Nutritional support has a pivotal influence in cats with HL and is an important component of at-home treatment in animals with slowly progressive hepatobiliary disorders. Proper nutritional support improves quality of life in animals with hepatic insufficiency prone to 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 for longer dietary support. Use of appetite stimulants remains controversial, because they may delay institution of regimented nutritional support. In addition, some commonly used drugs are metabolized in the liver. Diazepam and oxazepam may rarely lead to idiopathic fulminant hepatic failure in cats.
Dietary modification for animals with liver disease depends on their clinical status, the definitive diagnosis, and assessment of liver function. Diets should be balanced and supplemented with water-soluble vitamins. In severe cholestatic disorders that impede enteric access of bile (eg, EHBDO, advanced sclerosing cholangitis in cats), fat-soluble vitamins may become depleted. Vitamin K1 can be supplemented via parenteral injection of 0.5–1.5 mg/kg every week (titrated against a thrombotest [PIVKA assay] or PT). If vitamin K1 depletion is confirmed, vitamin E also likely needs supplementation. 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/day, PO). It is important to follow dosing recommendations, because excessive vitamin K can lead to hemolytic anemia (in cats), and excessive vitamin E can interfere with vitamin K function.
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). In rare circumstances, in animals prone to hypoglycemia, low-dose IV glucose may be transiently needed. Protein modification and restriction is used to address insufficient nitrogen detoxification (see below).
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.
Dietary Protein Allowance:
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.
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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).
Modified Protein Quality/Source:
Altering the type and quality of protein intake for dogs with HE can help achieve good life quality. A high energy:nitrogen ratio should be maintained, because this optimizes use of dietary protein. In dogs, dairy and vegetable quality protein (soy) sources 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. Using dairy quality and vegetable-derived protein can be estimated using the Nutritional Analysis Tool 2.0 ( http://archive.myfoodrecord.com/ human nutrition). In cats, which are pure carnivores, a meat-based protein source is recommended in a balanced diet that contains adequate arginine (~250 mg/100 kcal diet) and taurine for feline metabolism (several commercial prescription foods meet these requirements).
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.
Micronutrients and Vitamins:
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 Supplementa for Dogs and Cats with Liver Disease Formulation of a Fortified, Water-Soluble Vitamin Supplementa 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.