THE MERCK VETERINARY MANUAL
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Nutrition in Hepatic Disease in Small Animals

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Optimizing nutritional support is essential. It has pivotal influence as a treatment in cats with HL and is an important component of at-home treatment in animals with slowly progressive disorders. It also improves life quality in animals with hepatic insufficiency prone to episodic HE. Diets for animals with hepatobiliary disease should be easily digestible, highly palatable, calorically dense, easy for the owner to prepare and feed, and fed frequently as small meals. Objectives are to optimize food digestion and assimilation and to achieve voluntary food consumption.

If animals are anorectic, tube feeding should be considered. Nasogastric tubes are inexpensive, easily placed, and recommended as a short-term solution. Esophagostomy tubes are preferred in cats with HL. Use of appetite stimulants remains controversial. They may delay institution of regimented nutritional support. In addition, some of the commonly used drugs are metabolized in the liver. Diazepam and oxazepam may lead to idiopathic fulminant hepatic failure in some cats.

Modification of the diet in an animal with liver disease depends on clinical status, definitive diagnosis, and recent assessments of liver function. Diets should be balanced and supplemented with water-soluble vitamins. In severe cholestatic disorders that impede enteric access to bile (eg, EHBDO, advanced sclerosing cholangitis in cats), fat-soluble vitamins may become depleted. Vitamin K1 can be supplemented with parenteral injections: 0.5–1.5 mg/kg every week (titrated against a thrombotest [PIVKA assay]). If vitamin K1 deficiency is confirmed, vitamin E also likely needs repletion. Because vitamin E is a fat-soluble vitamin, a unique water soluble form may be necessary for oral administration: polyethylene glycol α-tocopherol succinate (10 IU/kg, PO, sid).

Liver function also has considerable influence on glucose homeostasis (glycogenolysis or gluconeogenesis from amino acids and lactate), detoxification of nitrogen (urea cycle), and ketogenesis (from fatty acids).

Energy allocation should be estimated based on ideal body weight. Feeding a new diet should be done slowly. For example, intake should be ~50% of the calculated daily energy requirement on day 1, increased to 75% on day 2, and then to 100% on day 3. The energy allowance may require adjustment after the diet has been accepted, the animal is stable, and weight and body condition score reassessments confirm a need for higher intake. Estimation of initial energy intake is calculated using formulas that predict resting energy requirements. Frequent reassessment is necessary, and energy allowance tailored to response. Formulas for estimation of initial energy allocations for dogs are 30 × body wt (kg) + 70 (for dogs 2–16 kg); 70 × body wt (kg)0.75 (for dogs <2 or >16 kg); and 99 × body wt (kg)0.67 (safe initial intake for a healthy dog).

For cats, the established formula is 60 × body wt (kg), unless the cat is quite obese or a subnormal metabolic rate or activity is suspected.

A diagnosis of liver disease should not automatically dictate a need for protein restriction. In fact, protein restriction can be detrimental in some patients, eg, cats with HL or animals with chronic but stable necroinflammatory liver disease that do not have APSS or HE. Nutritional support may be impaired in animals that reject dietary change and protein restriction. Protein restriction is appropriate when HE is suspected, ammonium biurate crystalluria is observed, or portosystemic shunting (congenital or acquired) is confirmed.

The protein allowance for an animal with HE should maintain a positive nitrogen balance and avoid catabolism. Because maintenance of lean body mass (muscle) provides a temporary respite from ammonia toxicity, body condition status should be monitored regularly for comparative estimates.

Protein should initially be restricted to 2.5 g/kg (<5 g/100 kcal diet) for dogs and 3.5 g/kg (<7 g/100 kcal) for cats. Sequential historical, physical, and clinicopathologic assessments judge treatment response.

Most protein-restricted diets are used in dogs with chronic, severe liver disease or with PSVA. If a dog responds well to an initial protein restriction, protein at 0.5 g/kg/day can be added, using a tofu or dairy-based protein source. Patients should be monitored every 1–2 wk for signs of HE and alterations in albumin, BUN, and appearance of ammonium biurate crystalluria. Three urine samples should be collected: first thing in the morning, 4–8 hr after feeding, and late in the evening.

Dietary protein should not be restricted in cats with HL because protein restriction compromises survival. Protein should not be restricted in most dogs and cats with chronic necroinflammatory liver disorders at the time of diagnosis; these animals may have higher protein requirements than a comparably sized healthy age-matched control for tissue repair and cell replication.

Modified Protein Quality/Source:

Altering the type and quality of protein intake in dogs with HE is helpful. A high energy:nitrogen ratio should be maintained because this optimizes use of dietary protein. In dogs, dairy quality protein and vegetable quality protein (soy) work best. Dairy quality protein (amount per 8 oz) can be found in the following products: whole milk (8 g in 157 cal), yogurt (8 g in 139 cal), cottage cheese (28–31 g in 200–250 cal), and cheddar cheese (57 g in 800–900 cal). Alternatively, in dogs calcium caseinate can provide 88 g protein, 2 g fat, and 370 kcal/100 g portion. In cats, meat-based protein in a balanced diet that contains adequate arginine (~250 mg/100 kcal diet) and taurine is essential.

There is no need to restrict dietary fat in most animals with hepatobiliary disease. Most animals have no problems with fat digestion or assimilation, and fat ingestion is important for provision of essential fatty acids and fat-soluble vitamins. One exception is animals with chronic EHBDO or cats with sclerosing cholangitis with symptomatic “ductopenia.” These patients have reduced enterohepatic circulation of bile acids, limiting the emulsification, digestion, and assimilation of ingested fat. Another exception is dogs with gallbladder mucoceles, some of which have idiopathic hyperlipidemia.

Water-Soluble Vitamins:

These should be supplemented in animals with chronic liver disease and cats with HL (see Table 1: Formulation of a Fortified Water-Soluble Vitamin Supplement (2 mL/L of IV fluid) in Dogs and Cats with Liver DiseaseTables). Cats are especially susceptible to thiamine (B1), cobalamin (B12), and vitamin K1 deficiency if they are chronically inappetent, treated with antimicrobials, have severe intestinal or pancreatic disease, or demonstrate chronic cholestasis. Hyperthyroid cats may develop malabsorptive problems and may be more prone to these complications when also affected with cholangiohepatitis or HL. Vitamin C is not recognized as a commonly depleted micronutrient. Dogs with copper storage hepatopathy and animals with large hepatic iron stores should probably not receive vitamin C supplements.

Table 1

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Fat-soluble Vitamins:

Supplementation of fat-soluble vitamins is important in animals with fat malabsorption and obstructed bile flow. Vitamin K1 depletion develops when the enterohepatic bile acid cycle is interrupted in animals demonstrating acholic feces (eg. EHBDO, severe sclerosing ductopenic cholangiohepatitis in cats), HL (cats), exocrine pancreatic insufficiency, severe malabsorptive intestinal disease, after feeding a vitamin K-deficient diet, as a result of chronic oral antimicrobial administration, and in severe liver disease. Vitamin K should be administered to any jaundiced animal with suspected liver disease as early as possible. Vitamin K1 should be given at 0.5–1.5 mg/kg, SC or IM, 3 times at 12-hr intervals before invasive procedures, insertion of catheters in large veins, cystocentesis, insertion of feeding tubes, hepatic aspiration sampling, or liver biopsy. In ductopenic feline sclerosing cholangitis or chronic EHBDO, animals require intermittent weekly vitamin K1 injections (eg, every 7–21 days), monitored by a PIVKA or PT clotting test. Overdosing with vitamin K1 can lead to symptomatic Heinz body hemolytic anemia in cats.

Vitamin E is an important antioxidant, antiinflammatory, and antifibrotic used in necroinflammatory and cholestatic liver disorders. Oral d-α-tocopherol acetate is given at 10 IU/kg/day. Higher dosages (100 IU/kg/day) are needed in animals with chronic EHBDO or ductopenic feline sclerosing cholangitis. Alternatively, α-tocopherol polyethylene glycol succinate (water-soluble vitamin E) can be used at 10 IU/kg/day. Dosing of Vitamin E should not exceed recommended amounts as too much vitamin E can interfere with vitamin K activity, provoking coagulopathies and also impart oxidant injury (accumulation of the tocopheroxy radical).

Last full review/revision March 2012 by Sharon A. Center, DVM, DACVIM

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