CLINICAL NUTRITION II

SNT 3033

CHAPTER 6:

Nutrition in Liver Disease

TOPICS
Nutrition in Liver Disease
Introduction
Diseases of liver
Laboratory assessment of liver function
Manifestations and complications of
cirrhosis
Nutritional management in liver disease
Liver
 Overview of anatomy & physiology
The liver :

the largest solid organ, ~ 1.2 - 1.5kg in adults, ~ 1/5 of total body wt.

The liver consists of four sections, or lobes. There are two main lobes--
the right lobe, which is by far the larger, and the left lobe. Two small
lobes lie behind the right lobe.
 Functions of liver
Excretion of bilirubin, cholesterol, hormones, and drugs
Metabolism of fats, proteins
Enzyme activation and storage of vitamins and minerals
Synthesis of plasma proteins, such as albumin, and clotting
factors
Blood detoxification and purification
Fighting infection
The liver has cells called macrophages that destroys the
bacteria and bacterial toxins that comes from the gut.
 Liver diseases
There are many kinds of liver diseases.
Viruses cause some of them, like hepatitis A, hepatitis
B and hepatitis C.
Others can be the result of drugs, poisons or
drinking too much alcohol.
If the liver forms scar tissue because of an illness, it's
called cirrhosis.
Jaundice, or yellowing of the skin, can be one sign of
liver disease.
Cancer can affect the liver.You could also inherit a liver
disease such as hemochromatosis.
Hemochromatosis http://www.ncbi.nlm.nih.gov/pubmedhealth/
Iron overload PMH0001368/

Hemochromatosis is too much iron in the body. It is also called

iron overload.
Causes, incidence, and risk factors
There are two types of hemochromatosis:
Primary hemochromatosis is a genetic disorder. People with this
condition absorb too much iron through their digestive tract.

Secondary (acquired) hemochromatosis is due to other blood-

related disorders (such as thalassemia or certain anemias) or
many blood transfusions. Sometimes it occurs in people with
long-term alcoholism and other health conditions.
Hemochromatosis affects more men than women.
 Hepatitis
Hepatitis is widespread inflammation of the liver with a
variety of etiologies. Eg:

The hepatitis A virus (HAV) causes acute viral hepatitis A

Hepatitis B virus (HBV) causes hepatitis B.
Hepatitis C, D, E and non-A, non-E viruses
alcohol
 Hepatitis A:

transmitted through fecal-oral route :

contracted through contaminated

drinking water, food and sewage

 symptoms:
i) anorexia (frequent & severe)
ii) Nausea
iii)Vomiting
iv)Right upper quadrant abdominal pain
v) dark urine
vi) jaundice
Adequate nutritional intake !!
Adult patient normally recover completely but serious
complications may occur in high risk patients (very young &
elderly)
 Hepatitis B and Hepatitis C can lead to chronic and carrier
states.

management in the acute phase is similar to that of hepatitis A

(adequate nutritional intake).

Hepatitis B and Hepatitis C are transmitted via blood, blood

products, semen and saliva.

These chronic active hepatitis can also develop into cirrhosis and
liver failure.
ii) Alcoholic Liver Disease (ALD)
The pathogenesis of ALD progresses in 3 stages:
Hepatic steatosis (fatty liver)
Alcoholic hepatitis
Cirhosis

Acetaldehyde, a toxic by-product of alcohol metabolism

causes damage to mitochondrial membrane structure and
function.
 Fatty infiltration or hepatic steatosis is caused by result of
metabolic disturbances:
an increase in the mobilization of fatty acids from adipose tissue
An increase in hepatic synthesis of fatty acids
A decrease in fatty acids oxidation
An increase in TG production
A trapping of TG in the liver

hepatic steatosis is reversible with the abstinence from alcohol.

If alcohol continues, cirhosis can develop
 Although nutritional factors may influence the hepatotoxic effect
of alcohol, adequate nutritional intake does not protect against
liver degeneration in the alcoholic.

In any case, nutritional implications remain strong, because of the

high prevalence of primarily and secondary malnutrition in ALD
and nutrition plays a vital role in its treatment
iii) Cirrhosis
Cirrhosis, the final stage of liver injury

Characterized by repeated episodes of liver necrosis followed

by regeneration resulting in fibrous (scar) tissue formation.

The fibrous tissue distorts and disrupts the normal

architecture of the hepatic lobules.
 This compresses the blood, lymph, and bile flow through the
liver, hence, the delivery of oxygen, nutrients, and hepatotoxic
substances.

The liver shrinks, losing parenchymal cells and function and the
condition is irreversible.

Liver biopsy aids in confirming diagnosis, type and severity of

cirrhosis.
 The increased pressure within the liver result in the increased
portal vein pressure, thus, creating portal hypertension.

As the low-pressure veins become distended with blood, they

enlarge and varices develop, most commonly in the esophagus
and stomach.
 A high number of patients die from an initial episode of GI
bleeding due to varices.

Another complications of portal hypertension is ascites (the

formation of fluid within the peritoneal cavity).

Low serum albumin also plays a part in the development of

ascites due to its role in maintaining oncotic pressure.

Jaundice occurs secondary to hyperbilirubinemia, although it can

be mild or absent in chronic liver failure.
 Other causes of cirrhosis:

Alcoholic liver disease

Right-sided congestive heart failure (cardiac cirrhosis),
primary sclerosing cholangitis, (infection of bile ducts)
chronic viral or autoimmune hepatitis,
biliary atresia and (common bile duct between liver and small
intestine)auto immune disorder
long-term chemical or drug exposure
Variable inherited metabolic disorders can lead to cirrhosis
iv) Hepatic failure (end stage liver
disease ESLD)
Actual hepatic failure occurs when liver function is
diminished to 25% or less.

This can occur when cirrhosis reaches the point of severe

parenchymal cell loss, or acutely which is termed fulminant
hepatic failure.

Fulminant failure can be caused by drug overdose,

hepatotoxic poisoning or circulatory failure.
 Portal systemic encephalopathy (PSE), formerly known hepatic
encephalopathy (HE) is a complication of liver failure,
manisfested by a variety of neuromuscular and personality /
behaviour alterations.
Symptoms :
mild confusion and impaired coordination (Grade I) to flapping
tremors and slurred speech (Grade II).
Grade IV encephalopathy is the most severe stage, characterized
by loss of consciousness and coma.

Grade III ??
 Ammonia is considered to be an important etiologic factor in the
development of encephalopathy.

When liver fails, it is unable to detoxify ammonia to urea.

Ammonia is direct cerebral toxin

Although serum and cerebrospinal fluid levels do not correlate

well with the degree of HE, treatment is based on lowering these
levels.
 Ammonia metabolites such as glutamine and alpha-keto glutarate
in cerebrospinal fluid have correlated more closely with severity
of encephalopathy.

The main source of ammonia is the endogenous production by

the gastrointestinal tract (eg: from bacteria degradation and
blood from GI bleeding).

Therefore, drugs such as lactulose and neomycin are given.

 Lactulose is a hyperosmotic laxative, is not digested or
absorbed in the small intestine and therefore reaches colon,
where it is fermented by the flora.
There, lactulose alters the metabolism of nitrogen resulting in
increased nitrogen excretion via fecal bacteria.
Lactulose may also inhibit ammonia generation itself by reducing
the colonic pH.
The acid environment produced traps ammonia as ammonium
ion NH4 and because lactuloses laxative effect, the ammonia is
excreted..
 Neomycin is an anti-infective agent, destroys the normal
bacterial flora that degrade protein and produce ammonia

Exogenous protein is also a source of ammonia, therefore dietary

modification is needed
 In addition, various metabolic abnormalities including hypoxia,
hypo volemia, hypotension, hypo albuminemia, hypoglycemia,
azotemia, electrolyte imbalance and several drugs may contribute
to this condition.
 Hepatic Encephalopathy
Hepatic encephalopathy may be triggered by:
Dehydration
Eating too much protein
Electrolyte abnormalities (especially a decrease in
potassium) from vomiting, or
from treatments such as paracentesis( a procedure
to take out fluid that has collected in the belly (peritoneal
fluid) or taking diuretics ("water pills")
Bleeding from the intestines, stomach, or
esophagus
 Hepatic encephalopathy Causes
Infections
Kidney problems
Low oxygen levels in the body
Shunt placement or complications
Surgery
Use of medications that suppress the central
nervous system (such as barbiturates or
benzodiazepine
Tranquilizers
Hepatic encephalopathy (Causes)
Alcohol intoxication
Complicated alcohol withdrawal
Meningitis
Metabolic abnormalities such as low blood
glucose
Sedative overdose
Subdural hematoma (bleeding under the skull)
Wernicke-Korsakoff syndrome(disorder of
CNS) caused by thiamine deficiency in
alcoholics
 Hepatic Encephalopathy (Contd)
Symptoms may be mild at first. Family members or caregivers
may notice that the patient has:
Breath with a musty or sweet odor
Change in sleep patterns
Changes in thinking
Confusion that is mild
Forgetfulness
Mental fogginess
Personality or mood changes
Poor concentration
Poor judgment
Worsening of handwriting or loss of other small hand
movements
 Dietary Counseling
1) Alcoholic liver disease:

help patient in the planning or preparation of appetizing,

nutrient-dense meals
Use of prescribed vitamins
Refrain from Alcohol consumption.
Weight loss
Help arrange for assistance at home
 Hepatic Encephalopathy Treatment
Hepatic encephalopathy may become a medical
emergency. Hospitalization is required.
The first step is to identify and treat any factors that may
have caused hepatic encephalopathy.
Gastrointestinal bleeding must be stopped. The intestines
must be emptied of blood. Infections, kidney failure, and
electrolyte abnormalities (especially potassium) need to
be treated.
Life support may be necessary to help with breathing or
blood circulation, particularly if the person is in a coma.
The brain may swell, which can be life-threatening.
Patients with severe, repeated cases of encephalopathy
may be told to reduce protein in the diet to lower ammonia
production.
 Hepatic Encephalopathy Treatment
. However, dietary counseling is important, because too little
protein in the diet may cause malnutrition.
Critically ill patients may need specially formulated
intravenous or tube feedings.
Lactulose may be given to prevent intestinal bacteria from
creating ammonia.
Neomycin may also be used to reduce ammonia production
by intestinal bacteria.
Sedatives, tranquilizers, and any other medications that are
broken down by the liver should be avoided if possible.
Medications containing ammonium (including certain
antacids) should also be avoided. Other medications and
treatments may be recommended. They may have varying
results.
v) Nonalcoholic fatty liver disease (NAFLD)
NAFLD encompasses simple fatty liver and nonalcoholic
steatohepatitis (NASH), which can lead to cirrhosis.

Vague right upper quadrant pain, fatigue and malaise may be reported.

Serum ALT and AST may be elevated two to fourfold.

Serum ferritin level and alkaline phosphatase may be elevated

Bilirubin, albumin and prothrombin time typically are normal

vi) Cholestatic liver disease
a) Primary Sclerosing Cholangitis (PSC)

sclerosing cholangitis is characterized by patchy inflammation,

fibrosis and destruction of the intra and extra hepatic bile ducts.

Common features include pruritus, jaundice, fatigue, and abdominal

pain.
Poor concentration of bile.

treatment to halt the disease : liver transplant

b) Wilsons disease
is an autosomal recessive disorder of copper metabolism characterised
by abnormal transport and storage of copper.

Copper accumulates in the liver, kidney, brain and cornea (Kayser-

Fleischer rings) and may have toxic effects on tissues.

Symptoms:
Hepatic, neurological and psychiatric dysfunctions.

Therapy : medications to remove copper or maintain balance

A low copper diet is advised.

Nutrition therapy
1) Assessment
diet history : special attention for:-
degree of anorexia
Postprandial fullness
Taste changes
Chronic diarrhea

1) Excess fluid retention

(ascites and edema)

2) Impaired protein metabolism

a) Anthropometric measurements
triceps skin fold and mid-arm muscle circumference will reflect
nutritional reserves.
b)SGA
Evaluation of Nutritional status
Physical Examination like oedema

c)24-hr urinary creatinine excretion

d)Total body potassium

e)Dual-energy X-ray (DEXA) _Measurement of body fat/tissue

mass
BIA
2) Energy Needs
most patients with liver disease have a normal metabolic rate .

for compensated cirrhosis or encephalopathy:

25-35 non-protein cal /kg/day

for inadequate or malnutrition:

35-40 non-protein cal / kg / day
3) Protein needs
protein restriction should not be considered routine

Basal protein requirements = 0.8 1g/kg/day

In stress = 2g/kg/day
For encephalopathic patients=0.5-0.6g/kg/day
4) Fat
most patients with liver disease are not able to tolerate dietary fat and
it should be used as an integral form of kilocalories in the diet

In cases of steatorrhoea (stool fat > 6g in 24hrs),

a diet restricted in dietary fat
but supplemented with medium-chain triglycerides (MCT) should be
considered

Why MCT??
5) Micronutrients
sodium restriction is only needed in cases of fluid retention (ascites
and edema)

a multivitamin to be taken daily

thiamin should be supplemented in alcoholic disease

Nutrient relationships in hepatic failure and hepatic encephalopathy

1) Increased sodium and fluid :

fluid retention

2) Decreased protein:
Swollen belly (ascites) from decreased albumin production

3) Decreased protein and fat with malabsorption:

somnolence, euphoria, asterixis, coma
6) Laboratory assessment
liver test:
aspartate aminotransferase (AST or serum glutamic oxaloacetic
transaminase (SGOT) )
Alanine aminotransferase (ALT or serum glutamic pyruvic
transaminase (SGPT))
Bilirubin
Prothrombin time (PT)
alkaline phosphatase
Gamma glutamyl-transpeptidase (GGT)
Serum cholesterol level
 Treatment
1) Oral Diet
for patients with fluid retention a 2g sodium diet should be
implemented

Fluid restriction should not be implemented unless serum sodium is <

120mmol/L

standard protein food sources and polymeric liquid formulas are

effective and well tolerated .
Food diaries and prospective calorie counts should be implemented to
ensure the patient is consuming their nutritional requirement
frequent meals should be encouraged
a night time snack is especially important for minimizing the
consumption of muscle tissue and fat stores during the non-prandial
state.
2) Branched-chain amino acids (BCAA)
The derangement in the balance of amino acids, specifically
imbalances in the ratio of plasma BCAA (valine, leucine, isoleucine) to
aromatic amino acids (AAA) (tyrosine, phenylalanine, tryptophan).
Vegetable Protein
- A higher fiber intake (which accelerates GI transit time
- a reduction in pH of the intestinal lumen to reduce the fermentation
of bacteria.
- a higher energy-to-nitrogen ratio
- diets > 50g : poorly tolerated (bloating, early satiety, flatulence)
2) Hepatitis:

Encourage small frequent meals

Educate patient about how to increase calorie, protein, and vitamin

intakes.
Ensure patient abstains from use of alcohol and drugs that are
hepatotoxic

Teach safe personal hygiene in regard to hand washing and use of

disinfectants especially when travelling overseas

Discuss other principles of food safety

3) Hepatic cirrhosis:

Identify if breakfast or another meal is best tolerated. Some pt sleep

late with a sleep reversal pattern.

Discuss use of nutrient dense foods and higher intakes of vegetable and
dairy sources of protein if intolerant to meat
Large meals increase portal pressure, therefore recommend to have
small frequent meals

Avoid skipping meals. Discuss proper menu planning

Avoid high dose of vitamin A and D, which may be toxic to liver

4) Hepatic failure, encephalopathy and coma
milk and eggs tend to produce less ammonia than meats or poultry.

discuss the importance of refraining the use of alcoholic beverages

To set meal timing.

Large meals increase portal pressure, therefore recommend to have

small frequent meals

Avoid skipping meals. Discuss proper menu planning

Avoid high dose of vitamin A and D, which may be toxic to liver

 Find out extra info:
1) Stages of alcoholism related effects (4 stages)
2) stages of hepatic encephalopathy
3) Signs of impending hepatic coma
4) herbs / supplements (milk thistle?? Probiotics for hepatic
encephalopathy??)
The diseases of gallbladder
Risk factors for gallbladder disease
Age : advanced age (>65yrs old)
Diet : western diet with high-energy, high fat, high
refined CHO, low fiber
Enzyme defects : such as sickle cell anemia and genetic
alterations
Gender : Female
Hormonal Imbalance : such as in pregnancy or DM
Medication : estrogens, insulin, oral contraceptives,
cholestyramine
Obesity : especially with highest BMI
Weight loss : rapid weight loss, fasting or crash dieting
1) Cholelithiasis
Means presence of the gallstones

Gallstones form if the gallbladder:

Does not Contract completely or
Does not Often enough empty bile

This can occur after eating too little or after periods of starvation

Preventive measures:
a controlled weight loss rate,
reduction of the length of overnight fast, maintenance of a small amount of fat in
the diet,
Reduce high intake of refine sugars & SFA
Eating nuts, vegetable protein, beans & soy may b preventive
more physical active
 Symptoms of cholelithiasis:

steady pain in the upper abdomen every 30 minutes to several hours

Pain in the back between the shoulder blades
Nausea
Vomiting
Abdominal bloating
Intolerance of fatty foods
Belching
indigestion
2) Cholecystitis
Inflammation of the gallbladder that is caused by gallstones

Surgery is needed to remove gallstones

Extracorporeal shock wave lithotripsy (ESWL) is effective in the
treatment of symptomatic cholecystolithiasis and preserves the organ
in pt

Laparoscopic cholecystectomy :
safe
reduce length of stay in hospital,
Can be performed in morbidly obese patients
Reduce the rate of preterm deliveries in pregnant women
3) Gallbladder cancer
Not common but usually due to late diagnosis, unsatisfactory
treatment and poor prognosis

More to women with gallstones for many years

Jaundice, pain above stomach, lumps in the abdomen and fever

should be addressed in pts who have gallstones
 Nutrition therapy for gallbladder diseases
Provide a calorie-controlled, balanced diet
For cholecystitis :
use low fat diet
Les spicy and gas forming vegetables, which cause distention, increased
peristalsis and irritation.
For cholelithiasis :
Diet high in fiber and when needed low in calories
Fat soluble vitamins may be needed.
Increase dietary intake of source of vitamin C such as citrus fruits and
juices. Use supplement forms if needed.
For gallbladder cancer:
Consume sufficient of selenium, zinc, vitamin E
 Dietary counseling for gallbladder diseases
After a cholecystectomy,
fat intake should be limited for several months to allow the liver to
compensate for the gallbladders absence.
Fats should be introduced gradually; excessive amounts of fat at one
meal should be avoided.
If diarrhea persists after surgery, try using ant diarrheal medications,
such as loperamide (Imodium) and high fiber diet for more bulk.

Avoid fasting and rapid weight loss schemes.

People who have had their gallbladders removed should have their
cholesterol levels checked periodically, as should every adult.
 To prevent new gallstones from forming,
maintain a healthy weight.

Dietary changes that lower plasma insulin levels,

such as a change in dietary fats and
Include a high fibre diet

Regular exercise has a beneficial effect on hyperinsulinemia, which is

frequently associated with gallbladder disease.
Pancreatic disorders
Pancreas
1) Acute Pancreatitis (AP)
The pancreas becomes inflamed and damaged by its own digestive
chemicals.Swelling and death of tissue of the pancreas can result.

The exocrine pancreas secretes proteolytic, lipolytic, and amylolytic

enzymes for nutrients digestion in the intestine.

Inflammation with edema, fat necrosis (death of body tissue) and

cellular exudate occur. (Exudate is fluid, such as pus or clear fluid,
that leaks out of blood vessels into nearby tissues).
 Enzymes become activated in the pancreas instead of the duodenum.

AP is common in men between the ages of 35 45 years

Causes :
primarily from alcohol abuse
secondarily from gallstones (cholelithiasis)
End-stage-renal disease
Lupus
Biliary tract disease
Abdominal trauma Its difficult to
Certain dyslipidemia (esp TG > 1000mg/dL) differentiate between
pancreatitis and acute
AIDS cholecystitis but need to
diagnose correctly due to
Pancreatic cancer different management
 Pancreas Tests

Physical Examination
CT scan using dye
MRI
(ERCP):Endoscopic retrograde cholangiopancreatography
Using a camera on a flexible tube advanced from the mouth to the
intestine, a doctor can access the area of the pancreas head. Tiny
surgical tools can be used to diagnose and treat some pancreas
conditions.
 PANCREAS TESTS
Pancreas biopsy: Either using a needle through the skin or a
surgical procedure, a small piece of pancreas tissue is removed
to look for cancer or other conditions.

Amylase and lipase: Blood tests showing elevated levels of

these pancreatic enzymes can suggest pancreatitis.
Nutrition therapy for acute pancreatitis
Controlling pain through medications and rest.
Restoring a normal fluid and electrolyte balance
Treating chemical dependency, if alcohol use is the cause of
pancreatitis.
Removing gallstones that can often be associated with
pancreatitis.
Draining fluid from pancreatic ducts with minimally invasive
surgery, including stent procedures.
Nutrition therapy for AP
Enteral products containing MCT are useful for tube feeding, esp
when there is steatorrhea. Omega-3 fatty acids are helpful.Transition
to jejunostomy .

Progress to a diet given in 6 daily feedings used with pancreatic

enzymes for all meals and snacks.

Alcohol beverages and nicotine are prohibited. Limit gastric

stimulants, such as peppermint and black pepper, if not tolerated.
Steatorrhoea reduce fat in the diet
 Diet should include adequate intake of vitamin C, B-complex vitamins
and folic acid for water soluble needs.

Antioxidants including selenium may be needed. Adequate calcium,

magnesium and zinc supplement should also be provided.
Discuss omission of alcohol from typical diet

Discuss tips of handling nausea and vomiting

coffee, tea and gas-forming foods may need to be omitted.

Advise on oral : low fat, high protein and high calories

 Enzyme therapy for mal absorption helps restore normal digestion and
reduces the amount of fat in the feces, leading to weight gain and
improved well-being.

Dietary changes such as eating smaller meals and limiting fats help
reduce the need for digestive enzymes.

Treatment of diabetes, if that develops

References:
1. Diseases of the Liver and Biliary System
Sherlock, Shiela Dooley, James
Pages: 724
Publisher: Wiley
Location: Chichester, GBR
Date Published: 2008
Language: en
LC Call Number: RC845 -- .S52 2002eb
eISBN: 9780470986813
pISBN: 9780632055821
Dewey Decimal Number:
OCLC Number: 646755480
Subjects: Liver -- Diseases. Biliary tract -- Diseases.
2) Liver Diseases : An Essential Guide for Nurses Andhealth Care Professionals
Sargent, Suzanne
Pages: 360
Publisher: Wiley-Blackwell
Location: Hoboken, NJ, USA
Date Published: 11/2009
Language: en
LC Call Number: RC845 -- .L585 2009eb
eISBN: 9781444322699
pISBN: 9781405163064
Dewey Decimal Number: 616.3/620231
OCLC Number: 646872962

3) Advancing Dietetics and Clinical Nutrition (2010)

Anne Payne & Helen Barker
Churchill Livingstone Elsevier
 References
Garcia-Tsao G. Cirrhosis and its sequelae. In: Goldman L, Ausiello D,
eds. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier;
2011:chap 156.
Nutrition and Diagnosis related Care-Sylvia Escott Stump,Sixth
Edition
Thank you