PROTEIN-CONTROLLED DIET FOR ACUTE AND REFRACTORY HEPATIC ENCEPHALOPATHY

Description
Adjustment of the amount and type of protein characterizes the Protein-Controlled Diet for Hepatic Encephalopathy. Energy and protein are provided to attempt maintenance of nitrogen balance and support liver regeneration.

Indications
The diet is used in the treatment of acute and refractory hepatic encephalopathy associated with hepatic disorders, which may include the following:

• hepatitis
• cholestatic liver disease
• cirrohosis with acute and/or chronic encephalopathy

        Liver disease causes numerous metabolic problems that can affect all major nutrients and the assessment parameters commonly used to evaluate nutritional status of the patient with hepatic disease.  The classic signs of liver disease are anorexia, weight loss, and nausea with marked deficiencies in energy, protein, vitamins, and minerals (1,2).  Because of the high risk for malnutrition in persons with hepatic diseases the American Society for Enteral and Parenteral Nutrition (ASPEN) recommends protein restriction be no less than 0.6 to 0.8 g/kg and reserved to those patients during acute or refractory episodes of encephalopathy.  Normal protein intake should be resumed of 1 to 1.2 g/kg after the cause of encephalopathy has been identified and treated (3).  The widespread practice of protein restriction for all patients with cirrhosis is not justified and often leads to iatrogenic protein malnutrition (3). 

Although malnutrition does not correlate with the type of liver disease, therapeutic modifications vary according to the type and severity of hepatic insufficiency.  Generally, fatty liver requires little to no nutrition intervention, while cirrhosis necessitates major changes in the patient’s food intake.  A major goal of medical nutrition therapy in liver disease is to prevent and treat hepatic encephalopathy (1,3).

    Hepatic disease can profoundly affect the nutritional status of the patient because of its effects on carbohydrate, fat, protein, vitamin, and mineral metabolism.  Metabolic disorders of the following are commonly seen in the clinical setting of patients with hepatic insufficiency:  

• Carbohydrates: Adverse effects can include hypoglycemia or hyperglycemia.  Hypoglycemia is most frequently seen in acute hepatitis or fulminant liver disease, probably due to impaired gluconeogenesis (1,3).  Hyperglycemia is commonly observed secondary to counteracting catabolic hormones and insulin resistance when superimposed by acute stress and injury (1).  Soluble fiber may be beneficial in managing hepatic encephalopathy.  Soluble fiber is fermented in the colon by the same mechanism as lactulose, which eliminates ammonia in the form of ammonium ion and bacterial proteins (3).
• Fats: Malabsorption may occur because of inadequate production of bile salts.  This may lead to steatorrhea, which could lead to deficiencies in fat-soluble vitamin and calcium levels.  Researchers have found an increase in serum lipids, reflecting lipolysis (1,3).
• Protein: The effect of hepatic injury on protein metabolism is more dramatic than is carbohydrate or fat metabolism.  There is a decrease in synthesis of serum albumin, the transportation of proteins, and the clotting factors (1,3).  The ability of the liver to synthesize urea decreases, which results in an accumulation of ammonia and a decrease in serum urea level.  This derangement in metabolism elevates the serum aromatic amino acids (AAAs) (phenylalanine, tryptophan, and tyrosine) and methionine and decreases the serum branched-chain amino acids (BCAAs) (valine, isoleucine, and leucine).  The only enzymes that metabolize AAAs are located in the hepatocytes.  In hepatic insufficiency, there is a decrease in hepatic oxidation of AAAs, leading to an increase in circulation of AAAs in the plasma.  In contrast, BCAAs are metabolized primarily by the skeletal muscle.  There is an increase in BCAA oxidation in the peripheral tissue during stress, causing a drop in plasma circulation (1).
• Vitamins and minerals: Hepatic injury results in decreased absorption, transport, and storage and may alter the metabolism of vitamins and minerals.  Cirrhotic livers have been reported to store decreased levels of thiamine; folate; riboflavin; niacin; pantothenic acid; vitamins B6, B12, and A; zinc; and cobalt (1,4).  In chronic liver disease, the hydroxylation of dietary and endogenous vitamin D to the active form (25-hydroxy derivative) is impaired and may lead to a deficiency state with concomitant osteomalacia.  Although there are possibilities of vitamin and mineral deficiencies, supplementation should be administered only when a specific nutrient deficiency is identified.  Supplementation should be monitored.  Vitamin K deficiency may be induced from malabsorption with steatorrhea, dietary deficiency, impaired hepatic storage, and/or decreased production of gut flora due to intake of antibiotics.  If vitamin K deficiency occurs, the rate at which prothrombin is converted to thrombin is affected, thus hampering the coagulation process and producing inadequate clotting factors (1).  Intravenous or intramuscular vitamin K often is given for 3 days to rule out hypopothrombinemia due to deficiency (4).

Nutritional Adequacy
Diets containing less than 50 g of protein may be inadequate in thiamin, riboflavin, calcium, niacin, phosphorus, and iron based on the Statement on Nutritional Adequacy.  Supplementation may be indicated but should be assessed on an individual basis.  This diet should be considered a transitional diet.  Normal protein intake should be resumed soon after the cause of encephalopathy has been identified and treated.  Long-term protein restriction should only be considered in patients with refractory encephalopathy (3).

How to Order the Diet
The diet order should specify the grams of protein required from food.  Base the grams of protein ordered on the patient’s actual weight or use ideal body weight in cases where weight cannot be measured or accurately accessed due to fluid issues (e.g, with ascites).  To calculate weight, see Estimating Energy Expenditures, or Weight for Height Calculation – 5’ Rule.  If a special formula is requested, the amount should be specified.  Specify any restriction such as sodium, fluid, or other nutrients.

Planning the Diet
The table below outlines the recommended nutrient prescription according to type of hepatic disease (3,5,6).

Meal size and frequency: Some patients require small portions and frequent feedings because ascites limits the capacity for gastric expansion.  Studies have shown that the metabolic profile after an overnight fast in patients with cirrhosis is similar to normal individuals undergoing prolonged starvation without any associated stress.  Cirrhosis can be considered a disease of accelerated starvation with early recruitment of alternative fuels.  A small-scale study showed patients with cirrhosis who received an evening snack to supply energy during sleeping hours were able to maintain a greater positive nitrogen balance than did other patients who were fed less frequently (2).

Commercial supplements: Supplementation with enteral formulas is often necessary to increase the patient’s intake. Modular products of carbohydrates and fat can increase energy intake without increasing protein intake.  The usefulness of special products containing BCAAs is controversial, and these products generally have a higher cost.  The guidelines for nutrition therapy in liver disease developed by the American Society for Enteral and Parenteral Nutrition (ASPEN) restrict the use of BCAA enriched formulas to patients with refractory encephalopathy not responding to medical therapy (7).

References

1. Wong K, Klein B, Fish J. Nutrition Management of the Adult with Liver Disease. In: Skipper A, ed.  Dietitian’s Handbook of Enteral and Parenteral Nutrition. 2nd ed. Gaithersburg, Md: Aspen Publishers; 1998.               
2. Levinson M. A practical approach to nutritional support in liver disease.  Gastroenterologist. 1995;3:234-240.
3. Teran TC, McCullough AJ.  Nutrition In Liver Disease.  In: Gottschlich M, ed.  The Science and Practice of Nutrition Support A Core Based Curriculum.  Dubuque, Ia: Kendall/Hunt Publishing Company; 2001.
4. Hasse JM, Matarese LE. Medical nutrition therapy for liver, biliary system, and exocrine pancreas disorders. In: Mahan K, Escott-Stump E, eds.  Krause’s Food, Nutrition and Diet Therapy. 10th ed. Philadelphia, Pa: WB Saunders; 2000:710.
5. Corish C. Nutrition and liver disease. Nutr Rev. 1997;55:17-19.
6. Shronts EP, Fish J. Hepatic failure. In: Merrit RJ, ed. The A.S.P.E.N. Nutrition Support Practice Manual.  Silver Spring, Md: Aspen Publishers;1998.
7. ASPEN Board of Directors and the Clinical Guidelines Task Force.  Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients[published erratum appears in JPEN J Parenter Enteral Nutr. 2002;26:144].  JPEN J Parenter Enteral Nutr. 2002;26 (suppl 1):1SA-138SA.

   PROTEIN-BASED EXCHANGES

Manual of Clinical Nutrition Management                                                     
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