Liver Disease In Small Animals

First things first, clinical signs:

Suggestions please!

One thing to consider is melena. What is the mechanism of this in a dog with liver disease?

And now onto ascites – we have that it can be caused by portal hypertension but there is another reason…

So now we have recognised that our poorly patient is looking like a good candidate for liver disease. What do we want to do next?

A word on jaundice:

Let’s think about BUN for a moment

Another test to consider is a bile acid stimulation test

Summary: bile acid stimulation test
So, to take a bile acid stim test, you need to have a patient that has been starved for 12 hours. You can then take bloods, feed the animal (fatty meal preferably) then re-sample in 2 hours.

Bile acids are synthesised in the liver from cholesterol, before being stored in the gall bladder in bile. The enterohepatic circulation involves the transport of bile acids back from the ileum and into the portal circulation. If there is disease altering the enterohepatic circulation then this results in increased levels of bile acids in serum.

Bile acid stimulation is the only way to test for liver function!

Now let’s think about ammonia:

So ammonia is useful but a bit of a tricky one to measure! There are some other things we can look at on our bloodwork as well as part of a routine biochemistry panel.

So, now we’ve had a think about general clinical signs and tests for liver disease, let’s move onto a more specific condition: portosystemic shunts

Portosystemic shunts

First up, what types of disease are possible?

And some general breed related rules of thumb

Also, we need to think about clinical signs

So a stunted, slobbery cat should get some alarm bells ringing!

Now we can recognise a possible shunt in our consulting room, what further tests are we going to want to run?

Making a diagnosis

So, on ultrasound we might be lucky and find our shunt if we’re very good, if not then we are also on the lookout for changes in liver architecture and size, big kidneys and urate crystals in the bladder (have a look here for a bit more on urate crystals: ) It is also worth bearing in mind that urate crystals are radiolucent, but are visible on ultrasound.

Let’s also quickly think about the kidney issue

Now, back to our ultrasound examination – what might we find?

How is best to go about taking samples from the liver?

Summary note: coagulation problems and liver disease
The liver is involved in synthesis of
anti-coagulant and coagulation factors and involved in platelet function. With severe liver disease, animals can have primary and secondary haemostatic defects.

Primary haemostasis

This is the initial response to
endothelial damage and involves formation of a
platelet plug and local


Secondary haemostasis

This involves strengthening and
reinforcing the platelet plug and then formation of a
stable fibrin clot


Tertiary haemostasis

Removal of the clot

Clotting pathways

Extrinsic pathway:
activated by tissue trauma

Intrinsic pathway:
damage to a surface

Both activate the
common pathway

Primary haemostatic tests
Buccal mucosal bleeding time (BMBT)

The upper lip is everted and an incision is made on the upper
lip with a simplate device. Blood is dabbed away with
filter paper, not dislodging the clot, and the filter paper is constantly turned. The BMBT is the time from incision to the time bleeding stops.
Normal times:

– Dog: 1.7-3.3 minutes

– Anaesthetised dog: 1.7-4.2 minutes

– Anaesthetised cat: <3.3 minutes

An increased BMBT indicates primary
haemostasis defective vWF, platelets and vascular defects


Platelet count

Take an EDTA blood sample and view ASAP to avoid clumping
a) Use a haemocytometer
b) Estimate from a blood smear on oil immersion
EDTA blood sampling
and ASAP to avoid clumping

If you use an automatic platelet count, you should always cross-check with a smear! 


Platelet count (x10-9/l) – dogs

– Normal:150-400

– Thrombocytopaenia: <100

– Haemorrhage may be induced: <50
– Spontaneous haemorrhage: <30

Secondary haemostatic tests

Activated coagulation time (ACT)

Place 2ml blood in ACT
tube containing the contact activator and incubate at 37*C for 60s. Check for clot
formation every 5-10s

Normal results 
– Dog: 60-110s

– Cat: 50-75s
Extended ACT with
90% deficiency of intrinsic pathway coagulation factors


Prothrombin time (PT)

Add tissue
thromboplastin and calcium ions to citrated plasma to activate the extrinsic pathway

It is prolonged when
factors <30% of normal


Activated partial prothrombin time (aPPT)

Add reagent to
citrated plasma to activate the intrinsic system (surface activator and phospholipid) and calcium

No tissue

Prolonged when
factors <30% of normal

You must ALWAYS check
haematology and clotting times before a liver biopsy

Let’s discuss the pros and cons of different sampling methods:

Management of liver disease

Now we’re all clued up on what to look for and how to test for it, how are we going to manage our liver cases?

A quick note on antioxidants:
– Oxidant stress is
induced in cases of liver disease due to the effects of inflammation, reduced
blood flow and mitochondrial damage from refluxed bile acids


Increases hepatic
and red cell glutathione levels

Particularly helpful
for toxic hepatopathies – especially steroid hepatopathies


Vitamin E

Effective in dogs
with liver disease

Should be used in
cases of copper storage disease



Has antioxidant

So, to summarise our treatment plan:

And a few others for more specific indications:
1. Spironolactone

2. Destolit (ursodeoxycholic acid)

So, that wraps up another successful #vetfinals session!

A nice resource for some more detailed reading is a series of In Practice articles on liver disease:
1. Diagnosis of canine liver disease: 
2. Treatment of canine liver disease – drugs and diet: 
3. Treatment of canine liver disease – managing signs and specific diseases: 
4. Liver disease in cats: 

Also, for a review in a hurry!;Entity=10MinuteTopUps&amp;ID=3