Nutrition-When the liver malfunctions



Anne O'Grady dispels some myths about the dietary management of patients with liver disease

Nutritional therapy is a very important tool in the overall management of patients with liver disease. Protein energy malnutrition (PEM) is present in 20% of patients with compensated liver disease and greater than 60% of patients with severe liver insufficiency.

The prevalence and degree of PEM does not relate to the aetiology of the liver disease and so is seen in all liver patient types.

PEM is associated with increased morbidity, mortality and an increased rate of complications. These complications include presence of and persistence of ascites, gastrointestinal bleeding, encephalopathy and increased rates of infection.

PEM has also been shown to impair liver function independently of liver disease.

The main causes of PEM are:

Assessment of nutritional status

Early referral and assessment of nutritional status is warranted for all patients with chronic liver disease in order to identify the type and degree of malnutrition if present. A full nutritional assessment should include information on nutrient intake with emphasis on total energy, protein, sodium, fluid, alcohol intake and use of vitamin or mineral supplements.

Any weight changes, nausea, vomiting, diarrhoea and steatorrhoea should also be noted. The use of body weight is limited as it can be influenced by the presence of ascites and peripheral oedema. Thus present, usual and estimated dry weight should all be calculated.

Upper body anthropometry is the most accurate indicator of malnutrition if ascites is present as minimal upper body ascites occurs.

Triceps skinfold thickness provides an estimate of body fat reserves and mid arm muscle circumference gives an estimate of muscle mass. Handgrip dynamometry can also be used as a measure of muscle function.

Vitamin, mineral, electrolyte levels and lab markers should also be noted. However, all biochemical markers need to be interpreted with caution as they can reflect degree of liver dysfunction and may not be accurate as measures of nutritional status.


Patients with compensated liver disease appear to have similar energy requirements to normal healthy individuals.

However, patients with severe liver disease are hypercatabolic and require nutritional support if hepatocyte regeneration is to be supported and the function of other organs and systems is to be maintained.


All patients with liver disease have higher protein requirements than normal healthy individuals. In the past, protein restriction was used in the treatment of hepatic encephalopathy (HE) yet there is no evidence that it has any clinical benefit.

Precipitating factors for HE include, constipation, GI bleeds, infection, sepsis, dehydration, electrolyte imbalance, acid/ base imbalance, alcohol binge, drugs, and portal systemic shunting.

Dietary protein induced HE is uncommon. A patient with liver disease is already at risk of infection and malnutrition and protein restriction can lead to a negative nitrogen balance and worsening HE. Thus the precipitating factor for the HE should be sought out and treated accordingly.

Protein restriction is not a routine treatment for HE. Protein should only be transiently restricted if a patient displays persistent HE, on maximum medical treatment, with no other precipitating factor being found. Medium to long-term protein restriction is never indicated.

Use of branch chain amINO acids, (BCAAs) and vegetable proteins as a better tolerated protein source in liver patients with HE, also remain inconclusive.

Thus the majority of liver patients should be advised on a high protein diet, with an even distribution of protein throughout the day. Always ensure energy requirements are met to allow full utilisation of protein ingested.


Steatorrhoea can occur in cholestatic liver disease when there is a reduced amount of bile salts reaching the small bowel. Restriction of dietary fat is only justifiable in patients with symptomatic steatorrhoea, ie. if they have severe symptoms, associated weight loss, or nausea and indigestion with fat intake which is unresponsive to medication.

The degree of fat restriction, if required, varies between patients, so individual dietary advice is required. If fat is restricted, the energy deficit needs to be made up and the use of glucose polymers, MCT fats and fruit juice supplements is useful.

Fat soluble vitamins may also require supplementation via the oral or IM route to prevent or correct deficiencies in chronic cholestasis. For patients who do not suffer from steathorrea, fat provides a palatable and useful source of concentrated calories and should not be restricted unless absolutely necessary.


Carbohydrate metabolism is altered in patients with end stage liver disease, (ESLD). Impaired glucose tolerance is common in patients with cirrhosis and around 10% develop diabetes.

For these patients a modified diabetic diet is recommended - low in simple sugars and high in fat with optimal use of oral hypoglycaemic agents +/- insulin.
Nutrient utilisation in patients with cirrhosis is also altered and ESLD patients may experience fasting hypoglycaemic episodes secondary to decreased glycogen synthesis. Thus regular meals, including a bedtime snack, are recommended for all end stage patients.


Ascites is the accumulation of protein rich fluid in the peritoneal cavity, a sign of liver decompensation. A trial has shown that the presence of ascites leads to an increase in resting energy expenditure (REE). This in turn increases the risk of developing PEM. Ascites also causes a decrease in appetite as a result of fluid in the peritoneum pressing on the stomach.

Treatment includes diuretic therapy, sodium restriction, paracentesis and, in some cases, placement of surgical or radiological shunts, eg. TIPS.

A diet very low in sodium helps ascites resolve more quickly than a less strict sodium diet. However, very low sodium diets are unpalatable and sodium restriction should never be at the expense of the patient's overall nutritional status.

Diuresis can be achieved at 88mmol of sodium a day, thus a no added salt diet (equivalent to around 80mmol of sodium/day), is generally used. Overall, sodium restriction depends on the degree/resistance of ascites, diuretic dosage, appetite, patient cooperation and social circumstances.


Fluid restrictions are usually only required when serum sodium falls below 125mmol/litre. The fluid allowed may vary from 500-1,500ml daily. Thus if a patient is on a fluid restriction they must be educated on efficient use of fluid volume and advised not to waste intake on fluids with poor nutritional value.

Energy-dense nutritional supplements and non-liquid supplements are often used in this patient group.

Vitamins and minerals

Micronutrient deficiencies have been observed in 10%-50% of patients with cirrhosis. Causes include inadequate diet, malabsorption, alcoholism, impaired metabolism, increased requirements and increased excretion, decreased hepatic storage and certain medications.

Fat-soluble vitamin deficiency can occur secondary to cholestasis or steatorrhoea. With any micronutrient deficiency, aim to correct deficiencies states.  There is no benefit in supplementing where there is no deficiency.

There is increased evidence to osteoporosis (20% - 50%) with cirrhosis and ESLD is now recognised as a risk factor for osteoporosis and subsequent fracture.  Excess alcohol intake, corticosteroid use and low body mass index (BMI), are also independent risk factors.  It is now recommended that all patients with chronic liver disease are advised to decrease alcohol intake, increase exercise, stop smoking, ain for BMI within the normal range and are supplemented with calcium 1g/day and Vitamin D 800IU/day as required.


Ann O'Grady is a dietitian at St. James Hospital, Dublin


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