Page 733 - Clinical Small Animal Internal Medicine

64 Canine Inflammatory Liver Disease 701

to the effects of inflammation, reduced blood flow, and Gastroprotectives
VetBooks.ir mitochondrial damage by refluxed bile acids. Oxidation leads to gut wall edema and potentially ulceration. This is
Portal hypertension is common in dogs with CH and
is a significant mechanism of hepatic damage, therefore
one of the most common causes of death in dogs with
antioxidant therapy is reasonable. SAM‐e increases
hepatic and red blood cell levels of glutathione, a potent chronic portal hypertension. Sudden GI bleeding can
antioxidant, and is also a critical enzyme in transmeth- precipitate an acute encephalopathic crisis due to the
ylation, transsulfuration, and aminopropylation path- high protein content of blood. An important way to
ways. As part of these pathways, SAM‐e is essential to all reduce the incidence of GI tract ulceration is to ensure
cells and is particularly important in hepatocytes because adequate enteral nutrition (see later), as anorexia predis-
of their central role in metabolism. It is widely available poses to GI ulceration. H2 receptor antagonists, or pro-
as a neutraceutical for dogs, sometimes in combination ton pump inhibitors, are often used in the prevention and
with silymarin. Although no experimental data exist, therapy of ulceration. However, there is some evidence
antioxidants are likely of benefit in CH. However, not all that gastric pH is actually elevated in human CH, and,
antioxidants are necessarily innocuous in liver disease; moreover, many ulcers are duodenal rather than gastric,
for example, ascorbate may increase liver damage by so the rationale for these drugs is unclear. Traditionally,
accumulating iron, so it is best to avoid supplementing ranitidine is preferred as an H2 receptor antagonist in
vitamin C. liver disease as it does not affect the cytochrome P450
system, and sucralfate should probably be used also.
Copper Chelators
Copper chelators include 2,3,2‐tetramine tetrahydro- Dietary Management
chloride (2,3,2‐T), 2,2,2‐tetramine tetrahydrochloride Appropriate dietary management is as important as drug
(2,2,2‐T), penicillamine, and zinc. 2,3,2‐T is the more therapy in the dog with CH. Each case is individual and
potent chelator but is not widely available in a drug for- the diet should be adjusted accordingly, so clinicians
mulation. Penicillamine is an alternative copper chela- should resist the temptation to think that “one diet fits
tor, but significant adverse effects can be associated all.” In particular, many dogs with CH are fed diets with
with its use. Copper chelators should be reserved for inappropriate and excessive protein restriction, which
dogs in which significant copper accumulation has been may restrict hepatic regeneration and result in protein‐
identified in liver tissues, primarily those animals with calorie malnutrition. Specific recommendations include
copper storage disease. Zinc is used as prophylaxis in the following.
dogs with copper storage disease, and commercially
produced hepatic support diets often contain increased ● Feed a palatable diet little and often (4–6 times a day)
zinc for this reason. The use of copper chelators for the as many dogs with CH may be inappetent. Frequent
management of copper-associated hepatitis is discussed feeding also reduces the development of HE.
in Chapter 62. ● Feed highly digestible, high‐quality protein in normal
amounts whenever possible. Good‐quality commer-
Diuretics cial diets are acceptable. Examples of high‐quality
Ascites in CH is usually due to portal hypertension, proteins include soya and these can be supplemented
although in some animals hypoalbuminemia may con- if weight or blood albumin decreases. If signs of HE
tribute to the pathogenesis. If blood albumin is normal or are suspected, feeding a normal amount of high qual-
near normal in the ascitic dog, portal hypertension is ity digestible protein little and often is recommended.
likely to exist. Portal hypertension leads to splanchnic Excessive protein restriction may result in protein‐
pooling of blood with subsequent reduction in systemic calorie malnutrition and the breakdown of highly
arterial pressure and activation of the renin‐angiotensin‐ ammoniagenic endogenous proteins.
aldosterone system (RAAS). RAAS activation then leads ● Dogs with CH may have impaired carbohydrate metab-
to further fluid retention and more ascites. Spironolactone, olism, so a diet containing highly digestible, complex
an aldosterone antagonist, is therefore the drug of choice carbohydrates should be fed.
in ascitic patients with portal hypertension, although it ● Normal amounts of fat should be fed, although fat can
can take 2–3 days to work. For this reason, spironolac- be restricted if steatorrhea develops.
tone combined with a thiazide diuretic or furosemide ● Fermentable fiber is helpful in dogs with HE as it acidi-
can be used in an attempt to increase its speed of action. fies the colon and traps ammonia. It also increases
Spironolactone also has the advantage that it does nitrogen incorporation into bacteria and reduces
not induce hypokalemia, which can precipitate hepatic bacterial ammonia production. Nonfermentable fiber
encephalopathy (HE) (hypokalemia allows ammonia to is helpful in preventing constipation, a predisposing
enter cells more easily). factor for hepatic encephalopathy.