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.

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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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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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