Hepatic Diseases (Liver)

HEPATIC DISEASES/DISEASES OF THE LIVER

The liver is the largest and the most complex organ in the body. It performs many functions that have an important bearing on the nutritional status of an individual. It plays a major role in intermediary metabolism

• CHO metabolism
• It is involved in synthesis, storage and release of glycogen
• Production of new glucose by the process of gluconeogenesis process
• Conversion of galactose and fructose into glucose

Protein metabolism

• Synthesis of plasma protein
• Deamination of amino acid
• Transamination of amino amino acid
• Formation of urea from ammonia
• Synthesis of non essential amino acid

Lipid metabolism

• Synthesis of lipoproteins, phospholipids, trglycerides and cholesterol
• Formation of bile and conjugation of bile salts
• Oxidation of fatty acids to energy

Mineral and vitamin metabolism

• Storage of Fe, mg, cu and Zn
• Storage of fat soluble vitamins and water soluble B12
• Conversion of carotene to Vitamin A
• Conversion of Vit K to prothrombin
• Conversion of Vit D to active form
• Protective factor- it detoxifies products of bacterial infection, poisons drugs including alcohol and deactivation of hormones.
• In case of liver disease those functions are affected such that there will be
• Decrease in plasma synthesis
• Increased level of ammonia
• Decrease urea output
• Increased serum lipids
• Decreased synthesis and secretion of bile salts
• Decrease in absorption and transport and storage of minerals and vitamins

Causes of Liver disease

• Toxins such as alcohol
• Infectious agents such as virus,
• Metabolic disorders or malnutrition
• Cancer
• Regardless the cause the pathological changes in the liver cells are similar
• Atrophy or reduction in cell size
• Fatty infiltration
• Fibrosis or excessive fibrous tissue
• Necrosis (death of the cells or tissue in the liver)

Symptoms and clinical findings in the liver disease

• Jaundice
• Yellow pigmentation of the skin, mucus membrane and other body tissues due to accumulation of bile pigments in the blood. The common one is the bilirubin
• Types of jaundice
• Obstructive jaundice-occur mainly due to interference to the flow of bile by stones, tumors or inflammation of the bile ducts
• Hemolytic jaundice- occur due to abnormal large destruction of the blood cells
• Toxic jaundice-due to poison, drugs or viral infections
• Weakness
• Fever
• Anorexia and weight loss
• Enlarged liver (hepatomegaly)
• Oedema (ascites- accumulation of fluids in the abdominal cavity
• Fatigue
• Joint and muscle pains.
• Anorexia
• Nausea
• Vomiting
• Diarrhea or constipation

Objectives of dietary management

• Maintain or improve the nutrition status of the patient through provision of adequate energy and nutrients
• Prevent further degeneration of the liver
• Enable regeneration of as much tissue as possible
• Enable the damaged liver to easily and efficiently perform its functions
• NB/
• Assessment of nutrition status may be done through clinical observation like presence of jaundice, presence of ascites
• Types of liver diseases:

Hepatitis

• This is a widespread inflammation of the liver. It is caused by drugs or virus. The viral type is more common.
• Viral hepatitis has three types i.e. hepatitis A, B and C.

Causes

• Type A/ infectious hepatitis: it is transmitted through contaminated drinking water and sewage, and general poor sanitation
• Epidemic may occur from time to time especially in the young children
• Common in overcrowded areas and in poor hygienic conditions

Symptoms

• Nausea, vomiting, fever, headache, fatigue and jaundice
• Recovery in adults is normally complete but however serious complications may occur in high risk groups like young children and the elderly
• Vaccine is available
• Type B: This is chiefly transmitted parenterally through contact with improperly sterilized needles, blood trasfussion from a carrier of the virus and body fluids e.g. saliva, blood and semen.
• Symptoms are like in type A but there are more severe and likely to progress to chronic state
• Type C: Can be transmitted through blood transfusion.
• Drug induced hepatitis: This is caused by use of some of the following substances: alcohol, heroine, marijuana or hypersensitivity to sulphur compounds, penicillin or carbon tetrachloride.

Dietary management

• Should be high in protein, high CHO and moderate fat
• Initially foods of liquid or soft consistency should be given if there is poor appetite, using concentrated commercial or blended formulas for frequent feedings
• As the patient improves appetizing and attractive food is needed
• Calories should be adequate to maintain weight or for weight gain- 35-45kcal/kg BWT or Increased energy of about 2500-3000kcl/day is needed for tissue regeneration for malnourished
• For CHO give complex CHO about 300-400gm/day

Proteins should be high to provide for tissue repair and replenish liver proteins (1.2-2g/kg/BWT) or about 100-150g of high biological value proteins. This will help overcome -ve nitrogen balance and prevent fatty infiltration of the liver cells

• Use low fat diet until the patient regains his/her appetite (MCT).
• Fat soluble vitamins in water soluble form should be provided in amount twice the normal RDAs other water soluble vitamins also require supplementation
• If steatorrhea is present MCT oil may be used for a brief time then regular vegetable oil products and small amount of butter fat may be resumed to ensure adequate amount of essential linoleic acid
• Allow spices to stimulate appetite
• Allow adequate time for food intake due to poor appetite
• Avoid alcohol
• Provide small frequent meals with in between high energy and high protein beverages

Liver cirrhosis

• It is a chronic liver disease characterized by degeneration of liver cells which is replaced by inactive fibrous tissue. There is loss of functional cells

Cause

• Chronic alcoholism
• Infectious hepatitis
• Long term chemical or drug exposure or exposure to other toxins
• Right side congestive heart failure
• Metabolic disorders eg excessive absorption and deposition of iron in the liver

Alcoholic liver disease (laennecs liver disease)

This is the most common type of liver cirrhosis caused by excessive alcohol consumption combined with malnutrition. Excessive consumption of disease can lead to poor dietary intake mal absorption of vitamins such as B1, B12, Vit C, Folic acid etc

• Pathological changes that occur include fatty liver, death of cells and fibrosis of tissue
• Mechanism
• Alcohol is converted to acetaldehyde group and hydrogen
• Acetaldehyde is toxic to the cells and causes inflammation and necrosis
• Excess hyderogen replaces fat as fuel and this leads to accumulation of fat in the liver (fatty liver)
• Other complications

Portal hypertension- the portal vein that carries nutrients rich blood from the GIT to the liver and hepatic artery that carries oxygenated blood from the heart to the liver carries huge vol. of blood due to scarred tissue. this cannot easily pass through the liver and therefore blood backs up and blood pressure builds in the portal vein

• Ascites - due to huge blood pressure in the portal veins which forces plasma from the vessel into the cavity causing swelling
• There is increased sodium and water retention

Oesophageal varices due to blockage of blood flow through the liver blood takes an alternative route (smaller vessels around the liver) they become distended, they enlarge and varices develops. This can lead to bleeding

• Elevated blood ammonia due to the failed function of the liver converting ammonia to urea
• General guidelines for management of hepatic Cirrhosis

Protein should be individualized and adjusted as the disease progress but it should be sufficient to regenerate the liver cells and prevent cirrhosis but not excess to aggravate ammonia build up (1.5-2g/kg BWT)

• If there are signs of coma it should be reduced to 35-50g/day and should be high biological value protein
• If there is hepatic coma it should further be reduced to 35gm/day
• Increase protein as the condition improves
• Fat mal absorption occurs in many patients leading to steatorrhea. Restrict fat to about 40gms per day
• Give long chain triglycerides
• CHO should be adequate to prevent protein catabolism and consequently building up of ammonia. Give 300-400g/day
• Fluids and sodium- if oedema and ascites are present restrict Na to 1-2g/day and 1-1.5 liters of fluids. Fluid restriction may also be as low as 500ml/day if edema is too much
• Vitamins and minerals supplements may be necessary especially B6, B2, B12, folic acid, vitamin C, Vit K
• Avoid alcohol
• Diuretics are used to remove fluids from the liver.
• If oesophageal varices develop, it may be necessary to give soft foods that are smooth in texture to prevent danger of rapture and haemorrhage

c. Hepatic encephalopathy (hepatic liver failure)

This is a clinical syndrome that develops in advanced liver disease characterized by impaired mental neurological and neuromuscular disturbances and altered consciousness. It is also referred to as end stage liver disease.

Manifestation

• Asterixis/flapping trmor- uncontrolled movements of the hands and legs
• Altered state of consciousness
• Confusion
• Restlessness
• Irritability
• Poor coordination
• Fector hepaticus-fecal oduor breath
• Coma
• Dysphagia

Cause

• The mechanisms leading to the changes are unclear but it is thought to include
• Hyper ammonia (liver cannot detoxify ammonia to urea)
• Entrance of nitrogen containing compounds including ammonia into cerebral circulation (CNS). Ammonia is a direct toxin to CNS)

Nutrition implications

• PEM (protein energy malnutrition).
• Malabsorption and maldigestion.
• Altered macronutrient metabolism

Aims of nutritional management

• To reduce ammonia levels in the liver
• To reduce nitrogenous substances in from the GIT

To provide adequate energy and proteins in order to facilitate hepatic cell regeneration. NB/ the GIT produces about 2/3rds of the body ammonia from the intestinal bacteria which makes ammonia from undigested proteins

• To correct vitamin and mineral deficiencies.
• To prevent and correct weight loss
• To avoid potential complications like hypoglycemia/hyperglycemia, fluid overload, electrolyte imbalance.
• General dietary guidelines for management of hepatic encephalopathy and coma
• Provide high calorie diet to avoid body tissue break down (1500-2000Kcal/day) or 35-50kcals/kgBWT.
• Restrict protein intake to 20-40g per day to reduce toxicity. Increasing the amount gradually (10-15g) as the patient condition improves to a maximum of 1g/kgBWT
• For severe cases limit 0-20g per day or 0.6g/kg BWT, then increase by 10-20g as the patient's condition improves

Vegetable proteins and casein from milk appears to be better tolerated than protein from meats as they are lower in aromatic amino acid (tyrosine, phenyalanine) and high in branched chain amino acid (valine, leucine, isoleucine ) which are not catabolised by the liver but are taken by other tissues meaning they can be catabolised without a healthy liver

Calorie intake should be chiefly from carbohydrates and not from either proteins or fats to avoid protein catabolism which results in hyper ammonia and excess fat deposition in the liver (50% of calories to come from carbohydrates and 30% fat contribution).

• High ammonia food such a cheese, onions, chicken , ham , peanut butter, potatoes should be avoided
• Food should be well prepared and presented as anorexia is a problem
• Use low sodium (Na) diet to avoid edema
• Ensure low fluid intake to avoid edema
• Supplement with B-complex, vitamin C, zinc and K.
• Avoid alcohol intake.
• NB/due to GIT discomfort as a result of fat indigestion there are feeding problems in liver disease thus giving small frequent meals that are nutrient and energy dense is recommended.

Guidelines for enteral support

• High-caloric density, low-sodium or modular products may be used for patients who need sodium and fluid restriction.
• Small-bore feeding tubes may be necessary for patients with esophageal varices.

The administration of 25 to 30 non-protein calories per Kg body weight should be adequate to meet the energy requirements in stable patients. For patients with increased stress due to infection, surgery or trauma 30 - 35KCalories/KgBwt may be needed.

Sufficient protein is needed to promote positive nitrogen balance. Estimated protein needs are 1 - 1.5g/Kgbwt (40 - 50g/day). Patients with end stage liver disease may not tolerate that level of protein if given as a standard protein. However the standard formulae should be attempted unless treatment with specialized formulae is indicated. Initiate feeding with a standard or high caloric density formulation at 20ml/hr. and increase as tolerated to the goal rate needed to meet caloric and protein requirements.

In encephalopathy or low-grade encephalopathy protein provided could be reduced by 10 to 20g/day, while ensuring adequate provision of energy. As condition improves protein can be increased in daily increments of 0.2g/Kgbwt until goal rate is achieved. If signs of encephalopathy re-occur protein should be reduced o previously tolerated levels. For worsening cases while receiving standard protein formula at a decreased rate, a Branched Chain Amino Acids (BCAA)- containing formula maybe be appropriate at this time. The modified amino-acid formula may also be used as an oral supplement for patients with chronic encephalopathy.

• Electrolytes, liver function tests, and input and output records should be monitored daily until stable.

Guidelines for parenteral support

• Standard amino acid solutions should be used as tolerated and increased to a goal of 1- 1.5g/Kgbwt depending on severity of the disease.
• As with enteral feeding specialized formulas could be used for those who worsen with a standard formula or present with grade II or higher encephalopathy.

If a modified formula is chosen it should be initiated at a rate to provide 0.5 - 0.7g protein/KgBwt and increased to a goal of 1.5g per Kg BWT. If clinical signs of encephalopathy ensure the modified solution should be increased to the previous level of tolerance.

Non-protein calories should be provided to meet the patients needs and prevent catabolism based on tolerance to parenteral nutrients. Avoid over feeding of lipids and carboydrates as it may lead to fat synthesis, cholestasis, steatosis, and glucose intolerance.

Micronutrients should be adjusted as necessary. Sodium and fluids may need to be restricted if ascites and edema are present. Potassium intake must be sufficiecnt to prevent hypokalemia when renal function is adequate and diuretic therapy is used. Vitamin K may need to be supplemented. Iron should be restricted in hemachromatosis and hemosiderosis. Additional supplements should be provided if a deficiency exists.

• General guiding principles in diet modification in liver diseases
• For those individuals whose liver damage is not so severe as to cause ascites or encephalopathy a balanced, adequate meal with all nutrients should be given.
• Portions should be small, well presented and appetizing.
• Between meal snacks such as milk drinks and biscuits should be available to maintain nutrient intake
• Likes and dislikes should be noted to ensure that food provided is eaten
• It may be appropriate to use sip feeds
• A protein intake of 1g/kg body weight is sufficient and this is easily provided by a normal diet.
• Excessive intake of proteins should be discouraged as it might precipitate encephalopathy
• Vitamin A, D, C, K, B complex and iron should be supplemented
• Alcohol is strictly forbidden