and include micro-
hepatica, enlarged kidneys and
urinary calculi. Although urate
stones are radiolucent, second-
ary infection may lead to struvite
deposition, which is radiopaque.
Medical managementThe aims of medical man-
agement are to correct fluid,
electrolyte and glucose imbal-
ances, and to prevent hepatic
encephalopathy.
Occasionally, animals will
present in hepatic encephalo-
pathic crisis. Seizures should be
treated initially with intravenous
(0.5mg/kg) or rectal diazepam
(1.0mg/kg to 2mg/kg), followed
by a loading dose of a longer
acting drug. The authors have
tended to use phenobarbitone
in dogs, 12mg/kg to 18mg/kg IV
followed by standard oral doses
of 2mg to 3mg/kg/day, and lev-
etiracetam in cats, 20mg/kg q8h.
However, given the potential
for hepatotoxicity, one could
consider the use of levetiracetam
in both species if justifi ed for use
under the cascade.
Lactulose enemas (preferably
as a 10 to 15-minute retention
enema; three parts lactulose
[20ml/kg in dogs] to seven parts
water) rapidly decrease colonic
bacteria, preventing further
absorption of toxic substrates.
Intravenous antibiotics, such
as clavulanic acid potentiated
amoxicillin 20mg/kg IV q8h,
will decrease the number of
ammonia-producing bacteria in
the gastrointestinal tract, reduc-
ing absorption.
Some clinicians use metro-
nidazole, but the hepatic metab-
olism of this drug should be
considered and neurological
side effects may be mistaken
for encephalopathy. For these
reasons, when metronidazole
is desired, a lower dose should
be used – for example, less
than 7.5mg/kg. Electrolytes and
glucose should be assessed and
corrected using intravenous
fluids spiked with potassium
or dextrose as required, and
changes in serum concentrations
monitored hourly.
Importantly, no oral food
should be provided while ani-
mals are severely encephalo-
pathic to minimise substrate
absorption, which could worsen
clinical signs. Thiamine has also
been recommended.
ManagementOnce animals are stabilised,
the mainstay medical manage-
ment comprises: � Diet. The main aim is to
provide moderate protein
restriction to reduce ammonia
production. Many commercially
available liver diets also pro-
CLINICAL SMALL ANIMAL
Figure 2. Hypersalivation may be evident, particularly in cats.
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Figure 3. Microcytic anaemia may be seen.
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STA
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PASO
ULI
OT
IS.
Pho
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ER
INA
RY
CLI
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AL
PAT
HO
LOG
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ATES
PR
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Figure 4. The distinctive “thorn apple” appearance of ammonium biurate crystals in the urine of an animal with a congenital PSS.
continued overleaf
VT40.45 master.indd 13 04/11/2010 16:58
14 Veterinary Times
vide L-carnitine, antioxidants,
restricted copper and increased
zinc. Normal fat metabolism
should be maintained and the
high energy available from fat
avoids excessive protein catab-
olism. Occasionally, animals
will be reluctant to eat these
preparations, and a diet of rice
or potato with high quality,
highly digestible protein (such as
cottage cheese, soya or white
chicken meat) may suffice.
Some controversy exists about
protein restriction in young
patients, given their need for
protein for growth. The authors
recommend that pat ients
are provided with a diet with suf-
fi cient protein for growth (mon-
CLINICAL SMALL ANIMAL
itor serum albumin and increase
the protein content of the diet
if this is decreasing), but not
enough to cause encephalo-
pathic signs. A good-quality
protein source can be added to
a liver diet, or a higher protein
diet can be selected if necessary. � Lactulose. This works by
decreasing colonic pH, increas-
ing entrapment of ammonium,
increasing faecal nitrogen excre-
tion, inhibiting protein and amino
acid metabolism, and decreas-
ing intestinal transit time. The
dosage is empirical, but should
be titrated until two or three
soft, but formed, stools per day
are passed. � Antibiotics. Once animals
are no longer encephalopathic,
oral antibiotics may be provided
and the authors prefer ampicil-
lin or amoxicillin. Occasionally,
lower dose metronidazole may
be used. � Regular, routine parasite
control. � Gastroprotectants. Gas-
trointest inal haemorrhage
may be seen in patients with
PSS. This is the equivalent of
a high-protein meal, making
encephalopathy more likely.
Gastroprotectants are not
used routinely and are reserved
for patients with documented
gastrointestinal bleeding, or a
history and investigation that are
highly suggestive.
Medical management alone
may be possible and up to one
third of dogs will do well. Ulti-
mately, once the animal is stabi-
Figure 5. Ultrasonographic image of a portocaval extrahepatic shunt. Caudal vena cava (CVC) and hepatic portal vein (HPV).
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.
Figure 6. Confi rmation of the shunting blood fl ow demonstrated using colour fl ow Doppler.
Figure 7. Ultrasonographic image of an intrahepatic PSS.
� PORTOSYSTEMIC SHUNTS IN CATS AND DOGS: SIGNS AND DIAGNOSIS – from page 13
lised medically, the authors pre-
fer to pursue surgical correction
where possible, and anecdotally
believe that the low postopera-
tive incidence of seizures seen at
their hospital is due to good pre-
operative medical management.
Without surgery, animals may
live for up to seven years and
survival has been correlated to
age at presentation and serum
BUN concentration.
Ultimately, more than half of
dogs managed medically will be
euthanised within 10 months
because of neurological dete-
rioration or progressive hepatic
fi brosis (Watson, 1998). How-
ever, long-term survival studies
for animals with surgically cor-
rected PSS are not available.
SummaryPSS are congenital or acquired
vascular abnormalities that con-
nect the portal and systemic
circulation. Haematological and
serum biochemical changes may
be suggestive of PSS, but defi ni-
tive diagnosis is achieved via
imaging or surgical evaluation.
Medical management should
be initiated in the fi rst instance,
the mainstay of which is an
appropriate diet, lactulose
and antibiotics.
Surgical management and
postoperative care will be dis-
cussed in a later article.
References and further readingBerent A C and Tobias K M (2009).
Portosystemic vascular anomalies,
Veterinary Clinics of North America:
Small Animal Practice 39: 513-541.
Center S A and Magne M L (1990).
Historical, physical examination and
clinicopathologic features or porto-
systemic vascular anomalies in the
dog and cat, Seminars in Veterinary
Medicine and Surgery Small Animal
5: 83-93.
Tobias K M (2003). Portosystemic
shunts and other hepatic vascular
anomalies. In Slatter D (ed) Textbook
of Small Animal Surgery (3rd edn),
Elsevier Science, USA: 727-752.
Tillson D M and Winkler J T (2002).
Diagnosis and treatment of porto-
systemic shunts in the cat, Veterinary
Clinics of North America: Small Animal
Practice 32: 881-899.
Watson P J and Herrtage M E (1998).
Medical management of congenital
portosystemic shunts in 27 dogs –
a retrospective study, Journal of
Small Animal Practice 39: 62-68.
Witte C L, Tobin G R, Clark D S
and Witte M H (1976). Relation-
ship of splanchnic blood flow and
portal venous resistance to elevated
portal pressure in the dog, Gut 17:
122-126. �
KELLY BOWLT qualifi ed from the University of Edinburgh in 2005. She spent two years in small animal practice in Nottinghamshire and one year as a junior clinical training scholar at the RVC. In 2008, she began an ECVS-approved residency in small animal surgery at the University of Bristol, where her interests include soft tissue surgery, particularly reconstructive surgery and management of trauma patients.
ED FRIEND graduated from the RVC in 1996 and worked in a mixed practice in Buckinghamshire for a year, before undertaking training positions at the RVC, University of Liverpool and University of Cambridge. He became a diplomate of the ECVS and a European specialist in small animal surgery in 2003. He joined the University of Bristol surgery department as a soft tissue surgeon in 2009 and enjoys ear, nose and throat surgery, thoracic surgery, trauma cases and wound management.
KATE MURPHY is senior clinical fellow in small animal emergency medicine and intensive care at the University of Bristol. She is interested in all aspects of internal medicine, but particularly enjoys the challenges posed by more critically ill patients.
Figure 8. Lateral cranial abdominal radiograph showing mesenteric portovenography of a portocaval shunt. Caudal vena cava (CVC), shunt (S) and hepatic portal vein (HPV).
Figure 9. Lateral abdominal radiograph showing mesenteric portovenography in the same animal as in fi gure 8. The shunt has been completely occluded and adequatearborisation of the contrast through the liver can be seen. Note excretion of the contrast through the kidneys. Renal pelvis (RP) and ureter (U).
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.
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