Nutritional Management of Liver Disease. Review the functions of the liver Review diseases of the...
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Transcript of Nutritional Management of Liver Disease. Review the functions of the liver Review diseases of the...
• Review the functions of the liver• Review diseases of the liver• Major complications of liver disease• Nutritional features of end stage liver disease• Nutritional management of end stage liver disease• Nutritional response to hepatic transplantation• Nutritional management of non alcoholic fatty liver
disease (NAFLD)• Hepatitis C
Functions of the Liver
Major role of the liver is the regulation of solutes in the blood that affect the functions of other organs for example: the brain, heart, muscle and kidneys
Strategically placed such that all blood passing from the small intestine must travel through the liver
Functions of the Liver
Storage and metabolism of macronutrients such as protein, carbohydrates and lipids
Metabolism of micronutrients – vitamins and minerals
Metabolism and excretion of drugs and toxins – endogenous and exogenous
Role of the Liver in Nutrient Metabolism
Storage and metabolism of macronutrients such as protein, carbohydrates and lipids
Carbohydrate Storage of carbohydrate as
glycogen Gluconeogenesis Glycogenolysis
Role of the Liver in Nutrient Metabolism
Protein Synthesis of serum proteins e.g. albumin Synthesis of blood clotting factors Formation of urea from ammonia Oxidation of amino acids Deamination or transamination of amino
acids
Role of the Liver in Nutrient Metabolism
Fat Hydrolysis of triglycerides, cholesterol and
phospholipids to fatty acids and glycerol
Formation of lipoproteins
Ketogenesis
Role of the Liver in Nutrient Metabolism
Fat Fat storage
Cholesterol synthesis
Production of bile necessary for digestion of dietary fat
Role of the Liver in Nutrient Metabolism
Vitamins Site of the enzymatic steps in the activation of
vitamins : thiamine
pyridoxine
folic acid
vitamin D(25 hydroxycholecalciferol)
Site of the synthesis of carrier proteins for vitamins: A, B12, E
Role of the Liver in Nutrient Metabolism
Storage site for fat soluble vitamins A, D,
E, K, B12
Minerals
Storage site for copper iron and zinc
Diseases of the Liver
Hepatitis Inflammation of hepatocytes Reversible Precipitants include:
Viral infections such as hepatitis A, B, C
Drugs such as paracetamolSome herbal preparationsAlcohol
Fatty Liver:Infiltration of the liver by fatPossible causes include:
alcoholobesitytype 2 diabetes mellitushyperlipidaemia
sudden rapid weight gain
hepatitis CTPN
NAFLD (Non Alcoholic Fatty Liver Disease)
Resembles alcohol induced fatty liver
Occurs in people who do not abuse alcohol
Has the potential to progress to cirrhosis and liver failure
Non Alcoholic Fatty Liver Disease (NAFLD)
Simple steatosis Steatohepatitis (NASH) Fibrosing steatohepatitis Cirrhosis
Non Alcoholic Fatty Liver Disease (NAFLD)
Factors involved in the development of NAFLD:
Lifestyle : Weight gain Weight loss Reduced activity
Childhood and adult obesity Type 2 diabetes
Non Alcoholic Fatty Liver Disease (NAFLD)
The major underlying risk factor for the development of NAFLD is insulin resistance
NAFLD (Non Alcoholic Fatty Liver Disease)
Prevalence of obesity in patients with NAFLD reported between 30% and 100%
Prevalence of type 2 diabetes in patients with NAFLD reported between 10% and 75%
Prevalence of hyperlipidaemia in patients with NAFLD reported between 20% and 92%
NAFLD - Symptoms
Often asymptomatic of liver disease at time of diagnosis
Fatigue or malaise and/or a feeling of fullness or discomfort on the right side of the abdomen
NAFLD - Symptoms
Mild to moderate elevation of the enzymes:
aspartate amino transferase
alanine amino transferase
Diagnosis confirmed on biopsy
Cirrhosis Refers to chronic scarring of the liver
Clearly delineated nodules form within the liver which contain connective tissue
This leads to a significant reduction in liver function
Fulminant Hepatic Failure Sudden massive necrosis of hepatocytes
The patient rapidly becomes encephalopathic and comatosed
Causes may be viral or a reaction to a drug such as paracetamol, sulphathiazone or some herbal remedies
Autoimmune liver diseases Diseases of the biliary tract and include
primary sclerosing cholangitis (PSC) and primary biliary cirrhosis (PBC)
PSC often occurs in association with ulcerative colitis
Serum cholesterol levels may be elevated and unresponsive to medication or dietary manipulation
Alcoholic liver disease
Alcohol is toxic to the liver
Caused by chronic alcohol abuse
All stages of the disease process – hepatitis, fatty liver fibrosis and cirrhosis
Alcoholic liver disease
Cessation of alcohol may result in recovery in the early stages of liver disease
Cessation of alcohol in patient with cirrhosis may result in an improvement in liver function and may also result in a slowing down of the disease progression
Wilson’s Disease
Copper storage disease
May result in cirrhosis if untreated
First presentation often in adults who present with cirrhosis
Wilson’s Disease
If detected in childhood management involves penecillamine which acts to bind Cu in the GIT
Value of dietary Cu restriction debatable in children; of no value in adults in the presence of cirrhosis
Hepatic tumours Often occur in association with Hepatitis B
or Hepatitis C
Occur independently
Include hepatocellular carcinomas, cholangiosarcoma (bile duct tumours)
Portal Hypertension
Occurs as a result of fibrous infiltration of the liver which in turn causes increased pressure in the portal vein
This pressure continues back through the system to the abdominal capillaries which then leak serous fluid into the abdominal cavity due to this increased pressure and low serum albumin levels
Portal Hypertension
Surgical interventions may be undertaken to alleviate this pressure (TIPSS). There are risks associated with these procedures – infection, failed shunts, encephalopathy
Decompensated cirrhosis
Symptoms of portal hypertension include: Ascites and/or peripheral oedema Jaundice Oesophageal and/or gastric varices Encephalopathy Hepatorenal failure Malnutrition
Ascites Refers to the accumulation of fluid in the
abdominal cavity
It contains protein, sodium and potassium
It is considered to be an active metabolic unit
Jaundice Refers to the yellow colour seen in
patients with liver disease
It is caused by high circulating levels of bilirubin
Severe itching may be present. May be alleviated by Questran/cholestyramine or by phenergan
Varices Distended/engorged veins that can occur at
any point in the venous system of the GIT
May bleed readily as patients with end stage liver disease (ESLD) have poor coagulation secondary to impaired synthesis of clotting factors
Encephalopathy Impaired mental state that results in impaired
mentation and coordination
May result in coma
Believed to be caused by increases in plasma ammonia and other nitrogenous waste products
These toxins cross the blood brain barrier and interfere with neuromuscular function and behaviour
Precipitants of encephalopathy include:
Peritoneal infection (subacute bacterial peritonitis – SBP)
GIT bleeding Poor compliance with lactulose (marketed
as Duphalac) therapy Nitrogen overload Fluid and electrolyte imbalance Medications Acid-base imbalance
There are four classifications of encephalopathy:
Grade1. foetor, impaired coordination, tremor, altered handwriting, reduced attention
span, mild confusion, mood swings and altered sleep
pattern
Grade 2. asterixis (impaired ability to draw a star), slurred speech, ataxia
inappropriate behaviour, lethargy, impaired memory and mild disorientation
Classifications of encephalopathy cont…
Grade3. bizarre behaviour, confusion, moderate to severe
disorientation, uncharacteristic anger, paranoia, somnolence, stupor and muscle rigidity
Grade 4. comatosed, dilated pupils
Nutritional Management of Liver Disease
Early Stages of Liver Disease: No specific dietary management
Healthy diet according to healthy eating guidelines
Beware of miracle cures
Acute Hepatitis:
High protein/high energy intake required to promote hepatocyte regeneration
• Fat restriction contraindicated• Nausea/anorexia• Consider oral supplementation such as
glucose polymers, fruit based high protein drinks, or high protein/ high energy drinks in the presence of nausea/anorexia
Caution against herbal remedies as some may be harmful and most have no scientific basis
Nutritional Features of End Stage Liver Disease
Look malnourished Low se protein levels
albumin, prealbumin, transferrin, retinol binding protein, insulin like growth factor-1
Vitamin deficienciesthiamine, vit A, D, E
Mineral deficienciesZn, Mg, Cu, Ca
Nutritional Features of Liver Disease
Weight and BMI do not reflect true nutritional status (ascites and/or oedema)
Oral intakes are not necessarily poor
Exhibit features of protein energy malnutrition
Nutritional Assessment of patients with ESLD
Weight? Weight history? Protein markers of nutritional status? Descriptive history of wasting? Skinfolds? Intake? Appetite?
Nutritional Assessment of patients with ESLD
SGA for patients with liver disease (Hasse) Anthropometry Food history Nausea Anorexia Taste changes Diarrhoea Early satiety Functional capacity
Grip strength
Nutritional Management of End Stage Liver Disease
Energy Requirements: Patients with compensated cirrhosis do not
appear to need modification of their energy intakes
Patients with decompensated liver disease require 35 – 40 non protein kcals/kg/day*
Ascites is a viable metabolic unit
*Plauth M, Merlim, Kondrup J, Weimann A, Ferenci P, Muller MJ.ESPEN Guidelines for Nutrition in Liver Disease and Transplantation. Clinical Nutrition 1997; 16: 43-55
Nutritional Management of End Stage Liver Disease
Energy Energy expenditure: currently there are no
metabolic equations which are able to estimate accurately the energy requirements of the patient with ESLD.
Harris-Benedict, Schofields and Muller all underestimate the energy requirements of this group
Indirect calorimetry
Nutritional Management of End Stage Liver Disease
Glycogen storage Reduced glycogen storage capacity
Unable to tolerate periods of prolonged fasting – increased protein breakdown in periods of prolonged fasting
Nutritional Management of End Stage Liver Disease
Fat Altered fat synthesis
Lipids are oxidised as a preferential substrate
Increased lipolysis
Active mobilisation of lipid stores
Decompensated Liver Disease
Fat restriction contraindicated in most patients
Symptoms of fat intolerance such as steatorrhoea, abdominal pain or nausea following a high fat intake are rare. If present fat modification may be necessary
Nutritional Management of End Stage Liver Disease
Protein Protein turnover in cirrhotic patients is normal or
increased Stable cirrhotics have increased protein
requirements¹ ²׳ Stable cirrhotic patients are capable of achieving
positive nitrogen balance during aggressive nutritional support regime¹ ²׳
¹Kondrup J, Neilsen K et al. Effect of long term refeeding on protein metabolism in patients with cirrhosis of the liver. Br J Nutr 1997; 77: 197-212
²Swart, GR et all. Minimal protein requirements in liver cirrhosis determined by nitrogen balance measurements at three levels of protein intake. Clin Nutr 1989; 8: 329-336
Nutritional Management of End Stage Liver Disease
Protein Protein turnover in cirrhotic patients is normal or
increased Stable cirrhotics have increased protein
requirements¹ ²׳ Stable cirrhotic patients are capable of achieving
positive nitrogen balance during aggressive nutritional support regime¹ ²׳
¹Kondrup J, Neilsen K et al. Effect of long term refeeding on protein metabolism in patients with cirrhosis of the liver. Br J Nutr 1997; 77: 197-212
²Swart, GR et all. Minimal protein requirements in liver cirrhosis determined by nitrogen balance measurements at three levels of protein intake. Clin Nutr 1989; 8: 329-336
Nutritional Management of End Stage Liver Disease
Protein Protein refeeding showed a 30% increase
in protein synthesis*
Protein refeeding did not show a significant increase in protein degradation*
*Kondrup J, Neilsen, K,and Anders J. Effect of long term refeeding on protein metabolism in patients with cirrhosis of the liver. Br J Nutrition (1997), 77, 197-212
Nutritional Management of End Stage Liver Disease
Protein Patients with cirrhosis have been shown to
have high protein requirements to maintain positive nitrogen balance*
*Konrup J, Nielsen K, Juul A. Effect of long-term refeeding on protein metabolism in patients with cirrhosis of the liver. Br. J. Nutr. 1997; 77: 197-212
Nutritional Management of End Stage Liver Disease
Protein The protein restricted diets used
traditionally have probably arisen historically from the response to a dietary protein load seen in cirrhotic patients who have some form of portocaval shunt surgery
Nutritional Management of End Stage Liver Disease
Protein requirements in episodic hepatic encephalopathy
62 patients with acute encephalopathy assessed – 32 excluded
30 patients randomised into two groups
All patients received lactulose enema and then identical oral neomycin dosage
Cordoba J, Lopez-Hellin J et al. Normal protein diet for episodic hepatic encephalopathy: results of a randomised study. J of Hepatology 41 2004) 38-43
Nutritional Management of End Stage Liver Disease
20 patients completed study
5 patients in each arm dropped out – 4 deaths in each. Group A: additional variceal bleed; group B: additional voluntary abandon
Nutritional Management of End Stage Liver Disease
2 groups – 15 in each group
14 days
Group A: 0g protein/day for 3 days. Protein increased incrementally to 1.2g protein/kg/day
Group B: 1.2g protein/kg/day
Protein synthesis and breakdown studied at day 2 and day 14
Nutritional Management of End Stage Liver Disease
Day 2: Increased protein breakdown in protein
restricted group
No statistically significant difference in protein synthesis
Nutritional Management of End Stage Liver Disease
Restricting protein intake did not have any positive effect on the evolution of episodic hepatic encephalopathy
Nutritional Management of End Stage Liver Disease
Protein Protein restriction is contra - indicated for
patients with decompensated cirrhosis Recommended protein intake for cirrhotics
is 1.0 – 1.5g protein/kg/day¹ Dietary protein restriction does not appear
to be of any benefit in episodic hepatic encephalopathy²
¹Plauth M, Merlim, Kondrup J, Weimann A, Ferenci P, Muller MJ.ESPEN Guidelines for nutrition in Liver Disease and Transplantation. Clinical Nutrition 1997; 16: 43-55²
²Cordoba J, Lopez-Hellin J et al. Normal protein diet for episodic hepatic encephalopathy: results of a randomised study. J of Hepatology 41 2004) 38-43
Nutritional Management of End Stage Liver Disease
Amino Acids in Encephalopathy Patients with advanced liver disease have an
altered ratio of branched chain amino (leucine valine, isoleucine) acids to aromatic amino acids (phenylalanine, tyrosine)
Aromatic amino acids are catabolised in the liver and their metabolism is impaired in cirrhosis resulting in an increase in circulating levels of AAAs
Nutritional Management of End Stage Liver Disease
Amino Acids in Encephalopathy Branched chain amino acids (BCAA) are
metabolised predominantly in the skeletal muscle and fat
Plasma BCAA levels fall due to their utilisation as an energy substrate and a substrate in gluconeogenesis
Nutritional Management of End Stage Liver Disease
Amino Acids in Encephalopathy The alteration in the ratio of BCAA:AAA
has been proposed as an aetiological factor in the development of encephalopathy*
*Fischer JE, Rosen HM, Ebeid AM et al. The effect of normalisation of plasma amino acids on hepatic encephalopathy in man. Surgery. 1976 Jul. 80 (1): 77-91.
Nutritional Management of End Stage Liver Disease
Amino Acids in Encephalopathy Marchesini et al carried out a multicentre
double blind randomised trial in which BCAA supplementation was compared with an isocaloric casein supplementation in 64 patients with encephalopathy*
*G Marchesini, FS Dioguardi, GP Bianchi et al. Long- term oral branched chain amino acid treatment in chronic hepatic encephalopathy. J of Hepatol, 1990; 11:92-101
Nutritional Management of End Stage Liver Disease
16/34 patients in the BCAA group regained normal mental state compared with 9/30 in the casein treated group (p<0.05)
After 6 months on BCAA treatment nitrogen balance improved and was suggestive of decreased nitrogen catabolism in the BCAA treated group
G Marchesini, FS Dioguardi, GP Bianchi et al. Long- term oral branched chain amino acid treatment in chronic hepatic encephalopathy. J of Hepatol, 1990; 11:92-101
Nutritional Management of End Stage Liver Disease
Long-term oral BCAA supplementation(6 months) resulted in an increase in body weight
G Marchesini, FS Dioguardi, GP Bianchi et al. Long- term oral branched chain amino acid treatment in chronic hepatic encephalopathy. J of Hepatol, 1990; 11:92-101
Nutritional Management of End Stage Liver Disease
15 centres over up to 15.5 months* 174 patients with Childs B or C cirrhosis
*Marchesini G, Bianchi G, Merli M et al. Nutritional supplementation with branched chain amino acids in advanced cirrhosis: a double blind randomised trial.
Gastroenterology 2003;124:1792-1801
Nutritional Management of End Stage Liver Disease
Methods: Three types of nutritional supplements.
Each 10g package supplied: 14.4g BCAA/day (leucine, isoleucine, valine
and saccharose providing 37.5 kcal) 2.1g lacto-albumin/day (lacto-albumin,
saccharose and mannitol providing 33.6 kcal) 2.4g maltodextrose/day (maltodextrose,
saccharose providing 34.9 kcal)
Nutritional Management of End Stage Liver Disease
Methods: All subjects were instructed to take 2
packets three times daily dissolved in 200ml water half an hour before meals
Patients were maintained on self selected diet. No new dietary restrictions were recommended or prescribed
Standard therapies (albumin, diuretics, lactulose) were allowed but registered
Nutritional Management of End Stage Liver Disease
Results: 115 patients remained in the study 59 patients were withdrawn for a variety
reasons:• Death• Deterioration in liver function• Non-compliance (palatability, nausea,
gastrointestinal discomfort and diarrhoea)• Psychiatric disease
Nutritional Management of End Stage Liver Disease
Results: Patients treated with BCAAs were admitted to
hospital less frequently:195 days in BCAA group; 327days in L-ALB group and 520days in M-DXT group
Length of stay varied within the treated groups: 0-24 days in BCAA group 0-31 days in the L-ALB group 0-77 days in the M-DXT group
Nutritional Management of End Stage Liver Disease
Results: Improved triceps skinfold thickness in the BCAA
group Improved midarm fat area in the BCAA group Reduction in the prevalence and severity of
ascites in the BCAA group Shift towards better scoring of health only in the
BCAA group M-DXT supplementation therapy did not require
increase in insulin therapy
Nutritional Management of End Stage Liver Disease
Results: Total bilirubin levels decreased in the BCAA
group and increased in the M-DXT group Improvement in the CTP score in the BCAA
group CTP was stable in the L-Alb group and M-DXT
group Reduced prevalence of anorexia in the BCAA
group
Nutritional Management of End Stage Liver Disease
To summarise: There are benefits to routinely supplement
patients with advanced cirrhosis with branched chain amino acids
Patient compliance
Nutritional Management of End Stage Liver Disease
Current Criteria for use of Oral BCAA Supplementation at RPAH:
chronic encephalopathy frequent hospital admissions due to
encephalopathysevere depletion of fat and muscle
storeselevated blood sugar levels
Nutritional Management of End Stage Liver Disease
Does the timing or frequency of meals of meals matter?
Nutritional Management of End Stage Liver Disease
Eating Pattern Swart and Zillikens demonstrated that
spreading food intake and inclusion of a late evening meal significantly improved nitrogen balance in cirrhotics*
*Swart G, Zillikens M. Effect of a late evening meal on nitrogen balance in patients with cirrhosis of the liver Med J 1989;299: 1202-3
Nutritional Management of End Stage Liver Disease
Eating Pattern A modified eating pattern should be
recommended to all patients with ESLD.
This would include eating at regular intervals – perhaps 5-7 small HP/HE meals/snacks per day
Include a pre-bedtime HP/HE snack to provide substrate for the liver to work with during sleep (supplements)
Ascites Patients with ascites usually have a high total
body sodium but often have a low se sodium
Generally have a poor intake secondary to abdominal distension
Early Satiety
Delayed gastric emptying
Frequent snacking important to achieve high energy intake
Ascites
Sodium restricted diet. Most common restriction is a no added salt diet which can range between 50Mm Na and 100Mm Na
Diuretics. Most commonly used are Lasix and Aldactone.
Salt substitutes contraindicated due to potassium sparing effect of aldactone
Ascites
Fluid restriction
Moderate (1500ml )to severe (≤ 800ml)
≤800ml used to treat intractable ascites unresponsive to diuretic therapy or when diuretic therapy no longer possible due to compromised renal function
• Don’t measure: custards, ice cream
Oesophageal Varices
Varices can occur at any point along the GIT
Oesophageal varices may bleed easily and bleeding further compromises the patient's nutritional status
Oesophageal Varices
Varices can occur at any point along the GIT
Oesophageal varices may bleed easily and bleeding further compromises the patient's nutritional status
Oesophageal Varices
Following an oesophageal bleed the patient will be nil by mouth
Varices will be banded
Oral intake recommenced when patient’s condition stabilises
Oesophageal Varices
When allowed to eat patients should be advise to:
Eat carefully and avoid large bolus of food which might dislodge a clot
Avoid over distension of the stomach which might lead to regurgitation or vomiting
Avoid foods with sharp bones that might be accidentally swallowed
Diabetes in Liver Disease
Patients with ESLD may present with impaired glucose tolerance. This may be due to a number of factors: Depleted hepatic glycogen stores
Impaired glucose tolerance
Hyperinsulinaemia
Insulin resistance
Diabetes in Liver Disease
Management involves diabetic education without restriction of energy intake
Insulin therapy
BCAA supplementation has been shown to facilitate control of blood sugar levels in patients with ESLD
Nutritional Management of End Stage Liver Disease
Achieve and maintain high energy intake(35-40 non protein kcal/kg/day)
Achieve and maintain a high protein intake(1.0-1.5g/kg/day)
Avoid unnecessary fat restriction
Encourage frequent snacking
Nutritional Management of End Stage Liver Disease
Restrict dietary sodium intake in the presence of ascites and/or oedema
Restrict fluid intake to assist in the management of ascites/oedema associated with hyponatraemia
Nutritional Management of End Stage Liver Disease
Consider branched chain amino acid supplementation
Significant pre-bedtime snack
Hepatotoxicity of Herbal Remedies
Herbs are potent medicines
The community is increasingly seeking out alternative or “natural” therapies
Patients with hepatitis C frequently seek out alternative therapies
Hepatotoxicity of Herbal Remedies
Important to be aware of the possible harmful effects of herbs
Some herbs are hepatotoxic and patients with known liver disease should avoid using them
Nutritional Management of NAFLD
Treatment centres around reducing insulin resistance Dietary intervention
Increased physical activity
Metformin
Nutritional Management of NAFLD
Weight loss strategies in presence of overweight/obesity. Weight loss results in improved lipid and carbohydrate metabolism.
Weight loss must be slow. Rapid weight loss results in worsening liver function tests and hepatomegaly
Rapid weight loss may promote or worsen NAFLD, NASH and may result in liver failure
Nutritional Management of NAFLD
• Normal weight subjects: dietary and pharmacological treatment of altered lipid and /or carbohydrate metabolism
• In overweight individuals with elevated aminotransferase levels weight loss of 10% or more corrects aminotransferase levels and decreases hepatomegaly
Nutritional Management of NAFLD
Modification in lifestyle which involves weight reduction and regular exercise are the mainstay of treatment and prevention of NAFLD