Avian Nutrition:
Nutritional management of liver disease

Author: Christal Pollock, DVM, Dipl. ABVP-Avian

Date: June 18, 2007

Keywords: Liver, liver disease, malnutrition, antioxidant, protein restriction, steatorrhea, hepatic encephalopathy, ascites, silymarin, milk thistle, carnitine, L-carnitine, liver failure, copper, zinc.

Key Points

• Chronic liver disease may lead to malnutrition and weight loss.
• Antioxidant supplementation may protect hepatocytes from further damage.
• Protein restriction is not required except in cases of liver failure and encephalopathy.
• In liver failure, temporarily restrict protein while feeding a highly digestible diet with moderate amounts of fiber.

Introduction

In mammals, chronic liver disease is often associated with decreased intake of food, mainly due to anorexia, nausea, and vomiting, as well as taste abnormalities, and the same appears to be true for the avian patient. Chronic liver disease may also lead to maldigestion and malabsorption, as well as metabolic abnormalities such as increased protein and lipid catabolism, glucose intolerance, depletion of hepatic glycogen stores, and decreased glucose oxidation. Therefore chronic liver disease may lead to significant malnutrition and weight loss, particularly in patients with severe hepatic dysfunction.

Assessment of the nutritional status of the patient with liver disease is challenging since many indicators are directly altered by liver pathology.

• Body weight is an insensitive indicator, especially in end-stage liver disease, when weight may be affected by total body salt and water retention.
• Measurement of plasma proteins, such as albumin and prealbumin, is also unreliable. Instead, low protein levels reflect a decrease in hepatic synthesis and an increase in catabolism of prealbumin.

Both in human and small animal patients, nutritional therapy of liver disease has been shown to be key in the management of patients, and nutritional therapy is the only effective treatment for hepatic lipidosis. The major goals in the nutritional management of the mammalian patient are to provide enough nutrients to correction malnutrition and support hepatocytes, while preventing complications such as hepatic encephalopathy and ascites. All of the recommendations listed below for the patient with liver disease are directly extrapolated from human and small animal medicine. There is very little bird-specific information available at this time.

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Antioxidant supplementation

Elevation of liver enzymes alone does not generally warrant a dietary change. However if liver enzymes are consistently elevated, supplemental antioxidants may partially protect hepatocytes from further damage. Healthy hepatocytes maintain an elaborate antioxidant system. Interruption of the free radical scavenger defense system by inflammation, infection, hypotension, and/or accumulation of copper is thought to play a major role in the pathogenesis and the progression of hepatic lesions. Dosing, efficacy, and the exact mechanism of action of these supplements is not fully understood, however antioxidants are known to be more effective when given in combination because of their synergistic action.

• Silymarin (Milk Thistle): 100-150 mg/kg divided q8-12h
• Vitamin C: 20-50 mg/kg IM q1-7d
• Vitamin E: 0.06 mg/kg IM q7d or 15 mg/kg PO once

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Energy and protein requirements

An adequate supply of energy and protein is essential to prevent weight loss and muscle wasting. Initially, calories should be provided as carbohydrates, an important energy source in chronic liver disease. Lipids may then be cautiously added to provide more calories. Restrict fat only in cases of significant steatorrhea (pale, bulky, foul-smelling stools).

Provide an adequate supply of high quality protein (i.e. highly digestible with an optimal amino acid profile). Protein restriction does not appear to be necessary in most patients with liver disease. In fact, unnecessary protein restriction can reduce the production of important proteins like albumin putting the patient at risk for abnormal fluid accumulation. Protein restriction is only crucial in treating patients with hepatic encephalopathy or ascites. Additionally, a moderate restriction of dietary sodium is indicated for ascites.

To avoid overwhelming the metabolic capacity of the liver, divide daily nutritional intake into smaller, more frequent meals. Whenever possible, feeding should be enteral. The first-pass effect of nutrients provides beneficial trophic effects on the liver and gastrointestinal tract.

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Vitamin/mineral supplementation

In mammals with liver failure, the most commonly reported deficiencies are for potassium, zinc, vitamin K, and vitamin B-complex.

• Hypokalemia may easily be corrected by fluid therapy. Dietary supplements may also be used cautiously.
• Zinc deficiency is essentially the result of anorexia and should correct when feeding resumes.
• B-vitamins are found in very high levels in the liver where they are stored as coenzymes. Therefore the need for vitamin B should be considered when refeeding. Supplement vitamin B-complex to satisfy at least twice the minimum requirements (Vitamin B1 or thiamine at 1-2 mg/kg IM q24h or 50 mg/kg PO q24h.
• In cases of abnormal bleeding, vitamin K injections (2.5 mg/kg IM q12-24h) are indicated.
• Depending upon the bird species, ascorbic acid synthesis may occur predominantly in the liver, kidneys, or both; therefore vitamin C supplementation may also be indicated (20-50 mg/kg IM q1-7d).

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L-carnitine

Although the site of L-carnitine production is unknown in birds, in mammals the liver is one of the main sites of L-carnitine synthesis. In patients with severe liver disease or in cases of hepatic lipidosis, carnitine supplementation has been recommended to promote hepatocellular regeneration.

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Liver failure

Patients with liver failure generally benefit from the same nutritional approach treatment described above for liver disease. Moderate amounts of dietary fiber are also recommended as they promote the uptake of ammonia by intestinal flora. These proteins are then excreted in the feces. By decreasing colonic pH, fermentable fibers also reduce the production and absorption of ammonia and potentially other toxins as well. Temporary protein restriction is also recommended for patients with liver failure with hepatic encephalopathy to minimize ammonia production.

A common feature of liver disease recognized in mammals is a decrease in plasma levels of branched chain amino acids (BCAA) (leucine, valine, isoleucine) and a rise in aromatic amino acids (phenylalanine, tyrosine). Because these latter amino acids are precursors of different neurotransmitters, changes in their concentrations could explain the clinical signs of encephalopathy. Diets enriched in BCAA have been used to theoretically normalize plasma amino acid levels in the hope of improving nitrogen balance and hepatic encephalopathy. However these formulas are not yet recommended in veterinary medicine due to their expense and controversial efficacy.

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Copper and zinc

In dogs, chronic hepatitis and severe cholestasis have been associated with the hepatic accumulation of copper. Therefore restricted intake of copper (± 1.25 mg/1000 kcal ME) is recommended to minimize hepatic parenchymal damage. Diets high in zinc have also been recommended for patients with liver failure since zinc induces the synthesis of metallothionein within enterocytes. Metallothionein, a compound recognized in several avian species, is a metal-binding protein that strongly binds copper blocking its absorption.

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Roudybush Formula AL Liver Care

The most important concepts for a diet fed to the patient with liver disease is that it be high quality and easily digestible. Although there is no empirical research to support its use, there is one formulated diet currently marketed for liver disease: Roudybush AL Liver Care. The two main ingredients of this product are barley and corn, and it contains a minimum crude protein of 7.5%, a minimum crude fat of 3.0%, and maximum crude fiber of 4.0%.

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Conclusion

In most cases of hepatic disease, nutritional modifications will be necessary for the life of the patient. The exception to this rule of thumb is hepatic lipidosis. Following treatment, the liver may return to normal function allowing the patient to return to its normal maintenance diet.

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Formulary

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References

Biourge V. Clinical Nutrition in Liver Diseases. 14th ECVIM-CA Congress, 2004

Dudrick SJ, Kavic S. Hepatobiliary nutrition: history and future. J Hepatobiliary Pancreat Surg 9:459-468, 2002.

Pollock CG, Antinoff N, Carpenter JW. Birds. In: JW Carpenter (ed). Exotic Animal Formulary, 3rd ed. St. Louis, MO, WB Saunders, 2005. Pp. 135-344.

Siriboonkoom W, Gramlich L. Nutrition and chronic liver disease. Can J Gastroenterol 12(3):201-207, 1998.