CIRRHOSIS :-

Studies to date have been able to show positive outcomes with parenteral and enteral nutrition in malnourished cirrhosis, including improvement in clinical complication of cirrhosis such as ascites, encephalopathy and infection in addition to decreased mortality. Regeneration of parenchymal cells occurs if appropriate diet therapy is initiated before the disease is well advanced. In early cirrhosis, the high protein, high carbohydrate diet outlined for infectious hepatitis is satisfactory. In advanced cirrhosis, however, further modification is needed. Energy requirements are increased to compensate for the extreme weight loss, which often occurs in cirrhosis.

Carbohydrate :-

Determining carbohydrate needs is often challenging in liver failure because of the liver's primary role in carbohydrate metabolism. The alteration in hormones also contributes to problems for glucose control. Metabolically, stable cirrhotic patients behave similarly to normal individuals under prolonged starvation.

Fasting hypoglycemia can occur because of the decreased availability of glucose from glycogen in addition to failing gluconeogenic capacity in end stage liver disease. Therefor, carbohydrate should provide most of the non-protein calories.

Protein:-

Protein is by far the most discussed and controversial nutrient in liver failure and also the most complex. Cirrhotic patients do appear to have an increase protein requirement due to increased degradation in order to supply energy. This occurs because in liver disease, carbohydrate and lipid metabolism are deranged and therefore, the body can not adequately utilize these macronutrients as fuel sources. In uncomplicated hepatitis or cirrhosis without encephalopathy, protein requirements range from 0.8 to 1 gm / kg dry weight per day to achieve nitrogen balance. Unnecessary protein restriction may only worsen body protein losses and therefore, must be avoided. In situations of stress such decompensated disease (sepsis, infection, Gl bleeding, severe ascites, at least 1.5 gm of protein /day should be provide.

Lipid (fat) :-
Cirrhosis is marked by impaired fat metabolism. Long chain triglycerides or dietary fat are incompletely metabolized in liver failure. Therefore overfeeding regardless of energy source should be avoided because excess calories can contribute to fat synthesis and accumulation in the liver. A range of 10 to 15 % of calories as fat is generally recommended. Fat absorption may also be improved in liver disease. It is estimated that steatorrhea of varying degrees, occurs in approx. 50% of cirrhotic patients. If significant steatorrhea is present replacement of some of the dietary fat with medium chain triglycerides (found in coconut oil) may be useful.

Vitamin and minerals :-
Deficiencies of fat-soluble vitamins have been found in all types of liver failure. Therefore, supplementation is necessary. Large doses of thiamine are given daily for limited time if deficiency is suspected. Mineral metabolism is also affected. Elevated serum copper levels are found in cholestatic liver disease.

Fluids and electrolytes :-
Cirrhosis is characterized by excess sodium and fluid retention with increased urinary potassium losses. These are further affected by diuretic therapy. In patients with ascites, sodium is commonly restricted to 2 g / day. More severe limitation may be imposed, however caution is warranted because of limited palatability. Fluid status is monitored closely by regular measurements of body weight and clinical assessment. Fluid intake is usually restricted to 1 liter per day, depending upon the severity of the edema, ascites, and hyponatremia

HEPATIC ENCEPHALOPATHY :-
In encephalopathy dietary treatment is geared towards reducing ammonia production and correcting plasma amino acid profile. The fundamental principle in the dietary management of hepatic coma is to reduce the protein intake to a minimum thus decreasing the amount of ammonia produced. Catabolism of tissue protein must also be avoided. Some clinicians omit protein completely for two or three days but this should be avoided, as some amount of protein is needed, to avoid catabolism of tissue protein. Twenty to 30 grams of protein daily or 0.6 to 0.8 gm/kg/day can be given safely. Vegetable protein and casein based diets have shown promise in reducing encephalopathy. The high fiber content of vegetable protein diet also plays a role in excretion of nitrogenous compounds. As the patient improves, the protein intake is gradually increased by increment of 0.2 g/kg/day to tolerable levels.

Levels of 40 to 50 gm protein daily may be used for long periods of time without detriment to nutritional status provided the diet is otherwise adequate. Nitrogen balance can be achieved on protein intake to as low as 25 to 35 gms daily if high - quality protein is used and caloric intake is adequate.

These patients pose problem in feeding because of anorexia and behavioral patterns ranging from apathy, drowsiness and confusion to irritability. The sugar fat emulsions, glucose in beverages or fruit juices may be used initially through oral or tube feeding.