HEPATOPATHY IN CANINES: PROTOCOLS

FOR INVESTIGATION & MANAGEMENT

Pardeep SharmaAssistant Professor (Veterinary Medicine)

Department of Teaching Veterinary Clinical Complex

DGCN - College of Veterinary & Animal Sciences

CSK HPKV Palampur-176062

EXAMINATION OF LIVER

INTRODUCTION

Most important vital organ

Largest gland of the body.

Large reserve capacity &

capable of regeneration(60% of liver will regenerate within a week)

Important function includes :

Metabolism : Fat, CHO, protein, drugs, hormones

Production & excretion of bile

Detoxification & excretion of toxic substances

Converts Ammonia into Urea

Act as a storage of Iron, B12 & Folic Acid.

CONSEQUENCES OF HEPATIC DYSFUNCTION

No. Function Product Conditions

I BILE

PRODUCTION

Bilirubin Prehepatic (hemolysis)

Hepatic (hepatocyte dysfunction/ cholestasis)

Post hepatic (cholestasis - Tumour, pancreatic, worm

Bile Acids Steatorrhoea (in gut)

II METABOLIC Hypoglycemia (Glycogen store/ gluconeogenesis affected / insulin

degradation, end stage liver diseases)

Hypoalbuminemia Ascites

III CIRCULATION Ascites oncotic Pr/ Hydrostatic Pr/ Sod.water retention

Portosystemic shunt

IV Detoxification Drug metabolism Hepatic encephalopathy

V OTHERS Bleeding Clotting factor

Vit K Malabsorption

Portal hypertension ( GI bleeding)

Polyuria/ polydipsia (rare)

CONSEQUENCES OF HEPATIC DYSFUNCTION

Wide spread

Acute lesions

Regenerate

Chronic lesion

Fatty liver

End stage

Necrosis

Fibrosis

Cirrhosis

ETIOLOGYNo. Course Etiology Consequences

i Acute liver

diseases

INFECTIOUS ICH

Leptospirosis

Toxoplasmosis

TOXINS Drugs like anticonvulsants &

glucocorticoids

Chemicals like heavy metals, CCl4

Plant toxins like Aflatoxin.

II

Chronic liver

diseases

Chronic hepatitis Chronic ICH

Leptospirosis

Drug Associated

Cirrhosis

Hepatic Neoplasia

Vascular malformation

Billiary tract diseases.

BREED PREDISPOSITION

High incidences of inherited copper storage hepatopathy in the Belington terrier.

Middle aged dogs of a number of breeds are over represented including American and English Cocker spaniels.

West Highland White terriers,

Dobermans (strong female predisposition),

Dalmatians and Labrador retrievers

DIAGNOSIS OF LIVER DISEASE

History

Signalment

Clinical signs

Physical examination

Radiological examination

Ultrasonography

Haematological examination

Biopsy

Liver function tests

DIAGNOSIS

Challenge for clinician as :

Clinical signs are vague & non-

specific.

Even jaundice/ascites if present

requires differentiation from causes

other than liver diseases.

Lack of clinical signs are partly due to

large functional reserve of liver &

Remarkable power of regeneration.

About 80 % of liver’s functional

mass may be lost before clinical

signs develop.

Icteric Conjuctival

Mucosa

Ascites in Pomeranian

Physical

Examination

CLINICAL SIGNS :

Clinical signs suggestive of hepatopathy are : Lethargy, anorexia & selective feeding

Weight loss,

Polydypsia & polyuria

Vomition, diarrhoea, constipation

Jaundice & Ascites.

Certain clinical signs are more

related with liver diseases like:

Alteration in liver size : Enlargement / reduction.

Jaundice : Prehepatic / hepatocellular / obstructive.

Ascites.

Hepatic encephalopathy.

Faecal changes & coagulation defects.

Melaena

HEPATIC ENCEPHALOPATHY

Signs vary

• Depression,

• Behavioral

changes

•Mania

• Convulsions

JAUNDICE :(BILIRUBIN > 2MG/DL)

Pre-hepatic : Babesiosis, Leptospirosis & Leishmaniasis.

Hepatocellular : Hepatitis, chronic active hepatitis, cirrhosis, ICH, Leptospirosis, Salmonellosis and Toxoplasmosis.

Obstructive : Intrahepatic – Cholangiohepatitis,

Cirrhosis, Cholestasis and Neoplasia.

Extrahepatic – Bile duct compression, Cholelithiasis and Duodenal obstruction.

Icteric oral mucosa

Icteric abdominal skin

ASCITES :

Can be associated with causes other than liver

disease.

If due to liver involvement : indicates chronic

process and occurs due to :

Portal hypertension

Hypoalbuminaemia

Increased hepatic lymph production

Sodium retention

Ascites in German Shepherd

LABORATORY ASSESSMENT :

Serum Enzymology :

(evaluate injury to liver)

AST

ALT

ALP

GGT

ALT and AST are injury enzymes and increased

in hepatitis and chronic active hepatitis.

ALP and GGT are cholestasis enzymes.

Enzymatic profile in hepatic dysfunctions

TEST BASED UPON HEPATIC SECRETION /

EXCRETION: EVALUATE FUNCTION

Bile pigments

Bile salts (concentration is increased)

Clearance of foreign dyes (BSP: t ½ is increased in hepatopathy.)

TEST BASED UPON Specific biochemical function:

Plasma Albumin : Hypoalbuminaemia occuring in chronic liver diseases.

Globulin may increase or decrease depending upon chronicity.

Ammonia metabolism : Increased ammonia level lead to hepatic

encephalopathy.

RADIOGRAPHY:

Normally the liver is confined within the costal

arch on both lateral and ventrodorsal view.

Hepatomegaly signs include rounding of

liver lobes and their projection beyond

costal arch.

Localised liver enlargement may be seen in

cases of neoplasia, hepatic cysts or

abscess.

In case of ascites radiograph shows ground

glass appearance and masking abdominal

details.

Severe ascites in case of hepatitis masking the details of abdominal organs

completely

ULTRASONOGRAPHY:

Normal liver paraenchyma is

hypoechogenic than spleen and

hyperechogenic / isoechogenic to renal cortex.

Hyperechoic liver is more

brighter & generally indicate chronicity like cirrhosis / fibrosis.

USG Gall bladder disorders like

cholecystitis, sludge &cholelithiasis

can also be detected.

Severe thickening of GB wall (>5mm) in case of cholecystitis

Cholecystitis

Diaphragm

GB

Normal echotexture of liver

Ultrasonogram of the liver in a

healthy dog

Rounding of liver lobe

Severe anechogenic peritoneal effusion

in case of hepatitis

HAEMATOLOGICAL EXAMINATION

No specific changes can be seen.

Anemia and reduction in haemoglobin, PCV,

and TEC may be recorded.

Clotting abnormalities can be seen, all

clotting factors are produced in liver except

factor VIIIBiopsy

Most satisfactory method to determine

nature and severity of liver dysfunction.

Hepatomegaly, jaundice,

neoplasia can be differentially diagnosed.

DIETARY MANAGEMENT OF LIVER DISEASE

Rest to the animal.

Correct malnutrition by fulfilling the basic

energy.

Provide carbohydrate rich diet & nutrient

requirements (amino acids, K & Zn, especially

vitamins B, C & K).

Administration of 5-10 % glucose I/V.

Support hepatocellular regeneration by

providing the limiting nutrients i.e. diet must be

low in protein.

High biological value protein like Proteinex

should be given.

To limit liver damage by preventing copper

TABLE 1. ANTIMICROBIAL TO PREVENT

BACTERAEMIA / SEPTICEMIA:

Drug Dosages Use Side effects

Amoxicillin-

clavulanate

13mg/kg PO Antimicrobial GI upset, diarrhea

Fluoroquinolone

s

2.5-5mg/kg/PO -do- GI upset ,cartilage

damage, retinal

degeneration

Cefotetan 30mg/kg s/c -do- Diarrhea

Meteronidazole 7.5mg /kg PO -do- Anorexia, weakness,

ataxia with large dose

Neomycin 20mg/kg PO Decrease

ammonia

Diarrhea, nephrotoxicity,

ototoxicity

Lactulose 0.5ml/kg PO -do- Diarrhea

TABLE 2: HEPATOPROTECTANTS & CHOLERETICS

NUTRACEUTICAL DRUGS

Drug Dosage Use Side effects

Ursodeoxycholic

acid

15 mg/kg PO Hepatoprotectant,

cholerectics

GI upset

Vit-E 400-500 IU/day PO -do- Rare

SAMe(Ademetionine)

18 mg/kg PO -do- None known

Milk thistle

(Silymarin)

4-8 mg/kg day

PO(human)

-do- GI upsets,

allergic skin

diseases in

human

L-Carnitine 250mg/day (cats) -do- Not known

Taurine 250-500mg/day PO

(Cats)

-do- -do-

MANAGEMENT (CONTD…) :

Management of Ascites :

Include rest, dietary restriction of sodium.

Administration of diuretic.

Spironolactone @ 2 mg / kg b. wt. or combination of

spironolactone and frusemide is used.

Abdominal paracentesis in cases of respiratory

distress. (tapping the abdomen utilizing a

drainage technique)

TABLE 3. IMMUNOSUPPRESSANT, ANTIFIBROTIC

& CUPRURETIC

Drug Dosage Use Side effects

Prednisone or

Prednisolone2.2 mg /kg/day

PO then taper

every 2-4wk to

lowest effective

dose

Immunosuppress

ant, antfibroticPossible

exacerbation of

encephalopathy,

infection, GI

ulceration

Dexamethasone 0.3 mg/kg PO Immunosuppress

ant,antifibroticEncephalopathy, GI

infection

Azathioprine 50 mg/m2 PO Immunosuppress

ant

Bone marrow

suppression

pancreatitis,

hepatotoxicity.

Colchicine 0.03 mg /kg PO Antifibrotic Nausea, vomiting,

diarrhea

Elemental Zinc 100 mg PO Antifibrotic,

cupruretic

GI upset, hemolysis

D-Penicillamine 10-15 mg/kg PO Cupruretic Nausea, anorexia,

vomiting.

TAKE HOME MESSAGE

Specific attention in high risk breeds

Non specific clinical signs

Increased ALT – initiate diagnostic steps

Rule out extra hepatic causes

Avoid / reduce hepato toxic drugs

THANKYOU

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