Page 635 - Small Animal Internal Medicine, 6th Edition

CHAPTER 36 Hepatobiliary Diseases in the Dog 607

of gut-derived and peripherally derived encephalotoxins, intestinal origin. Dogs with experimental PSS and animals
eliminating precipitating factors, and correcting acid-base and humans with acquired PSS actually have a higher dietary
VetBooks.ir and electrolyte abnormalities. A variety of encephalotoxins protein requirement than do normal animals or people. In-
flammatory mediators are also thought to be important pre-
are implicated as causes of HE (see Chapter 33), but the most
cipitators of HE. It is known that clinically relevant episodes
important from the point of view of treatment is ammonia.
It was once believed that the most important source of am- of HE in dogs with congenital or acquired PSS are often
monia was undigested protein in the colon metabolized by precipitated by stress and infections, not just by feeding,
gut bacteria, but emphasis has now shifted to interorgan me- emphasizing the role of hypermetabolism, inflammation,
tabolism of ammonia and small intestinal enterocyte gluta- and breakdown of body protein in the development of HE
mine catabolism in patients with HE rather than production (see Chapter 33). HE is also triggered by negative nitrogen
of ammonia in the large intestine from dietary protein itself, balance and breaking down of muscle mass (see Fig. 36.5),
which is considered a less important source (see Chapter 33 particularly in dogs with acquired PSS and protein-calorie
for more details). There are high amounts of ammonia in malnutrition, and in these cases starvation and protein re-
the portal circulation, particularly after a meal, but the main striction will worsen the HE.
source is obligate catabolism of glutamine by small intestinal A combination of careful dietary manipulation, locally
enterocytes as their main energy source; intestinal glutamin- acting agents that discourage the formation of readily absorb-
ase concentrations seem to increase for unknown reasons able ammonia and hasten evacuation of the intestinal tract
in humans with cirrhosis, increasing gut ammonia produc- (lactulose), antibiotics to suppress bacterial populations that
tion. There are no published studies showing the relative generate ammonia and other gut-derived encephalotoxins,
contribution of small and large intestine–derived ammonia and treatment of any precipitating cause is the standard
to HE in dogs, but the observed tendency for dogs to show approach for the long-term management of chronic HE
signs of HE 1 to 2 hours after feeding would support a small (Box 36.6). Dietary management and treatment of the

BOX 36.6

Long-Term Medical Management of Hepatic Encephalopathy

Dietary Management • Fermentable fiber reduces hepatic encephalopathy in
• Feed normal amounts (if possible) of high-quality, highly the same way as lactulose. Nonfermentable fiber is
digestible protein to minimize the chance that any also important because it prevents constipation and
protein will reach the colon to be converted into NH 3 . therefore reduces contact time for colonic bacteria to
Some veterinarians recommend increasing branched act on feces and produce ammonia.
chain amino acids and reducing aromatic amino acids • Zinc supplementation may reduce encephalopathy
such as tryptophan, but there is no evidence that because zinc is used in many metalloenzymes in
changing the dietary levels affects cerebrospinal fluid the urea cycle and in the muscle metabolism of
levels. Consider adding ornithine aspartate, which ammonia.
provides substrates for conversion of NH 3 to urea
(ornithine) and glutamine (aspartate). Restrict protein Lactulose
only if absolutely necessary to control neurologic signs • Lactulose is a soluble fiber that acidifies colonic
and monitor muscle mass and blood protein contents, reducing ammonia absorption, and also
concentrations carefully. increases colonic bacterial cell growth, therefore
• Prevent protein-calorie malnutrition by avoiding incorporating ammonia into the bacterial cell walls.
prolonged fasting and/or excessive protein restriction Cats should be given 2.5–5 mL PO q8h, and dogs,
because this will lead to hyperammonemia from the 2.5–15 mL PO q8h. Start at the low dose, and titrate
breakdown of body protein. to effect (two or three soft stools daily).
• Feed small amounts often to reduce the amount of liver
work required, reduce energy demands and thus Antibiotics
glutamine metabolism in small intestine, and lessen the • Give amoxicillin (22 mg/kg PO q12h) to reduce
potential for undigested food to reach the colon. gastrointestinal flora and also protect against
• Fat needs no special recommendations, although it bacteremia.
should be fed in normal amounts and not restricted
unless clinical steatorrhea develops (rare). Avoid diets Identify and Treat Concurrent Infections and Inflammation
that are very high in fats, particularly with cholestasis • Pay particular attention to identifying and treating any
or portal hypertension, in which GI signs may be urinary tract infections (pyelonephritis or cystitis).
exacerbated.
• Carbohydrates should be highly digestible as a primary
calorie source, reducing the need for hepatic
gluconeogenesis from fat and protein.