Page 1127 - Small Animal Clinical Nutrition 5th Edition

Hepatobiliary Disease 1173

1996b; Marks et al, 1994a). The amino acid composition of Table 68-9. Relative copper content of selected human foods.
VetBooks.ir these protein sources is not significantly different from that of Foods with very high copper content
meat sources, suggesting that other food factors such as di-
Liver
gestibility and levels of digestible (soluble) carbohydrate and
fermentable fiber are important. Fermentable carbohydrates Shellfish
increase microbial nitrogen fixation, reduce intraluminal am- Foods with high copper content
monia production in the gut and promote colonic evacuation Cocoa
(Center, 1996b). (See Fiber below.) Heart
Kidney
Superficial necrolytic dermatitis (hepatocutaneous syn- Legumes
drome) is an uncommon skin disease associated with systemic Mushrooms
metabolic disease. Afflicted dogs commonly have concurrent Nuts
Skeletal muscle (meat)
skin erosions and ulcerations with alopecia, exudation and thick
adherent crusts on the footpads and around mucocutaneous Foods with low copper content
junctions. The hepatopathy grossly has the appearance of Cheese
Cottage cheese
macronodular cirrhosis but is characterized by regenerative hy- Rice
perplastic nodules separated by fibrous septa containing ductu- Tofu
lar structures and is void of inflammation. Some authors believe
this condition results from exaggerated amino acid catabolism
and the resultant hypoaminoacidemia is responsible for the skin
and liver lesions (Gross et al, 1990, 1993). Most affected dogs to 0.25% DM for dogs and 0.07 to 0.3% DM for cats.
also have low plasma amino acid concentrations and parenteral Recommended DM chloride levels are typically 1.5 times sodi-
amino acid replacement with nutritional protein supplementa- um levels (NRC, 2006).
tion may resolve the skin lesions (Gross et al, 1993). In these
cases, high protein foods, various protein supplements and Copper
intravenous amino acid solution administration is recommend- Avoiding excessive copper intake is important for dogs with
ed. Note that rapid amino acid infusion can result in HE. copper-associated hepatotoxicosis, especially when serious
Repeated amino acid infusions are given weekly as needed if a hepatic injury has not yet occurred. The minimum recom-
clinical response is observed using this protocol. mended allowance for dietary copper in foods for healthy adult
dogs is 6 mg/kg DM (NRC, 2006). However, studies have
Potassium shown that Bedlington terriers achieve copper balance when
Cats with hepatic lipidosis may develop hypokalemia due to consuming approximately 0.4 mg copper/day (Brewer et al,
inadequate potassium intake, vomiting, polydipsia and 1989).This equates to approximately 2.6 mg/kg of food. Foods
polyuria, magnesium depletion and concurrent chronic renal for dogs with suspected or confirmed copper-associated hepa-
failure. In one study, hypokalemia was present in 19 of 66 cats totoxicosis should not provide more than 5.0 mg/kg DM cop-
(29%) with severe hepatic lipidosis (Center et al, 1993). Hypo- per from an available copper source. Hepatic copper content is
kalemia was significantly related to nonsurvival in this group of also increased (although not to the levels found in patients with
cats. Dogs with chronic liver disease and HE also frequently inherited copper-related hepatotoxicosis) in patients with cho-
develop hypokalemia due to vomiting and alkalosis (Meyer, lestasis. Therefore, moderate copper restriction is recommend-
1998). Hypokalemia is exacerbated by ascites due to activation ed for most patients with cholestatic liver disease. The role of
of the renin-angiotensin-aldosterone axis. Hypokalemia, espe- copper in cats with liver disease has not been adequately inves-
cially in combination with alkalosis (which is also a common tigated but it is generally considered that copper plays a mini-
feature in the same patients due to decreased use of bicarbon- mal part, if any, in feline liver diseases.
ate in the urea cycle and vomiting), is dangerous because it may Feeding selected commercial veterinary therapeutic (i.e.,
prolong anorexia and exacerbate expression of HE. This is due those formulated for patients with liver disease) or homemade
to intracellular trapping of ammonia in hypokalemic alkalosis. foods to patients with liver disease can control copper intake,
Foods for cats with hepatic lipidosis should be potassium especially those with cholestasis. For patients with copper-asso-
replete (0.8 to 1.0% DM potassium), or potassium supplemen- ciated hepatotoxicosis, copper restriction should be more
tation (2 to 6 mEq potassium gluconate per day) should be aggressive and copper chelating agents (Box 68-3) or dietary
considered. zinc supplementation (See below.) should be used. Dogs should
not be fed supplements containing copper or table foods that
Sodium and Chloride have a high copper content (Table 68-9). Certain fiber sources
Excessive dietary sodium chloride should be avoided in liver and minerals in food inhibit copper absorption (Chapters 5 and
disease patients with ascites, portal hypertension and/or signif- 6). The appropriate levels of these nutrients in foods for
icant hypoalbuminemia. Dietary sodium chloride restriction to patients with copper toxicosis have not been determined. Zinc
levels recommended for patients with renal and cardiac failure supplementation is important for blocking copper absorption
is appropriate. Thus, sodium levels should be restricted to 0.08 and is discussed below.