Page 600 - Small Animal Internal Medicine, 6th Edition

572 PART IV Hepatobiliary and Exocrine Pancreatic Disorders

stomach) and vitamin E (≈100 IU daily) is also logical cats with sclerosing cholangitis may have hepatomegaly on
because bile is a potent oxidizing toxin in the liver. A recent radiography, which is unexpected; cirrhosis usually results in
VetBooks.ir retrospective study of 26 cats with lymphocytic cholangitis, a small liver in dogs. Presumably, this reflects the biliary tract
dilation and florid peribiliary fibrosis in these cases. Treat-
with a preponderance of older male cats and Norwegian
Forest cats, suggested that cats had a longer survival time
associated with portal hypertension, as outlined in Chapter 36.
when given prednisolone alone than when given ursodeoxy- ment is supportive, with treatment of only the clinical signs
cholic acid alone (Otte et al., 2013). Further prospective
studies are necessary to evaluate these therapies individually Liver Fluke Infestation
and together in a wider range of ages and breeds before the
results can be generalized to all cats with lymphocytic chol- Etiology and Pathogenesis
angitis. Again, it is important to ensure that affected cats eat Liver fluke infestation is regularly observed in cats from
to prevent the development of concurrent hepatic lipidosis; areas endemic for the family Opisthorchiidae (Platynoso-
as discussed earlier, a highly digestible, high-quality diet mum spp., and occasionally Amphimerus pseudofelineus and
without protein restriction is indicated. A diet formulated Metametorchis intermedius). It is estimated that, in Florida
for feline intestinal disease (e.g., Eukanuba feline intestinal, and Hawaii, the prevalence of Platynosomum fastosum (the
Procter & Gamble, Cincinnati, Ohio; Royal Canin feline most common feline liver fluke) is as high as 70%; the clini-
selected protein; or Hill’s i/d) might be the most appropriate cal feline disease is referred to as lizard poisoning. The flukes
because of the relatively high prevalence of concurrent IBD. require two intermediate hosts: water snails and lizards,
Tube feeding should be considered if necessary (see earlier, amphibians, geckos, or fish, depending on the species. The
“Hepatic Lipidosis”). Cats with more acute signs, particularly cat is the final host and is infested by ingesting the metacer-
associated with concurrent intestinal and/or pancreatic cariae in the second intermediate host. The immature flukes
disease, may require hospitalization and IV fluid therapy. migrate from the intestine to the liver via the bile ducts and
The prognosis for cure appears to be poor because the become adult and patent by 8 to 10 weeks. Eggs can then
disease appears to wax and wane chronically in spite of treat- be found in the feces (inconsistent) or bile aspirates (more
ment. However, few cats with lymphocytic cholangitis die as reliable). The severity of associated disease seems to depend
a result of their disease and those that do die have a high on the parasite load and on individual responses. Many cases
prevalence of concurrent pancreatic and intestinal disease, are mild. In some cases the pancreas may also be affected.
which may explain their poor outcome (Callahan Clark The clinical signs are caused by peribiliary inflammation
et al., 2011). This is likely because, as opposed to dogs, the and fibrosis in the liver, culminating, in severe cases, in an
disease does not generally progress to end-stage cirrhosis. obstructive jaundice. In experimental infestations, hepatic
lesions are visible histologically starting approximately 3
Sclerosing Cholangitis weeks postinfestation. There is an initial distention of proxi-
Sclerosing cholangitis, or biliary cirrhosis, involves an end- mal bile ducts and a neutrophilic and eosinophilic inflamma-
stage fibrotic liver and is uncommon in cats except in asso- tory response, which progresses chronically to adenomatous
ciation with liver fluke. Cats appear to be very resistant to duct hyperplasia and surrounding florid fibrosis. Eosinophils
hepatic fibrosis. The condition is characterized histologically may be absent in the later stages of disease, and flukes and
by diffuse proliferative fibrosis of the bile duct walls spreading eggs may not be seen on histology.
to involve the hepatic lobules and disrupting their architecture
and circulation. It is thought in most cases to represent an Clinical Signs
end stage of chronic biliary tract disease, usually complete Commonly, cats with low-grade infestations remain asymp-
obstruction or chronic severe liver fluke infestation (see the tomatic. However, heavy infestations can be associated with
next section). It is unusual for neutrophilic or lymphocytic severe and often fatal disease (Haney et al., 2006; Xavier
cholangitis to progress to sclerosing cholangitis in cats. Some et al., 2007). In these cases clinical signs are typically those
cases of ductal plate abnormality may be misdiagnosed as of posthepatic jaundice combined with those of inflamma-
sclerosing cholangitis in cats (see later section). Affected cats tory liver disease (e.g., jaundice, anorexia, depression, weight
present with typical clinical signs of chronic biliary tract disease loss, lethargy). Diarrhea and vomiting have been features of
(see previous “Cholangitis” and later “Extrahepatic Biliary clinical cases but do not occur in experimental cases; affected
Tract Obstruction”). Affected cats may also develop chronic cats may also have hepatomegaly and ascites.
portal hypertension, with the resultant development of ascites,
gastrointestinal ulceration, and/or an acquired portosystemic Diagnosis
shunt (PSS) and HE (see Chapter 33). Acquired PSSs are much Diagnosis is made after a history of exposure (cats often have
less common in cats than in dogs. Sclerosing cholangitis is a history of hunting lizards), combined with finding the
diagnosed on hepatic biopsy; again, it is very important to flukes or eggs in feces or bile. Supportive findings are high
evaluate hemostasis profiles before biopsy and to administer liver enzyme levels typical of cholestasis; ALT, AST, and bili-
vitamin K 1 (0.5 mg/kg SC or IM q12h for up to 3 days) as rubin concentrations are particularly high, but the ALP level
necessary because vitamin K deficiency is common in cats is surprisingly often only mildly increased. Eosinophilia is
with chronic biliary tract obstruction. It should be noted that inconsistent. Ultrasonography reveals changes typical of