Vachon 1

Jennifer Vachon
Nutrition 580
16 December 2016
Case Study 6: Chronic Renal Disease
I. Understanding the Disease and Pathophysiology
1. The liver is an extremely complex organ that has a particularly important role in nutrition
metabolism. Identify three functions of the liver for each of the following:
(a) Carbohydrate metabolism
The liver forms and stores glycogen, a storage form of glucose carbohydrates. It also converts
galactose and fructose to glucose. In addition the liver can convert amino acid residues to
glucose via gluconeogenesis.
(b) Protein metabolism
The liver forms plasma proteins such as albumin. It also deaminates, transaminates, and
synthesizes non-essential amino acids. In addition the liver synthesizes and processes
lipoproteins.
(c) Lipid metabolism
The liver forms lipoproteins which are important for the transport of fats. It also oxidizes fatty
acids to Acetyl CoA for its use in the TCA cycle. In addition the liver can convert carbohydrate
and protein intermediates to fat via lipogenesis.
(d) Vitamin and mineral metabolism
The liver converts vitamin D to 25-hydroxycholecalciferol. It also stores iron as ferritin. In
addition the liver stores vitamins A, D, E, K, and B12.

2. The CT scan and live biopsy confirm the diagnosis of cirrhosis. What is cirrhosis?
Cirrhosis is an end stage of severe chronic liver disease resulting in hepatocyte destruction. The
inflammation associated with liver disease leads to the formation of fibrous scar tissue which
thickens the tissue and may cause blockages. Regenerative nodules form in a failed attempt to
regenerate the liver resulting in clusters of newly formed cells within the scar tissue.

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3. The most common cause of cirrhosis is alcohol ingestion. What are additional causes of
cirrhosis? What is the cause of this patients cirrhosis?
Cirrhosis can be caused by a chronic autoimmune disease like primary biliary cirrhosis which
slowly destroys the bile ducts. It may also be caused by idiopathic hemochromatosis, a genetic
disorder affecting the way in which the body handles iron. Viral hepatitis may also cause
cirrhosis. Cholestasis is biliary obstruction with a blockage in the biliary ducts resulting in the
accumulation of bile in the liver which can cause cirrhosis. Liver necrosis of undetermined
cause, obesity in the form of nonalcoholic steatohepatitis, and metabolic disorders like Wilsons
disease may also cause cirrhosis.
This patients cirrhosis is likely caused by chronic hepatitis C.

4. Explain the physiological changes that occur as a result of cirrhosis.

An obstruction in the bile duct prevents conjugated bilirubin from being excreted by the liver.
Conjugated bilirubin is released to body tissues. The increase in conjugated bilirubin causes dark
urine, pale stools, and jaundice. Jaundice is the yellowing of the skin particularly the whites of
the eyes.
Ascites can occur as a result of cirrhosis. This is the accumulation of fluid in the peritoneal
cavity. Since the liver is not functioning and the scar tissue has accumulated causing some
blockage, hepatic pressure may increase. Excessive fluids begin to leaker through the outer
surface of the liver directly into the abdominal cavity.
Prolonged elevation of hepatic blood pressure can develop into collateral circulation in which
blood is diverted into systemic veins. This can lead to varices which may rupture and cause
bleeding. Varices can occur in the esophagus or rectum and cause hemorrhaging. The collateral
circulation also causes toxic substance like ammonia to accumulate in the blood since the liver is
unable to extract ammonia from the blood and convert it to urea. When the ammonia is deposited
within brain tissues this condition is known as hepatic encephalopathy.
Night blindness, bone disorders, neuropathy, bleeding tendencies, glossitis, and cheilosis are
other changes which may occur as a result of decreased absorption, transport, and storage of the
fat soluble vitamins A, D, E, and K. Thiamin, folate, and vitamin B12 deficiencies may occur
particularly in cases of cirrhosis caused by alcohol intake. The liver cannot produce glucose via
gluconeogenesis so hypoglycemia may occur.

5. List the signs and symptoms of cirrhosis, and relate each of these to the physiological changes
discussed in question 4.

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Jaundice- obstructed bile duct causes conjugated bilirubin from being excreted by the liver
Ascites- excess fluid leaks into peritoneal cavity due to liver failure and increased hepatic
pressure
Malaise/lethargy- decreased kcal intake r/t anorexia
Bloating- increase of fluid in peritoneal cavity
Esophageal varies- prolonged elevated hepatic blood pressure leading to collateral circulation
Nausea/Vomiting- increase of toxic substances in the body, attempt to rid the body of them
Anorexia- painful ingestion due to varices
Dyspepsia- altered gut motility, abdominal pain, nausea, bloating
Bruising- decreased stores of Vitamin K and production of blood clotting factors, decreased
Vitamin C
Dermatitis- Vitamin a malabsorption
Glossitis- decreased vitamin B12, folate, niacin
Weight loss- decreased intake of food due to anorexia
Confusion- elevated serum ammonia levels
Night blindness- decreased vitamin a storage
Bone disorders- Vitamin D malabsorption
Hypoglycemia- decreased ability to produce glucose due to liver failure

6. After reading this patients history and physical, identify her signs and symptoms that are
consistent with the diagnosis.
Anorexia, fatigue, weakness, jaundice, nausea/vomiting, bruising of skin not related to injury,
weight loss of 10 pounds, enlarged esophageal veins, telangiectasias on chest

7. Hypoglycemia is a symptom that cirrhotic patients may experience. What is the physiological
basis for this? Is this a potential problem? Explain.

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The liver stores glucose in the form of glycogen. Insulin, epinephrine, growth hormone,
glucagon, and the thyroid hormone work to regulate the levels of glucose in the blood. When
dietary intake is decreased as it normally is with anorexia, hypoglycemia can ensue since the
body cannot mobilize this stores glucose from glycogen. The damaged liver is also not able to
respond to hyperinsulinemia by breaking down its glycogen and releasing glucose back into the
blood to regulate insulin and glucose levels. Hypoglycemia is a potential problem. Clinical
manifestations include cardiac palpitations, shakiness, and sweating. Hypoglycemia may also
progress to glucose intolerance or diabetes.

8. What are the current medical treatments for cirrhosis?

The current medications for the treatment of cirrhosis include lactulose, neomycin, Rifaximin,
and metronidazole. Lactulose is a nonabsorbable disaccharide which acidifies the gut, inhibits
ammonia production, and increases gut motility. Neomycin, metronidazole, and Rifaximin are
used to decrease the colonic concentration of ammonia-producing bacteria. Nutritional
deficiencies are corrected with vitamin and nutritional supplements paired with a high calories
and moderate to high protein diet. Protein needs increase to 1.5-2.0 g/kg body weight in the
absence of hepatic encephalopathy. Protein needs decrease to 0.6-1.0 g/kg body weight if signs
of hepatic encephalopathy appear. Carbohydrate needs are 30-35 kcal/kg dry weight in order to
replenish glycogen reserves. A 2 g sodium restriction helps decrease fluid retention and reduces
edema. The diet must be mechanically soft in order to prevent varice rupture.
9. What is hepatic encephalopathy? Identify the stages of encephalopathy and outline the major
theories regarding the etiology of this condition.
Hepatic encephalopathy is the condition of confusion, altered mental state, agitation, irritability,
sleep disturbances, disorientation, and possible coma as a result of liver failure. It occurs when
portal blood is diverted into general circulation via collateral vessels. Toxic substances such as
ammonia accumulate in the blood since the liver is not able to remove them. These substances
reach the brain causing mental alterations.
Stage I: Mild confusion, agitation, irritability, sleep disturbance, decreased attention
Stage II: Lethargy, disorientation, inappropriate behavior, drowsiness
Stage III: Somnolence but arousable, incomprehensible speech, confusion, aggression when
awake
Stage IV: Coma
The exact cause of hepatic encephalopathy is unknown. It is triggered by the accumulation of
toxins in the blood due to the livers inability to breakdown these toxins. It may also be triggered

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by a result of excessive nitrogen load from kidney disorder or excess of protein in the diet,
electrolyte or metabolic disturbance resulting from dehydration, drugs and medications which
suppress the immune system or central nervous system such as barbiturates, or infection like
pneumonia.
10. Protein-energy malnutrition is commonly associated with cirrhosis. What are the potential
causes of malnutrition in cirrhosis? Explain each cause.
Many patients with cirrhosis also experience anorexia, nausea, and vomiting. These
complications lead patients to decrease intake. The stomach is also not able to easily expand due
to ascites. This would further prevent consumption. Dyspepsia makes eating uncomfortable.
Portal hypertension impairs digestion and nutrient absorption. Fat-soluble vitamins in particular
are not absorbed since they are stored in the liver and there is a reduction in bile salt
concentrations. The liver is not able to synthesize proteins leading to further loss of body protein
and wasting.

II. Understanding the Nutrition Therapy

11. Outline the nutrition therapy for the following stages of cirrhosis with the rationale for each:
Diagnosis
Stable cirrhosis

Sodium
2 g/day

Potassium
Monitor
intake if
furosemide
or other
potassium
wasting
diuretic is
used

Protein
1.5-2.0 g/kg
body weight
to correct
malnutrition,
regenerate
functional
liver tissue,
replenish
plasma
protein
Cirrhosis
1-2 g
Monitor
0.6-1.0 g/kg
w/acute
restriction intake if
body weight
encephalopathy to reduce furosemide to minimize
edema
or other
nitrogenous
and fluid potassium waste and
retention wasting
toxic effects
diuretic is
used

Micronutrients Fluid
Multivitamin to No
correct
restriction
deficiencies, fat
soluble vitamins
in water
miscible form

Other Modifications
Moderate fat intake to
prevent steatohhrea, no
alcohol

Multivitamin to No
correct
restriction
deficiencies, fat
soluble vitamins
in water
miscible form

Probiotics may help treat

hepatic encephalopathy,
no alcohol, moderate fat
intake to prevent
steatohhrea

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Cirrhosis
w/ascites and
esophageal
varices

1g
restriction
to reduce
edema
and fluid
retention

Monitor
intake if
furosemide
or other
potassium
wasting
diuretic is
used

1.5-2.0 g/kg
body weight
to correct
malnutrition,
regenerate
functional
liver tissue,
replenish
plasma
protein

Multivitamin to
correct
deficiencies, fat
soluble vitamins
in water
miscible form,
liquid form of
vitamins to
prevent varice
rupture

Restrict
to 1.2-1.5
L to
reduce
edema
and fluid
retention

Mechanical soft diet to

avoid varice rupture, no
alcohol, moderate fat
intake to prevent
steatohhrea

III. Nutrition Assessment

12. Measurements used to assess nutritional status may be affected by the disease process and
not necessarily be reflective of nutritional status. Are there any components of nutrition
assessment that would be affected by cirrhosis? Explain.
Due to fluid accumulation in cirrhosis patients, body weight and BMI values would not be an
accurate indication of nutritional status. Patients may also experience muscle wasting and
subcutaneous fat loss which would alter skin fold thickness and arm muscle circumference.
Dietary intake may indicate a balanced intake but due to vomiting and malabsorption the amount
of nutrients available to the body would likely differ from the amount of nutrients consumed.
Serum albumin and creatinine in patients with cirrhosis are affected negatively by liver
dysfunction are less likely to be markers of nutritional status. Albumin, pre-albumin, transferrin,
and coagulation factors are synthesized in the liver. A deficiency in these values is likely to be
the result of liver dysfunction not malnutrition. Bioelectrical impedance analysis and dual energy
X-ray absorptiometry are used to estimate fat mass. However, the extracellular water in patients
with ascites is likely to alter these results.

A. Evaluation of Weight/Body Composition

13. Dr. Horowitz notes Ms. Wilcox has lost 10 lbs since her last exam. Assess and interpret Ms.
Wilcoxs weight.
Current weight: 125 lb
Usual weight: 135 lb
% UBW: (125/135)(100%)= 93%
IBW: 100 lb + (9 x 5 lb) = 145 lb

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Current %IBW: (125/145)(100%)= 86%
Usual %IBW: (135/145)(100%)= 93%
Current BMI: 18.5 kg/m2 low end of normal weight
Usual BMI: 19.9 kg/m2 Normal weight
Ms. Wilcoxs weight loss is likely due to her anorexia, nausea, vomiting, and malabsorption due
to cirrhosis. Nutrition therapy should focus on increasing energy consumption.

B. Calculation of Nutrient Requirements

14. Calculate the patients energy and protein needs.
30-35 kcal/kg dry weight (135 lb)
(30 kcal)(135lb/2.2)= 1841= 1800 kcals
(35 kcal)(135lb/2.2)=2148= 2100 kcals
Energy needs: 1800-2100 kcals
Protein due to hepatic encephalopathy: 0.6-1.0 g/kg (greater than 40g per day)
(0.6 g/kg)(135lb/2.2)=36.8=40 g
(1.0 g/kg)(135lb/2.2)=61.4=60 g
Protein needs: 40-60 g

15. What guidelines did you use and why?

For energy needs I used 30-35 kcal/kg dry weight because glucose is needed to replenish
glycogen reserves and to prevent further PEM. I used her usual weight to calculate these needs.
She does not have any edema but has lost 10 lbs. unintentionally in 6 months so a goal of
nutritional therapy should be to replenish these losses. I used 0.6-1.0 g/kg requirement for her
protein needs. She is exhibiting signs of hepatic encephalopathy with her inability to get enough
rest. In order to minimize nitrogenous wastes and their toxic effects, her protein needs are
decreased to 0.6-1.0 g/kg but should still total at least 40g to discourage further PEM.

C. Intake Domain

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16. Evaluate the patients usual nutritional intake.
Breakfast: calcium-fortified orange juice, a good choice considering it provides fruit, vitamin C,
and calcium
Lunch- soup and crackers with Diet Coke, CHO in the crackers, salt on the crackers and in the
soup could promote edema, diet Coke is high in sugar and has little nutritional value, crackers
could rupture varices
Dinner- Chinese or Italian carry-out, protein if she is consuming meat, potential CHO in noodles,
pastas, or breads, could be high in sodium which could promote edema
Ms. Wilcoxs anorexia has altered her dietary intake. She is not consuming enough fruits,
vegetables, water, or dairy. Increasing her dairy consumption would help to increase her protein
intake and prevent further PEM. Increasing the amount of food she is consuming once her
anorexia is addressed will help her to regain her lost weight. The crackers she is consuming for
lunch serve as a threat to rupturing her esophageal varices if they are not first softened in the
soup.

17. Her appetite and intake have been significantly reduced for the past several days. Describe
the factors that may have contributed to this change in her ability to eat.
Signs of cirrhosis include nausea, vomiting, dyspepsia, and anorexia. Anorexia is a general loss
of appetite which would naturally result in a decrease intake since she is not hungry. Nausea and
vomiting would make it unpleasant for Ms. Wilcox to continue eating. The dyspepsia would
make her feel uncomfortable after she eats and would likely reduce the number of times she is
eating. She is also experiencing fatigue which may decrease her ability to prepare or consume
food. Her enlarged esophageal veins likely due to varices could be limiting the amount of food
she is physically able to swallow in a given setting.

18. Why was a soft, 4-g Na, high-kcaloric diet ordered? Should there be any other modifications?
Ms. Wilcox has enlarged esophageal veins which indicate she may have esophageal varices. A
soft diet prevents these varices from rupturing and causing possible hemorrhage. The 4-g Na diet
was likely ordered to prevent potential edema. The patient is not currently exhibiting edema so a
restriction beyond 4 grams is not necessary at this disease stage. She needs to consume a highkcaloric diet in order to prevent further PEM and to help her to regain the 10 lbs. she has lost.
The diet order should also specify protein consumption so that nitrogenous wastes can be limited
while providing enough protein to prevent further PEM. A multivitamin/mineral supplement with
water soluble forms of vitamins a, d, e, and k would help to address the micronutrient

Vachon 9
deficiencies and malabsorption she is experiencing. I would restrict her sodium intake to 2g per
day since this is the recommendation for most cirrhosis patients. She should consume no more
than 30 percent of her total kcals from fat in order to decrease the risk of steatorrhea.

19. This patient takes multiple dietary supplements. Identify the possible rationale for each and
identify any that may pose a risk for someone with cirrhosis.
400 mg vitamin E: antioxidant, protects RBCs from hemolysis
May cause fatigue, weakness, nausea, bruising, bleeding in some people which Ms.
Wilcox is already experiencing and at risk of
600 mg calcium: aids in bone and teeth health, reduced pepsin activity by elevating gastric pH,
increases esophageal sphincter tone, strengthens gastric mucosal barrier
Side effects include nausea, vomiting, loss of appetite which she already is experiencing
400 IU vitamin D: increases absorption of calcium
Side effects include weakness, fatigue, sleepiness, loss of appetite, nausea, vomiting
which she already is experiencing
Multivitamin/mineral: bone growth, tissue health, retinal function
Fat soluble vitamins must be in water soluble form since fat absorption is hindered due to
liver failure
200 mg milk thistle (2x): main ingredient Silymarin is an anti-inflammatory and antioxidant,
may slightly improve liver function, may improve blood sugar control
May cause nausea, bloating, upset stomach which is a problem considering Ms. Wilcox is
already experiencing nausea which is decreasing her ability to eat
3 g chicory (3x): acts as a mild laxative, increases bile from gallbladder, decreases swelling,
source of beta-carotene, may increase appetite
May decrease desire to eat resulting in weight loss which is a problem considering Ms.
Wilcoxs weight loss and anorexia
500 mg ginger (2x): treats nausea/vomiting and loss of appetite, may reduce inflammation, may
decrease dyspepsia by speeding up how quickly food empties from the stomach

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May increase the risk of bleeding which is a problem considering cirrhosis patients are at
an increased risk of bleeding due to Vitamin K malabsorption and decrease in production
of proteins

D. Clinical Domain
20. Examine the patients chemistry values. Which labs support the diagnosis of cirrhosis?
Explain their connection to the diagnosis.
Ms. Wilcoxs bilirubin, albumin, aspartate amino transferase, alanine amino transferase,
triglyceride, phospholipid, and ammonia labs support the diagnosis of cirrhosis. Serum bilirubin
concentration increases when the liver is not able to excrete conjugated bilirubin. Albumin is a
good indicator of chronic liver disease due to its long half-life but its value is not specific to liver
disease. Aspartate amino transferase is a marker of functional liver cell injury. Increased levels
indicate damage to hepatocytes which causes the release of enzymes into general circulation.
Alanine amino transferase is another important marker of functional liver cell injury which is
limited primarily to the liver. Triglyceride and phospholipid serum levels are likely to be
increased because the liver is not able to breakdown fats. Serum ammonia would be increased
because of the decreased ability of the liver to breakdown this metabolic nitrogen waste.

21. Examine the patients hematology values. Which are abnormal, and why?
Ms. Wilcoxs albumin, transferrin, bilirubin, alt, ast, alk phos, and triglyceride levels are
abnormal. . Serum bilirubin concentration increases when the liver is not able to excrete
conjugated bilirubin. Albumin is a good indicator of chronic liver disease due to its long half-life
but its value is not specific to liver disease. Aspartate amino transferase is a marker of functional
liver cell injury. Increased levels indicate damage to hepatocytes which causes the release of
enzymes into general circulation. Alanine amino transferase is another important marker of
functional liver cell injury which is limited primarily to the liver. Triglyceride and phospholipid
serum levels are likely to be increased because the liver is not able to breakdown fats. Serum
ammonia would be increased because of the decreased ability of the liver to breakdown this
metabolic nitrogen waste. Additionally her RBC count was low due to chronic inflammatory
disease, hemorrhage, or nutritional deficiency. Low hemoglobin indicates a chronic disease or
cirrhosis. Low hematocrit is likely due to cirrhosis. Both of these decreased values contribute to
Ms. Wilcoxs feeling of fatigue. Her MCV is elevated because of her liver disease. Her
prothrombin time was increased due to biliary obstruction, prolonged cirrhosis, and vitamin K
deficiency.

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22. Does she have any physical symptoms consistent t with your findings?
She is fatigued which evidences her low albumin, hemoglobin, hematocrit, MCV, and RBC
count. Ms. Wilcoxs jaundice correlates with increased bilirubin. Her inability to rest is evidence
of potentially stage one hepatic encephalopathy which would be consistent with her high levels
ammonia.

23. What signs and/or symptoms would you monitor to determine further liver decompensation?
I would monitor Ms. Wilcoxs appetite, energy levels, weight, and cognitive status. I would
monitor her cognitive status and energy levels to ensure she did not develop further stages of
hepatic encephalopathy. Weight status would indicate a development of edema or ascites if
weight increased. A decrease in weight or appetite would indicate further PEM with potential
nutrient deficiencies. Ms. Wilcoxs degree of jaundice would be an indication of increased
bilirubin in the body tissue and further liver decompensation. The presence of steatorrhea could
also indicate further liver decompensation as fat began to accumulate in the stool.

24. Dr. Horowitz prescribes two medications to assist with the patients symptoms. What is the
rationale for these medications, and what are the pertinent nutritional implications of each?
Rationale for Rx
Spironolactone: Increases the
excretion of Na and water
from the body. Potassiumsparing diuretic
Propranolol: Beta blocker
used to treat hypertension

Nutritional Implications
Avoid excess K intake, low Na
diet recommended, avoid
alcohol
Low Na diet recommended,
avoid alcohol

25. If the patients condition worsens (e.g., acute varices, bleeding, progression to hepatic
encephalopathy), the following medications could be used. Describe each drug classification and
mechanism.
Drug
Vasopressin

Classification
Antidiuretic hormone

Lactulose

Laxative, synthetic sugar

Mechanism
Acts on 3 receptors which
initiate vasoconstriction, liver
gluconeogenesis, platelet
aggregation
Laxatives and ammoniadetoxifying actions allows

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Neomycin

Aminoglycosides antibiotic

Ferrous sulfate

Iron supplement

Bisacodyl

Stimulant laxative

Docusate

Stool softener

Diphenhydramine

Antihistamine

lactulose metabolites to draw

water into the bowel to soften
stools, draws ammonia out of
the body to treat hepatic
encephalopathy
Irreversibly binds to proteins
which interferes with reading
of mRNA so incorrect amino
acids are inserted into the
polypeptide leading to the
breakup of polysomes into
nonfunctional monosomes
Supplemental iron to prevent
and treat iron deficiency
anemia, promotes formation
of hemoglobin
Induces diarrhea which cleans
colon, promotes fluid
accumulation in colon and
small intestine
Prevents constipation, reduces
the surface tension of liquid
contents of the bowel,
promotes incorporation of
liquid into stool
Reduces the effects of
histamine in the body

E. Behavioral-Environmental Domain
26. What is the recommendation regarding alcohol intake when cirrhosis is caused by the
hepatitis C virus?
It is recommended that alcohol intake is eliminated when cirrhosis is caused by the hepatitis C
virus. This reduces the potential of causing further damage to the liver. Alcohol intake is
associated with fibrosis progression and the worsening of cirrhosis. Alcohol is also likely to
reduce the effectiveness of the Spironolactone and Propranolol medications which Ms. Wilcox is
prescribed.

27. Ms. Wilcox asks if she can use a salt substitute at home. What would you tell her?

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I would tell her that she is not able to use a salt substitute at home. Salt substitute is KCl which
contains potassium. Ms. Wilcox is taking Spironolactone which is a potassium-sparing diuretic.
This means she needs to limit the amount of potassium in her diet. I would suggest she use herbs
rather than salt or a salt substitute to add flavor to her foods.

28. What suggestions might you make to assist with compliance for the fluid restriction?
One of the most complicated aspects of adhering to a fluid restriction is to deal with thirst.
Avoiding foods which trigger thirst such as salty and spicy foods in addition to a general salt
reduction and the use of low sodium products may reduce thirst. Liquids should be spread
throughout the day and should be consumed cold. Some beverages could be made into ice so that
they last longer in the mouth and may help to alleviate thirst. Consuming hard candy or cold
produce may help to reduce thirst as well. It is important to stay cool. By recording her food and
fluid consumption she would be able to keep track of her fluid intake.

VI. Evaluation and Monitoring

29. When you see Ms. Wilcox 1 month later, her weight is now 140 lbs. She is wearing flip-flops
because she says her shoes do not fit. What condition is she most probably experiencing? How
could you confirm this?
It is likely Ms. Wilcox is experiencing edema, an increase of fluid accumulation in the peritoneal
cavity and extremities like the feet. It is likely her weight gain is due to the fluid excess and her
inability to fit into her shoes is due to swelling. This could be confirmed via albumin, electrolyte
levels, or urinalysis. Hypoalbuminemia and low electrolyte levels would be expected in patients
with edema. Plasma proteins no longer sustain osmotic pressure to counterbalance hydrostatic
pressure which results in further edema. A urinalysis would indicate low protein levels since the
liver is not able to form urea.

30. Her diet history is as follows:

Breakfast: 1 slice toast with 2 tbsp peanut butter, 1 c skim milk
Lunch: 2 oz potato chips, grilled cheese sandwich (1 oz American cheese with 2 slices of wholewheat bread; grilled with 1 tbsp margarine), 1 c skim milk
Supper: 8 barbeque chicken wings, French fries- 1 c, 2 c lemonade

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What changes might you make to her nutrition therapy? Identify foods that should be eliminated
and make suggestions for substitutions.
Since Ms. Wilcox has developed edema I would restrict her fluid intake to 1.2-1.5 L with a
sodium restriction of 1g per day in order to reduce water retention. The potato chips, American
cheese, and French fires contain a lot of sodium. These foods should be eliminated. She could
consume sauted spinach and carrots rather than chips to increase her vegetable intake.
Replacing American cheese with goat cheese decreases Ms. Wilcoxs sodium intake and
increases her protein intake since goat cheese contains less sodium and more protein. She could
eat roasted sweet potatoes instead of French fries to decrease sodium and increase vegetable
intake. The barbeque chicken wings likely contain high sodium. She could consume grilled
chicken instead. Unsalted butter would be a good replacement for the margarine.

31. Over the next 6 months, Terris cirrhosis worsens. She is evaluated and found to be a good
candidate for a liver transplant. She is placed on a transplant list and, 20 weeks later, receives a
transplant. After the liver transplant, what diet and nutritional recommendations will the patient
need before discharge? For the long term?

Kcal
Protein
Fat
CHO
Sodium
Fluid
Calcium
Vitamins

Immediate Posttransplant
(First 2 months)
30-35 kcals/kg
1.3-2 g/day
30% of calories
50-70% calories
Less than 2 grams
1.2-1.5 L
1200-1500 mg/day
Multivitamin/mineral
supplement

Long-Term Posttransplant
25 kcals/kg
1 g/kg depending on activity
level
<30% calories
50-70% calories
Less than 1.5 grams
1.2 L
1500 mg/day plus Vitamin D
Multivitamin/mineral
supplement