Page 607 - Small Animal Internal Medicine, 6th Edition

CHAPTER 35 Hepatobiliary Diseases in the Cat 579

in cats with PSS (see Fig. 35.10), but this is not a consistent Treatment
feature. Treatment involves complete or partial ligation of the shunt-
VetBooks.ir in cats, which helps in distinguishing congenital PSS from cellophane, or ameroid constrictors; however, a detailed
ing vessel using one of several methods, including silk or
Because of the low portal pressure, ascites is not a feature
explanation is beyond the scope of this text. The procedure is
the rare feline cases of acquired PSS, in which ascites is
expected because of portal hypertension. best reserved for referral centers, particularly in cats, which
are more prone to complications than dogs. The postop-
Diagnosis erative mortality in cats appears to be higher than in dogs,
A suspicion for congenital PSS can be gained from the which is often caused by intractable, severe neurologic signs.
history of recurrent neurologic signs combined with high Pretreatment with phenobarbital has been attempted, but
fasting and/or postprandial bile acid or ammonia concentra- too few cases have been reported to assess its value. Propofol
tion in a young cat. Traditional ammonia tolerance tests are infusions are often used for HE-associated seizures in dogs,
not recommended because they can precipitate severe HE. but care must be taken in cats because of their susceptibil-
Postprandial ammonia or bile acid determinations are safer ity to Heinz body hemolytic anemia when they are given
alternatives. Serum bile acid levels should be measured propofol infusions.
before and 2 hours after feeding (see Box 34.3). If the Cats should be managed medically before surgery and for
ammonia level is measured instead, the postprandial sample a period of about 2 months after surgery while the portal
should be taken 6 hours after feeding (Walker et al., 2001). vasculature and liver mass recover. This involves careful
Other typical (but not pathognomonic) clinicopathologic dietary management (see later) with additional antibiotics
findings in some cats include a low serum urea concentra- (usually amoxicillin, 15-20 mg/kg PO q8h) and sometimes
tion, mildly increased liver enzyme levels, and microcytosis. also a soluble fiber source such as lactulose (2.5-5 mL PO
Notable differences from dogs are that decreases in total q8h, to effect). Some anecdotal data suggest that changes in
protein or albumin levels, hypoglycemia, and anemia are medical management should be made more gradually in cats
much less common in cats. Urine specific gravity is low in than in dogs to prevent the risk of seizures (e.g., change the
many dogs but occurs in fewer than 20% of affected cats. If diet first, add antibiotics after 1 week or more, and then add
fasting bile acid concentrations are very high, it is not neces- the soluble fiber source later). Details of the medical man-
sary to obtain a postprandial sample, but the diagnostic sen- agement of HE are given in Chapter 36. Cats do not tolerate
sitivity of doing both is higher than only measuring fasting marked dietary protein restriction because of their high obli-
concentrations. If biliary stasis (which also causes high bile gate protein requirement, and in fact dietary protein restric-
acid concentrations) is ruled out and the cat does not have tion is no longer indicated in affected animals. Little and
hepatic lipidosis (which causes hepatocellular failure and often feeding of a highly digestible diet is recommended. A
HE, with increases in bile acid and ammonia concentration diet manufactured for cats with gastrointestinal disease (e.g.,
in many cases), it is likely that the cat has a congenital PSS Hill’s i/d or Royal Canin intestinal) is appropriate and, unlike
because other causes of HE and high bile acid concentrations in dogs, homemade diets based on dairy protein should be
are uncommon in cats. A recent case report noted significant avoided in cats because dairy protein is relatively deficient in
increases in postprandial ammonia and bile acid concentra- arginine, which is essential for the urea cycle. Such a defi-
tions in a cat with congenital hypothyroidism, which resolved ciency will further predispose to hyperammonemia. Medical
with treatment of the hypothyroidism. The reason for this management alone is effective in some dogs long term (see
was unknown, but this is an important, albeit rare, differen- Chapter 36) and anecdotally, some cats do well with medical
tial diagnosis for PSS in a young cat (Quante et al., 2010). treatment of congenital PSS, although this is less common
Hypocobalaminemia can also cause signs of HE with ele- than in dogs probably because of their high obligate protein
vated ammonia but normal bile acids. This is more common metabolism; this would make them more susceptible to
in dogs but has been reported in a cat (Simpson et al., 2012). hyperammonemia, regardless of the diet fed.
Abdominal radiographs show a small liver in 50% of cases
(Lamb et al., 1996) but, for definitive diagnosis, the shunting Prognosis
vessel must be visualized. The prognosis appears to be good if the PSS can be ligated.
Visualization of the shunting vessel is achieved by ultra- Medical management is worth attempting if the client
sonography, portal venography, or computed tomography declines surgery although insufficient cases have been
(CT) angiography (see Chapter 34). A liver biopsy should reported to assess the long-term prognosis with either
be taken at the time of surgery or portovenography, after medical or surgical management in cats. However, clients
evaluation of hemostasis profiles, to rule out other or con- should be warned that the short-term mortality rate after
current conditions. This shows histologic features similar surgery is relatively high.
to those in dogs, typical of portal venous hypoperfusion,
with loss of smaller portal veins, increased numbers of HEPATOBILIARY INFECTIONS
arterioles, hepatocellular atrophy with lipogranulomas,
and sometimes periportal sinusoidal dilation but minimal Several infectious organisms can infect the liver as a primary
inflammation. target or as part of a more generalized infection (Box 35.5).