Nutritional support has a pivotal influence in cats with hepatic lipidosis (HL) and is an important husbandry consideration for home management of animals with progressive hepatobiliary disease. Proper nutritional support demonstrably improves quality of life for animals with hepatic insufficiency prone to hepatic encephalopathy (HE).
Diets for animals with hepatobiliary disease should be easily digestible, highly palatable, calorie 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. It is important to restrict protein content only in patients with clinical signs of HE or demonstrating ammonium biurate crystalluria due to liver disease.
Prescription canine diets for liver disease deliver better-tolerated protein (not red meat or fish origin) and decrease protein intake to 2.0–2.5 g protein/kg. Otherwise, feeding a protein-restricted prescription liver diet is inappropriate.
Because prescription liver diets currently are the only diets reliably restricted in copper content, these are recommended for management of dogs with copper-associated hepatopathy. However, in those cases, protein intake is adjusted upward by adding low copper-containing protein supplements (ie, white meat chicken) to achieve 3.5–4.0 g protein/kg intake for maintenance canine needs.
If animals are anorectic, tube feeding should be considered. Nasogastric tubes are inexpensive, easily placed, and recommended only as a short-term solution. Esophagostomy tubes are preferred in cats with HL for longer dietary support and also used in dogs.
Use of appetite stimulants remains controversial because they may delay institution of regimented nutritional support. In addition, some commonly used appetite stimulants 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, extrahepatic bile duct obstruction, advanced sclerosing cholangitis in cats that have become ductopenic), fat-soluble vitamins may become depleted. Vitamin K1 can be supplemented via parenteral injection of 0.5–1.5 mg/kg once or twice per week; in the absence of bile acids, oral fat-soluble vitamins are not absorbed.
Because vitamin E is a fat-soluble vitamin, a unique, water-soluble form, polyethylene glycol alpha-tocopherol succinate (10 U/kg, PO, every 24 hours), may be necessary for oral administration. Empirically, injectable vitamins A and D administered SC or IM used in patients needing supplementation (injectable depot vitamins A and D containing 500,000 U vitamin A and 75,000 U vitamin D3 per mL would be 0.01–0.015 mL/kg every 4–6 months; Dr. J. Loftus, Cornell University). It is important to follow dosing recommendations for vitamin supplements, because excessive vitamin K can lead to hemolytic anemia (in cats), excessive vitamin A to hepatic fibrosis, and excessive vitamin D to hypercalcemia, 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 are used to address insufficient nitrogen detoxification.
Energy Allowance in Hepatic Disease in Small Animals
Energy allowance for animals with hepatic disease 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 days 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 (in kcal) for dogs are as follows:
for dogs 2–16 kg: 30 × BW + 70
for dogs < 2 or > 16 kg: 70 × BW0.75
safe initial intake for a healthy dog: 99 × BW0.67
where BW is body weight in kg. For cats, 60 × BW 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 in Hepatic Disease in Small Animals
A diagnosis of liver disease should not automatically dictate a need for restricted dietary protein allowance. 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 acquired portosystemic shunts (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 (< 5 g protein per 418.4 kJ [100 kcal] diet) for dogs and 3.5 g protein/kg (< 7 g protein per 418.4 kJ [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 portosystemic vascular anomaly (PSVA). If a dog responds well to an initial protein restriction, ~0.25−0.5 g/kg/d can be added, using a tofu- or dairy-based protein source or, if necessary, white meat chicken. Animals should be monitored for signs of HE and ammonium biurate crystalluria during dietary protein titration. Three urine samples should be collected: first thing in the morning, 4–8 hours 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 humans 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 quality of life; however, it should only be done when HE is definitively evident. A high energy:nitrogen ratio should be maintained, because this optimizes dietary protein utilization.
In dogs, dairy and quality vegetable protein (soy) sources work best in dogs demonstrating protein-related episodic HE. Quality dairy protein (amount per 227 g) can be found in whole milk (8 g per 656.9 kJ [157 kcal]), yogurt (8 g per 581.6 kJ [139 kcal]), cottage cheese (28–31 g per 836.8–1,046 kJ [200–250 kcal], and cheddar cheese (57 g per 3,347–3,766 kJ [800–900 kcal]). Alternatively, in dogs, calcium caseinate provides 88 g protein, 2 g fat, and 1548 kJ (370 kcal) per 100 g portion. The amount of dairy or vegetable-derived protein to feed in other foodstuffs can be estimated using the USDA food tables.
In cats, which are pure carnivores, a meat-based protein source is essential in a balanced feline diet containing adequate arginine (~250 mg/418.4 kJ [100 kcal] diet), taurine and other essential amino acids, arachidonic acid, and fatty acids for feline metabolism. If protein restriction is deemed appropriate, there are several protein-restricted feline commercial prescription renal diet foods that meet these requirements.
Dietary Fat in Nutrition in Hepatic Disease in Small Animals
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 extrahepatic bile duct obstruction (EHBDO) or cats with sclerosing cholangitis (destructive cholangitis) with clinical ductopenia (pale acholic feces, bleeding tendencies, marked jaundice). These animals have decreased 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 in Hepatic Disease in Small Animals
Water-soluble vitamins should be supplemented (via IV fluids) in animals with chronic liver disease and cats with HL (see table). 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.
Supplemental fat-soluble vitamins are important in animals with fat malabsorption or obstructed bile flow. Vitamin K1 depletion develops when the enterohepatic bile acid cycle is interrupted, in animals with acholic feces (eg, EHBDO, severe ductopenia [eg, destructive cholangitis as observed in some cats with severe lymphocytic cholangitis]), feline HL, severe chronic exocrine pancreatic insufficiency, and severe chronic enteric malabsorption, and in those receiving a vitamin K–deficient diet. In addition some animals chronically treated with oral antimicrobials and some animals with severe hepatic insufficiency (not just portosystemic shunting) also develop vitamin K depletion.
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-hour intervals) before invasive procedures (insertion of catheters in large veins, cystocentesis, feeding tube placement, hepatic aspiration sampling, or liver biopsy). In ductopenic feline cholangiohepatitis (ie, sclerosing cholangitis) or chronic EHBDO, animals require intermittent vitamin K1 administration (eg, every 7–21 days). Overdosing with daily administration of injectable vitamin K1 can lead to clinical Heinz body hemolytic anemia in some cats.
Vitamin E is an important antioxidant and has anti-inflammatory and antifibrotic properties. Supplementation of vitamin E is often prescribed for animals with necroinflammatory or cholestatic liver disorders. Oral d-alpha-tocopherol acetate is given at 10 U/kg, PO, every 24 hours. Higher dosages (100 U/kg, PO, every 24 hours) are needed in animals with chronic EHBDO or severe ductopenia (causing jaundice). Alternatively, polyethylene glycol alpha-tocopherol succinate (water-soluble vitamin E) can be used at 10 U/kg, PO, every 24 hour in chronic EHBDO or severe ductopenia.
Dosing of vitamin E should not exceed recommendations because too much vitamin E can interfere with vitamin K activation, provoking coagulopathies. Too much vitamin E also can impart oxidant injury secondary to accumulation of the tocopheroxyl radical.
