HEPATIC

DISEASES AND
TREATMENT BPHA 4652
 RESOURCES
https://www.merckvetmanual.com/
Veterinary Clinical Drug Information Monographs(VCDIM): VCDIM: https://
www.aavpt.org/page/43
 https://www.aavpt.org/page/48
OBJECTIVES
After completing the topic, student will be able to:
discuss diseases, parasites and pathologies that affect the liver
gain basic idea of common liver diseases in our animals
discuss which drugs to use, dosage, amount and time or duration of treatment.
 INTRODUCTION
These are diseases affecting the liver and areas associated with liver.
The conditions can be due infection or non infection.
The diseases are common in both small and large animals
Some of the organisms responsible for the diseases can be transmitted to human
 LIVER DISEASES
Small animal liver diseases and treatments
Large animal liver diseases and treatments
Tyzzer Disease,
Wesselsbron Disease and
 Infectious Canine Hepatitis with treatments.
OTHER CONDITIONS
Liver fluke
splenomegaly
diabetic Hepatopathy
bile duct obstruction
 DISEASES IN SMALL ANIMALS: SHARON A. CENTER , DVM, DACVIM, CORNELL UNIVERSITY,
COLLEGE OF VETERINARY MEDICINE

The liver performs numerous functions, including but not limited to lipid,
carbohydrate, and protein metabolism; storage, metabolism, and activation of
vitamins; storage of minerals, glycogen, and triglycerides; extra medullary
hematopoiesis; and synthesis of coagulant, anticoagulant, and several acute
phase proteins.
It also influences immunologic responses and contributes to digestion through
synthesis and enterohepatic circulation of bile acids and detoxification of many
endogenous and exogenous compounds, toxins, and xenobiotic.
The liver has a large functional reserve and the ability to regenerate, the
hepatic injury must be considerable or chronic and recurrent to cause overt
hepatic dysfunction or failure.
 PATHOLOGY
In Pigs: Vitamin E or selenium deficiency (hepatosis dietetica), aflatoxicosis, ascarid
migration, bacterial hepatitis, and ingestion of toxic substances (eg, coal tar,
cyanimide, blue-green algae, plants, gossypol) are associated with hepatic injury in
swine.
PATHOLOGY OF LIVER
DISEASE.
Active liver injury is accompanied by increased liver enzyme activity,
with cytosolic transaminases (ALT, AST) acutely reflecting altered
membrane permeability or viability or the phenomenon of membrane
blebbing, and membrane-affiliated enzyme induction (alkaline
phosphatase [ALP], γ-glut amyl transferase [GGT]) reflecting
cholestasis and increased protein transcription (enzyme induction)
The liver is predisposed to secondary injury owing to its sentinel
position between the systemic circulation and GI tract and because it
contains the largest population of fixed macrophages in the body.
Macrophage phagocytosis can initiate release of a cascade of
inflammatory cytokines, leading to local cellular damage and
recruitment of inflammatory infiltrates
CLINICAL SIGNS
The accumulation of other toxic products, hepatic copper and/or iron can initiate, and
augment liver injury through oxidative mechanisms.
Common clinical features may include anorexia, vomiting, diarrhea, weight loss, and
fever. With severe, diffuse liver injury, animals may become jaundiced and
demonstrate polyuria and polydipsia (PU/PD), coagulation abnormalities, and ascites.
Ascites, indicates development of portal hypertension
Hepatic encephalopathy
Hepatomegaly
Fecal color may change with complete occlusion of bile ducts (acholic or pale-
colored feces) or because of increased enteric bilirubin elimination (green fecal color)
 MISCELLANEOUS HEPATIC DISORDERS IN LARGE ANIMALS: JONATHAN H. FOREMAN , DVM, MS,
DACVIM (LAIM), COLLEGE OF VETERINARY MEDICINE, UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN

Hepatic disease is common in large animals. Increases in serum hepatic enzymes and total
bile acid concentration may indicate hepatic dysfunction, disease, or failure. Although liver
disease is especially common in horses and foals, progression to liver failure is not.
Horses and Foals:
Diseases that frequently result in hepatic failure in horses include Theiler disease, Tyzzer
disease (foals), pyrrolizidine alkaloid toxicosis, hepatic lipidosis, suppurative cholangitis or
cholangiohepatitis, cholelithiasis, and chronic active hepatitis.
Obstructive disorders (biliary stones etc), aflatoxicosis, pancreatic disease, Klein grass or
alsike clover poisoning, hepatic abscess, and perinatal herpesvirus 1 infections sporadically
result in hepatic failure
Hepatic failure is associated with end toxemia, steroid administration, inhalant anesthesia,
drug-induced amyloidosis, parasite damage, iron toxicity.
Cows: Hepatobiliary disease is associated with hepatic lipidosis, hepatic abscesses, end
toxemia, pyrrolizidine alkaloid and other plant toxicoses, certain clostridial diseases,
liver flukes, mycotoxicosis, and mineral toxicosis (copper, iron, zinc) or deficiency
(cobalt).
 SIGNS
Clinical signs of hepatic disease may not be evident until >60%–80% of the liver parenchyma
is nonfunctional or when hepatic dysfunction is secondary to disease in another organ system.
Onset of signs of hepatic encephalopathy and liver failure is often acute regardless of whether
the hepatic disease process is acute or chronic. Clinical signs and severity of hepatic pathology
reflect the degree of compromise of one or more of the liver’s vital functions.
Weight loss, or abnormal behavior are common in horses with liver disease and hepatic failure
Bilateral pharyngeal paralysis, causing respiratory difficulty, diarrhea, or constipation, may be
present
Hepatic encephalopathy is associated with behavioral changes in horses, ruminants, and swine;
depression, lethargy, aggressiveness, head pressing.
Diarrhea or constipation may be seen in animals with hepatic disease.
Recurrent colic, intermittent fever.
Anemia may be seen in animals with liver dysfunction due to parasitic diseases, chronic copper
toxicity (in ruminants), some plant poisonings, or chronic inflammatory disease.
Clinical signs of severe or terminal hepatic failure include coagulopathies and hemorrhage due
to decreased production of clotting factors by the liver and possibly increased utilization in
septic or inflammatory processes.
TESTING DIAGNOSIS
Laboratory tests often detect liver disease or dysfunction before hepatic
failure occurs.
Routine biochemical tests such as serum enzyme concentrations are
sensitive indicators of liver disease, but they do not assess hepatic function.
 Dynamic biochemical tests that assess hepatic clearance provide
quantitative information regarding hepatic function.
Tests of hepatic function are useful diagnostic and prognostic tools and provide a
guide for the modification of drug-dosing regimens.
Ultrasonography
Liver Biopsy
Radiography
 TREATMENT AND MANAGEMENT
Initial treatment of animals with signs of hepatic disease or insufficiency is often
supportive and started before the underlying cause and extent of hepatic damage is known.
History, clinical signs, and laboratory data may give some clue as to the nature of the
hepatic disease process, but liver biopsy is usually required to make a definitive diagnosis
and to determine the degree of hepatic injury.
Specific therapies for hepatic disease depend on cause, presence of liver failure,
chronicity, degree of hepatic fibrosis or biliary obstruction, and species affected. Increases
in hepatic enzymes without hepatic disease may not require specific therapy for the liver
but rather for the primary disease.
Therapy is most successful when intervention is early, hepatic fibrosis is minimal, and
evidence of regeneration in the liver exists.
Horses with hepatic encephalopathy may be aggressive or demonstrate repetitive
behaviors that make restraint difficult. To ensure safety of the animal and handlers,
sedation is required.
 ENCEPHALOPATHY
Horses with hepatic encephalopathy may be aggressive that makes
restraint difficult-give tranquilizers which are metabolized in liver so
minimal doses should be initiated with less frequency.
Xylazine or detomidine given in small doses to effect can be used to
control horses.
Avoid diazepam in animals with hepatic encephalopathy, because it
may enhance the effect of GABA on inhibitory neurons and worsen
neurologic signs.
Acepromazine should also be avoided, because it may lower the
seizure threshold.
DEHYDRATION IN ENCEPHALOPATHY AND LIVER FAILURE
MGMT.
Dehydration, acid-base and electrolyte imbalances, and hypoglycemia
should be corrected with appropriate IV fluids.
If IV infusion is not possible in ruminants, rehydration may be attempted
by oral administration of fluids if rumen motility is normal.
Acidosis should be corrected gradually by IV administration of fluids
with a high concentration of electrolytes.
Supplemental vitamins are optional. Adequate fresh water should be
available if the animal can swallow normally.
Glucose as a 5%–10% solution is given to correct hypoglycemia if
present, also to reduce blood ammonia concentration.
IV glucose should be used in combination with balanced electrolyte
fluids and not as the sole fluid source.
INFECTION IN LIVER
Treatment with broad-spectrum antimicrobials is warranted if infectious hepatitis is
suspected.
Trimethoprim-sulfa combination is a good empiric choice because of its activity
against gram-negative bacteria and its high concentration in bile.
Penicillin in combination with an aminoglycoside has a broad spectrum of action and
may be of
Enrofloxacine has also been recommended.
First- and second-generation cephalosporins have been used in foals and in other
species: Ceftiofur has a broader spectrum than most early generation cephalosporins
and has proved useful to treat acute or recurrent ascending bacterial
cholangiohepatitis.
Metronidazole may be administered when anaerobic infection is suspected in horses.
Specific antimicrobial therapy based on culture and sensitivity of a liver biopsy is
ideal.
 PAIN AND INFLAMMATION
Pain may be controlled with appropriate doses of an NSAID (eg, Flunixin Meglumine,
1.1 mg/kg, IV, bid, or phenylbutazone 4.4 mg/kg, IV or PO, bid). Vitamin K1 (up to 1
mg/kg, SC; 40–50 mg/450 kg, SC) and plasma transfusions (1–2 L/100 kg) may be
given when coagulopathies develop or hypoalbuminemia is present.
In some horses with acute hepatic disease and failure, antioxidant (dimethyl sulfoxide,
acetyl cysteine, vitamin E, S-adenosylmethionine [SAMe]), and anti-inflammatory
(Flunixin Meglumine, phenylbutazone) therapy may be useful
Mannitol has been recommended for treatment of suspected brain edema in fulminant
hepatoencephalopathy.
Horses with hepatic disease should be protected from sunlight.
 DIETARY
Dietary management is essential for management of animals with hepatic encephalopathy or
acute or chronic Hepatopathy but remember dysphagia is present.
The diet should meet energy needs with readily digestible carbohydrates, provide adequate but
not excessive protein, have a high ratio of branched-chain amino acids to aromatic amino acids,
and be moderate to high in starch to decrease need for hepatic glucose synthesis.
Fat and salt should not be added to the diet
Feeds used successfully in horses include grass or oat hay, corn, and sorghum.
Small amounts of molasses may be added to improve palatability and add energy.
Linseed meal and soybean meal have an excellent branched-chain to aromatic amino acid ratio
and may be used as a protein supplement in small quantities.
 DIETARY MANAGEMENT
CONT.
Beet pulp may be substituted for oat or grass hay. Beet pulp may be soaked first to
allow full expansion before being fed but watch out for choke!
Parenteral or enteral supplement with branched-chain amino acids helps restore the
normal ratio of branched-chain to aromatic amino acids

Supplementation with vitamins A, D, E, and K might be indicated, because these fat-

soluble vitamins are not stored effectively or readily available from a diseased liver.
Vitamin K1 may be indicated in animals with a coagulopathy.
Excessive fat may lead to a fatty liver
INFECTIOUS HEPATITIS AND HEPATIC ABSCESSES IN LARGE
ANIMALS

Tyzzer disease is caused by Clostridium piliforme (previously Bacillus piliformis) and affects a wide
range of animals in many regions of the world.
Cholangiohepatitis is a severe inflammation of the bile passages and adjacent liver, which may hepatic
failure in horses and ruminants. It occasionally occurs secondary to cholelithiasis, duodenitis, intestinal
obstruction, neoplasia, parasitism, and certain toxins in horses. The fungal toxin sporidesmin from
Pithomyces chartarum may cause cholangiohepatitis in sheep and cattle.
Treatment based on culture and sensitivity results from liver tissue often gives favorable results. Therapy
consists of longterm (≥4–6 wk) antimicrobial administration.
Initially, broad-spectrum antimicrobials effective against gram-negative, gram-positive, and anaerobic
organisms should be administered.
A combination of penicillin with either a trimethoprim-sulfa or an aminoglycoside or enrofloxacin may
be used. Ampicillin or a cephalosporin can be used instead of penicillin. Ceftiofur sodium has an
enterohepatic cycle and broader spectrum and may prove valuable in treatment. Metronidazole can be
used in horses to treat anaerobic bacteria.
 HEPATIC ABSCESSES
Hepatic abscesses are generally polymicrobial infections; anaerobes are
common.
The primary etiologic agent of liver abscesses in cattle is Fusobacterium
necrophorum. In goats, most abscesses are due to Corynebacterium
pseudotuberculosis, Trueperella pyogenes, and Escherichia coli.
Organisms less frequently isolated include Proteus sp, Mannheimia
haemolytica, Staphylococcus epidermidis, S aureus, Rhodococcus equi,
Erysipelothrix rhusiopathiae, and the yeast Candida krusei.
In horses, hepatic abscesses often contain Streptococcus spp (S equi equi,
S equi zooepidemicus), C pseudotuberculosis, or enterobacteria after
ascending cholangiohepatitis or intestinal disease, and anaerobes.
In pigs, hepatic abscesses develop after migration of ascarids into the bile
ducts.
 TREATMENT
Hepatic abscesses are most prevalent in ruminants and uncommon in horses.
Signs may be similar to those seen with other abdominal abscesses and include
intermittent colic, intermittent fever, and weight loss in cattle and horses.
Hepatic ultrasound may prove diagnostic.
Prognosis is generally poor because of lack of response to antimicrobial therapy or
incomplete resolution.
Tylosin phosphate fed at 10 g/ton of feed significantly reduces the number of liver
abscesses and increases feed efficiency and weight gain.
Virginiamycin fed at 16 g/ton of feed or chlortetracycline fed continually at 70
mg/head/day during the finishing period is also used.
Percutaneous drainage and longterm therapy with procaine penicillin G (22,000 IU/kg)
can be attempted, but the prognosis is poor in cattle.
RESEARCH AND READ THE
FOLLOWING BELOW
1. CANINE HEPATITIS
2. LIVER FLUKE
3. DIABETIC HEPATOPATHY
4. BILE DUCT OBSTRUCTION
5. VIRAL DISEASE OF
ANIMALS
TREATMENT AND
MANAGEMENT
DRUG PROFILES
Prepare drug ( commonly used) profiles used in liver diseases in small and large
animals
VIDEOS
Search and view videos on hepatic diseases in small and large animals:
Dogs: https://www.youtube.com/watch?v=hBUvvxCbkps
Cat: https://www.youtube.com/watch?v=cjdW_ZPvFcY
Large animal: https://www.youtube.com/watch?v=tC4or8qhBms
https://www.youtube.com/watch?v=T4V0IsHDUtohttps://
www.youtube.com/watch?v=T4V0IsHDUto
https://www.youtube.com/watch?v=Bw7pcK0zc4Y
Please view the videos on the ppt by copy and paste on your youtube page
Pay attention to the food/ nutrition given or restricted. Note the drugs mentioned on the videos as
wellPay attention to the food/ nutrition given or restricted. Note the drugs mentioned on the videos
as well