Nutrition in Hepatic Disease in Small Animals

Energy allocation should be estimated based on ideal body weight, with modified diets gradually introduced. Initial intake should be no greater than 50% of the calculated daily energy requirement on day 1, increased to 75% on day 2, and then to 100% by day 3–5. Energy allowances may require adjustment after the diet is accepted, the animal is stable, and weight and body condition reassessments confirm a need for higher or lower intake. Estimation of initial energy intake is calculated using formulas that predict resting energy requirements in healthy animals. 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); or 99 × body wt (kg)^0.67 (safe initial intake for a healthy dog).

For cats, 60 × body wt (kg) is often used, unless the cat is markedly overconditioned or has a subnormal metabolic rate or activity level. Frequent reassessment is necessary with energy allowances tailored to response.

A diagnosis of liver disease should not automatically dictate a need for protein restriction. In fact, protein restriction can be detrimental in some animals, eg, cats with HL or animals with chronic but stable necroinflammatory liver disease that do not have APSSs or HE. Unfortunately, altering nutritional support can be difficult and challenging in animals that reject novel diet modifications. Protein restriction is appropriate when HE is suspected, ammonium biurate crystalluria is observed in an animal with suspected hepatic insufficiency, or portosystemic shunting (congenital or acquired) is either confirmed by imaging studies or suggested by protein C assessments.

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

When protein restriction is deemed necessary, initial restriction to 2.5 g protein/kg body wt (<5 g protein/100 kcal diet) for dogs and 3.5 g protein/kg body wt (<7 g protein/100 kcal) for cats is advised. Sequential historical, physical, and clinicopathologic assessments judge treatment response and guide further tailoring of these recommendations.

Most protein-restricted diets are used in dogs with chronic, severe liver disease or that have PSVA. If a dog responds well to an initial protein restriction, ~0.25−0.5 g/kg/day can be added, using a tofu or dairy-based protein source. Animals should be monitored every 1–2 wk for signs of HE and alterations in albumin, BUN, and appearance of ammonium biurate crystalluria during dietary protein titration. Three urine samples should be collected: first thing in the morning, 4–8 hr after feeding, and late in the evening to optimize scrutiny for ammonium biurate crystalluria.

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, because many of these animals may have higher protein requirements than a comparably sized, healthy, age-matched control for tissue repair and cell replication. In people with similar health status, nitrogen requirements increase as needed for increased nitrogen utilization (tissue repair and regeneration).

There is no need to restrict dietary fat in most animals with hepatobiliary disease, because these animals typically have no problems with fat digestion or assimilation. Fat ingestion is important to provide essential fatty acids and fat-soluble vitamins. One exception is animals with chronic EHBDO or cats with sclerosing cholangitis (destructive cholangitis) with symptomatic “ductopenia” (pale acholic feces, bleeding tendencies, marked jaundice). These animals have reduced entry of bile into the alimentary canal and impaired enterohepatic circulation of bile acids, limiting emulsification, digestion, and assimilation of ingested fat. Another exception is dogs with gallbladder mucoceles, some of which have idiopathic hyperlipidemia; in these, feeding a high-fat diet can facilitate rapid maturation of the gallbladder mucocele.

Water-soluble vitamins should be supplemented (via IV fluids) in animals with chronic liver disease and cats with HL (see Table: Formulation of a Fortified, Water-Soluble Vitamin Supplement^a for Dogs and Cats with Liver Disease). Cats are especially susceptible to thiamine (B₁), cobalamin (B₁₂), and vitamin K₁ deficiency when 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 in either dogs or cats. Dogs with copper storage hepatopathy and animals with large hepatic iron stores should probably not receive vitamin C supplements, because this may augment oxidative injury associated with transition metal accumulation.

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 destructive [sclerosing ductopenic] cholangiohepatitis in cats), HL (cats), exocrine pancreatic insufficiency, severe malabsorptive intestinal disease, after feeding a vitamin K–deficient diet, animals chronically treated with oral antimicrobials, and in animals with severe liver disease causing insufficiency. Vitamin K should be administered to any jaundiced animal with suspected liver disease as early as possible (0.5–1.5 mg/kg, SC or IM, three 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 vitamin K₁ injections (eg, every 7–21 days), monitored by PIVKA or PT clotting tests. 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 feline destructive cholangitis (ductopenic 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, because too much vitamin E can interfere with vitamin K activity, provoking coagulopathies. Too much vitamin E also can impart oxidant injury secondary to accumulation of the tocopheroxy radical.