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Diseases of the liver

Primary diseases of the liver, with the exception of the fat cow syndrome of cows in early lactation, seldom occur in farm animals except as a result of poisoning.

Principles of hepatic dysfunction

DIFFUSE AND FOCAL HEPATIC DISEASE

The liver has a large reserve of function and approximately three-quarters of its parenchyma must be rendered inactive before clinical signs of hepatic dysfunction appear.

Diffuse diseases of the liver can be classified as hepatitis and hepatosis according to the pathological change.

HEPATIC DYSFUNCTION

There are no specific modes of hepatic dysfunction. The liver has several important functions and any diffuse disease of the organ interferes with most or all of the functions to the same degree. Variations occur in the acuteness and severity of the damage,but the effects are the same and the clinical manifestations vary in degree only.

PORTAL CIRCULATION

The liver depending upon the portal vein for its supply of nutrients and the portal flow depending upon the patency of the hepatic sinusoids.
The portal flow is unusual in that blood from the gastrosplenic area and the lower part of the large intestine passes to the left half of the liver and the blood from the two intestines to the right half, without mixing the two streams in the portal vein. The restriction of toxipathic hepatitis of one half of the liver and the localization of metastatic abscesses and neoplasms in specific lobes results from the failure of portal vein blood from different gut segments to mix. The localization of toxipathic hepatitis may be because of selective distribution of the toxin or of protective metabolites.


The passage of blood from the portal circuit through the liver to the caudal vena cava is dependent upon the patency of the hepatic vascular bed, and obstruction results in damming back of blood in the portal system, portal hypertension, interference with digestion and absorption, and in the final stages the development of ascites.

Manifestations of liver and biliary disease

JAUNDICE

Jaundice is a clinical sign that often arises in diseases of the liver and biliary system

but also in diseases in which there are no lesions of these organs. It does not always occur and may be clearly absent in acute hepatitis.
Although jaundice is a result of the accumulation of bilirubin, the staining is much more pronounced with conjugated (direct) bilirubin than with unconjugated (indirect) bilirubin. Thus
the jaundice is more intense in cases of obstructive and hepatocellular jaundice than in hemolytic jaundice.

The levels of bilirubin in blood also affect the intensity of the jaundice, the obstructive form often
being associated with levels of bilirubin that are ten times higher than those commonly seen in hemolytic anemia.

The staining of jaundice is due to staining of tissues, especially elastic tissue, and not to
accumulation in tissue fluids, so that it is best detected clinically in the sclera , and jaundice that may be detectable easily at necropsy may not be visible on clinical examination.

The primary differentiation has to be made between jaundice with and without impairment of bile flow.
The only accurate basis for the differentiation between jaundice with impaired bile flow
and jaundice without impaired flow is the examination of the urine for the presence of bilirubin and urobilinogen and the determination of the relative amounts of conjugated and unconjugated .
Bilirubin present in the serum.
Unconjugated (indirect) bilirubin that has not passed through hepatic cells is not excreted by the kidney, so that in hemolytic jaundice the indirect bilirubin content of serum is increased markedly and, although the urine contains an increased amount of urobilinogen, no bilirubin is present.


In those cases in which jaundice is caused by impairment of bile flow there is a marked
increase in the serum level of conjugated (direct) bilirubin, and the bilirubin content of the urine is greatly increased. The amount of urobilinogen varies depending on whether any bilirubin reaches the intestine to be metabolized to urobilinogen and reabsorbed.

In complete extrahepatic biliary obstruction urobilinogen is not present in the urine.

OVERPRODUCTION OR HEMOLYTIC JAUNDICE

Hemolytic jaundice is common in animals and may be associated with bacterial toxins, invasion of erythrocytes by protozoa or viruses, inorganic and organic poisons and immunological reactions.

Diseases :

Bacillary hemoglobinuria of cattle
Leptospirosis.
Babesiosis, anaplasmosis, eperythrozoonosis .
Equine infectious anemia.
Chronic copper poisoning, selenium poisoning in sheep, phenothiazine poisoning in horses,
pasturing on rape and other cruciferous plants and bites by some snakes are other
common causes.
Postparturient hemoglobinuria
Isoimmunization hemolytic anemia of the newborn is caused by an immunological reaction between the sensitized cells of the newborn and antibodies in the colostrum of the dam.


Hemolytic jaundice is characterized clinically by a moderate degree of yellowing of the mucosae, and by the presence of hemoglobinuria in severe cases.

Clinicopathological findings indicate the presence of anemia, an increase in urobilinogen and an absence of bilirubin in the urine, and a preponderance of indirect bilirubin in the serum.

JAUNDICE DUE TO HEPATIC CELL DEGENERATION

The cause may be any of those diffuse diseases of the liver that cause degeneration
of hepatic cells ( hepatitis ). Because there is only partial obstruction of biliary excretion, the changes in serum and urine lie between those of hemolytic jaundice and extrahepatic biliary obstruction.
Serum levels of total bilirubin are increased because of retention of direct bilirubin, which also passes out in the urine, causing an elevation of urine levels. The urobilinogen levels in the urine also rise.

EXTRAHEPATIC BILIARY OBSTRUCTION

Obstruction of the bile ducts or common bile duct by biliary calculi or compression
by tumor masses is a rare occurrence in farm animals. Commonly listed causes are obstruction of the common duct by nematodes and inflammation of the bile ducts by extension from an enteritis or by infestation with trematodes.
Parasitic cholangitis and cholecystitis also occur due to fascioliasis and infestation with Dicrocoelium dentriticum.

JAUNDICE DUE TO INTRAHEPATIC PRIMARY CHOLESTASIS

The mechanical stasis of biliary flow caused by fibrous tissue constriction and obliteration of the small biliary canaliculi may occur after hepatitis and in many forms of fibrosis. Cholelithiasis, the
formation of biliary calculi, is frequently reported as a cause of cholestasis in humans and has been reported in horses and cattle.

NERVOUS SIGNS (HEPATIC ENCEPHALOPATHY)

Nervous signs include:
Hyperexcitability
Convulsions
Muscle tremor and weakness
Dullness
" Yawning
Compulsive walking
Head-pressing
Failure to respond to signals
Mania in some cases.

These are common with any severe hepatocellular insufficiency or major circulatory bypass of the liver. Terminally, hepatic coma may occur.

Many factors, including hypoglycemia and failure of normal hepatic detoxification mechanisms, leading to the accumulation of excess amino acids and ammonia, or of acetylcholine, and the liberation of toxic breakdown products of liver parenchyma, have all been suggested as causes and
significantly elevated in cattle with hepatic disease.

Clinical signs of hepatic encephalopathy such as blindness, head pressing, excitability, ataxia and weakness, together with fever and jaundice, are grave prognostic signs.


EDEMA AND EMACIATION

Failure of the liver to anabolize amino acids and protein during hepatic insufficiency is manifested by tissue wasting and a fall in plasma protein. This may be sufficiently severe to cause edema because of the lowered osmotic pressure of the plasma.

Hepatic edema is not usually very marked and is manifested most commonly in the intermandibular space (bottle jaw). If there is obstruction to the portal circulation, as may occur
in hepatic fibrosis, the edema is much more severe but is largely limited to the abdominal cavity.

DIARRHEA AND CONSTIPATION

In hepatitis, hepatic fibrosis and obstruction or stasis of the biliary system, the partial or complete absence of bile salts from the alimentary tract deprives it of the laxative and mildly disinfectant qualities of these salts. This, together with the reflex effects from the distended liver in acute hepatitis, produces an alimentary tract syndrome comprising anorexia, vomit ion in some species and constipation punctuated by attacks of diarrhea.
The feces are pale in color and, if there is an appreciable amount of fat in the diet, there is steatorrhea.

PHOTOSENSITIZATION

Most photosensitizing substances, including phylloerythrin, the normal breakdown
product of chlorophyll in the alimentary tract, are excreted in the bile. In hepatic or biliary insufficiency excretion of these substances is retarded and photosensitization occurs.

H EMORRHAGIC DIATH ESIS

In severe diffuse diseases of the liver there is a deficiency in prothrombin formation
and a consequent prolongation of the clotting time of the blood. Abnormality of the prothrombin complex is not the only defect, deficiencies of fibrinogen and thromboplast also occurring. Prothrombin and other factors in the prothrombin complex depend upon the presence of
vitamin K for their formation and an absence of bile salts from the intestine retards the absorption of this fat-soluble vitamin. Parenteral administration of vitamin K is advisable before surgery is
undertaken in patients with severe hepatic dysfunction.


ABDOMINAL PAIN

Two mechanisms cause the pain in diseases of the liver: distension of the organ with increased tension of the capsule, and lesions of the capsule. Acute swelling of the liver occurs as a result of engorgement with blood in congestive heart failure and in acute inflammation.
Inflammatory and neoplastic lesions of the capsule, or of the liver parenchyma just beneath the capsule, cause local irritation to its pain end organs. The pain is usually subacute, causing abnormal posture, particularly arching the back, and disinclination to move. Tenseness of the
abdominal wall and pain on deep palpation over the liver area may also be detected in the majority of cases.

ALTERATION IN SIZE OF THE LIVER

Great variation in the size of the liver is often seen at necropsy but clinical detection
is not easy unless the liver is grossly enlarged. This is most likely to occur in advanced congestion of the liver due to congestive heart failure, in some plant poisonings in horses and when multiple
abscesses or neoplastic metastases occur.
In acute hepatitis the swelling is not sufficiently large to be detected clinically and in terminal fibrosis the liver is much smaller than normal.
weight while the right lobe in horses with

DISPLACEMENT OF THE LIVER

The liver may be displaced from its normal position and protrude into the thoracic cavity through a diaphragmatic hernia, causing respiratory distress and abnormal findings on percussion of the chest.

RUPTURE OF THE LIVER

Rupture of the liver is an occasional accident in animals, occurring usually as a
result of trauma. In most instances rupture results in death from hemorrhage.