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680 Section 7 Diseases of the Liver, Gallbladder, and Bile Ducts
Supportive care includes restoration of the fluid and resulting from liver dysfunction depend on the extent of
VetBooks.ir electrolyte balance. Ammonia (if available), electrolytes liver necrosis, and vary from general illness and lethargy
to hepatic encephalopathy. Anorexia and vomiting may
(sodium and especially potassium), and pH should be
monitored to permit supportive care directed at hepatic
liver.
encephalopathy if indicated. occur as a result of impaired detoxifying function of the
Prognosis Diagnosis
Owners need to be warned that the prognosis is gener- The presence and severity of any liver changes can only
ally guarded, with roughly half of cats surviving. be confirmed by histologic examination of a liver biopsy.
Moreover, therapy can be prolonged, sometimes consist- These changes are specific and therefore confirmatory.
ing of several weeks to months of enteral nutrition. The An impression of the severity and course of the liver
prognosis is quite good if the condition is diagnosed and necrosis is provided by measurements of the liver
treated early. However, cats with severe hepatic encepha- enzymes and bile acids in serum, but they may also be
lopathy have a worse prognosis. elevated in any other hepatobiliary disease and are by no
means specific. The diagnosis of the underlying disease
causing anemia or shock is not discussed here.
Liver Changes Due to Anemia and Shock
(Acute Hypoperfusion)
Therapy
Etiology/Pathophysiology Management primarily involves treatment of the under-
Liver degeneration or necrosis can occur with acute lying cause of hypoxia. There is no specific treatment
hypoxia of the liver. In this context, it is important to possible for the hepatic lesions, and the liver will recover
remember that the blood supply of the liver is predomi- spontaneously in most cases after resolution of the
nantly venous and therefore any adaptation to hypoxia underlying condition. In cases of severe damage, the
requires time. Possible causes for such lesions are acute impaired liver function may become life‐threatening.
hemolysis or massive blood loss. Histologically, there is Only symptomatic supportive therapy for liver dysfunc-
necrosis of the centrilobular zone 3 (the oxygen‐poor tion can be given, to allow time for the liver to regener-
part of the liver lobule). Extensive necrosis may occur in ate. Specific measures to prevent or reduce hepatic
rare cases with confluent and bridging necrosis, forming encephalopathy may be important. Remember that the
connections between necrotic centrilobular areas. course of liver regeneration cannot be evaluated by the
Necrosis induces a secondary inflammatory reaction of degree of icterus.
polymorphonuclear cells, and there is usually wide-
spread cholestasis. In cases of hemolysis, there is eryth- Prognosis
rophagocytosis and/or accumulation of iron pigment in The prognosis is very variable and primarily depends on
the reticuloendothelial system, and sometimes extramed- the underlying cause of hypoxia. If the underlying cause
ullary hematopoiesis is seen. In addition to the general can be addressed, hepatic changes are likely to be
illness and icterus, hepatic encephalopathy can also reversible.
occur in severely affected cases.
These changes explain why hemolytic anemia is so
often accompanied by an increase in conjugated biliru- Amyloidosis
bin, and this is sometimes marked. It is the cholestasis, Etiology/Pathophysiology
rather than the hemolysis, that determines the degree of Amyloidosis of the liver is very rare in dogs or cats.
icterus. Hence, bilirubin is predominantly the conju- Amyloidosis is often a systemic disease involving a num-
gated direct reacting type. ALT, AST, ALP, and gamma‐ ber of organs. In cases of generalized amyloidosis, there is
glutamyl transferase (GGT) can be severely elevated. usually also deposition of amyloid in the liver and kidneys,
Sometimes, the liver dysfunction is so severe that, in but this seldom leads to clinical signs relevant to the liver.
spite of adequate treatment of the hemolysis, it leads to The severe glomerular damage leading to urinary protein
death. loss is almost always the most important clinical phenom-
enon. In the liver, deposits of amyloid are visible as amor-
History and Clinical Signs phous hyaline and eosinophilic material in the space of
Clinical signs are usually acute in onset, and a history of Disse when Congo red staining is used. Depending on the
recent shock may be present. In hemolytic anemia, the amount of amyloid, the liver may be enlarged on abdomi-
mucous membranes may be jaundiced and are usually nal palpation. However, it is often a normal size. Liver
pale. Clinical signs are in part those of anemia, namely enzymes and bile acids may be increased, although some-
lethargy and exercise intolerance. Subsequent signs times they are within the normal reference interval.