Nutritional Management of Specific Feline Liver Diseases

Nutritional Management of Specific Feline Liver Disease

Acute Liver Disease

Cats are more likely to have chronic liver disease, since they are good at hiding early signs of any disease. Acute liver disease is mostly caused by hepatotoxins, and its management includes removal of the toxin (if known), and supportive treatment with fluids and antioxidants (vitamin E, SAMe). Tube-feeding may be necessary if the cat remains anorexic, since anorexia may predispose it to the development of hepatic lipidosis.

Chronic Liver Disease

Dietary management is particularly important in chronic liver disease. Treatment is essential in restoring the energy balance, especially by providing protein. The amount fed should at first be based on an estimation of the cat’s energy requirements. Every effort should be made to get the cat to eat voluntarily, although force-feeding should be avoided in order not to create food aversion. Food should be palatable and fed in small portions several times daily. Cats that refuse to eat or consume insufficient amounts to meet minimum requirements require tube feeding, usually initially via an indwelling nasoesophageal tube, in order to halt the vicious cycle of excessive muscle catabolism and worsening signs of liver dysfunction. Protein restriction should only be instituted when there are signs of HE. It is also essential that the diet contains increased zinc levels and a mixture of antioxidants including vitamin E and C. Zinc supplementation is useful because it is an antioxidant, and also has antifibrotic properties and can reduce the severity of HE.

Hepatic Lipidosis

The key to treatment is for the cat to receive adequate protein and fat calories via tube feeding to correct the nutritional imbalance that has been created by the disease (Figure 19). Since these cats are usually profoundly anorexic, tube feeding is indicated as an initial treatment. An esophagostomy or a gastrostomy feeding tube should be placed as soon as the cat is stabilized. Ideally, a moderate to high protein (30 - 40% of calories), complete and balanced diet that has been specifically formulated for cats should be utilized unless the cat has or develops signs of HE. The energy requirements of cats with hepatic lipidosis are presumed to be similar to healthy cats (50 - 60 kcal/kg/day), divided into equal sized portions. In addition, a predisposing condition (e.g., stress, pancreatitis, cholangiohepatitis) should be investigated and managed. Attention should also be given to appropriate protein intake, at least 3.8 - 4.4 g/kg/day. The goal is to restore the energy balance and supplement amino acid deficiencies, especially arginine and taurine. L-carnitine may also be an important nutritional factor because as it may help the beta oxidation of fatty acids by the hepatocytes.

Figure 19. Liver histology of a cat illustrating the capacity of the cat to recover quickly from hepatic lipidosis. (© V. Biourge).

Cats should derive their caloric intake via the feeding tube for the first 7 - 10 days of therapy. At this time, the cat can be offered food orally. If the cat remains anorexic, tube feeding should continue for another 5 - 7 days prior to offering food again. The feeding tube can be removed after the cat has has started eating voluntarily and is maintaining its caloric intake and body weight. Several dietary supplements have been recommended, but not critically evaluated by various authors. These include L-carnitine (250 - 500 mg/cat/day), taurine (250 - 500 mg/cat/day), vitamin B complex, zinc (7 - 10 mg/kg elemental zinc/day), and vitamin E (20 - 100 mg/cat/day). Weekly parenteral vitamin K1 (0.5 - 1.5 mg/kg SQ) is indicated for those cats with documented coagulopathies.

Hepatic Encephalopathy

HE is a metabolic disorder affecting the central nervous system, which develops secondary to hepatic disease (Michel, 1995). In cats, it is usually a result of congenital portosystemic shunts and less commonly due to severe hepatocellular disease. Signs are typically intermittent, may be precipitated by a high-protein meal, and vary from anorexia, vomiting, diarrhea and polyuria/polydipsia to disorientation, apparent blindness and seizures. Stunted growth or failure to gain weight may occur in young cats with congenital shunts. A high index of clinical suspicion is important, since appropriate management of HE will greatly improve the patient’s demeanor and may restore appetite.

Cats with signs of HE are initially offered a protein-restricted diet (<20 - 25% of calories) in combination with medication aimed at reducing colonic absorption of ammonia (lactulose, oral antibiotics) (Figure 20). Protein quantity is gradually increased at weekly or biweekly intervals when the cat becomes neurologically asymptomatic. Serum protein should be monitored to prevent hypoalbuminemia, in which case dietary protein content should be increased in association with more aggressive adjunct treatment. Maintenance of a positive nitrogen balance is essential in reducing the risk of HE.

Figure 20. Overview of nutritional management of cats with liver disease.

The source of proteins is important in the management of HE, since ammonia production and absorption can be minimized by providing highly digestible sources of protein. When hepatic encepalopathy persists despite a protein-restricted diet and adjunct medication, it may be helpful to replace meat proteins with highly digestible vegetables (e.g., soy hydrolysate) and/or milk proteins (e.g., casein, cottage cheese). Milk and vegetable proteins are better tolerated in human patients with hepatic encephalopathy. Soy and milk protein diets are low in nitrogen compared to meat diets, which could contribute to their beneficial effects.

The addition of soluble fiber (psyllium 1 - 3 tsp mixed with food daily) adds bulk to the stool and prevents constipation.

Conclusion

Diets for cats with liver disease should be highly digestible with a high energy density provided by fat and carbohydrates (Table 7). Protein restriction should be avoided as much as possible, especially in cats with acute inflammatory hepatic disease or necrosis. Moderate protein restriction may be necessary in cats with clinically evident HE, but in general, it is important to feed cats the highest level of protein they can tolerate without precipitating signs of encephalopathy.

Protein quality should be very high. In addition, the diet should contain high normal to increased levels of watersoluble vitamins, enhanced zinc (>43 mg/1000kcal), restricted sodium (<0.5 g Na/1000 kcal) in case of ascites, and a moderate amount of predominantly soluble fiber.

Correction of enteric bleeding, constipation, infection, alkalosis, hypokalemia and azotemia is important in reducing the risk of hepatic encephalopathy. Maintenance of a positive nitrogen balance (muscle mass) is essential.