Case StudyMr. D B: Cirrhosis and Ascites

Erica Bennett

I. Primary Disease Process: Cirrhosis

Cirrhosis of the liver is the final stage of chronic hepatic diseases, characterized by fibrosis

(permanent scarring) and loss of function of the hepatic tissue. As the satellite cells of the liver

respond to chronic injury and inflammation, they transform into fibroblasts and begin producing

collagen, which stiffens the organ and cuts off much of the hepatic circulation, leading to portal

hypertension.8

In the year 2010, cirrhosis was the eighth leading cause of death in the United States, leading

to 49,500 deaths nationwide.16 The main etiologies of cirrhosis are chronic viral hepatitis (HBV

and HBC), alcoholism, and nonalcoholic fatty liver disease. 8

Cirrhosis can be diagnosed most definitively by liver biopsy, but can also be detected by

MRI, CT scan, and ultrasonography, especially in patients who are symptomatic. Symptoms are

not always apparent in compensated cirrhosis, where the liver is damaged but still able to

perform its functions, or may be so nonspecific that it is hard to ascertain the cause. Some more

specific symptoms of later-stage compensated cirrhosis include muscle wasting, hardened liver,

spider angiomas, esophageal varices, and palmar erythema, or redness of the palm.6 Symptoms

of decompensated cirrhosis include ascites, edema, hematemesis (suggestive of variceal

bleeding), osteopenia and osteoporosis, diabetes, jaundice, vitamin and mineral deficiencies,

hepatocellular carcinoma (HCC), and hepatic encephalopathy. 1

Cirrhosis can be classified into one of four stages upon diagnosis by the presence of certain

complications. Stages one and two of cirrhosis are considered compensated, with stage one

characterized by presence of cirrhosis without esophageal varices or ascites, and stage two

characterized by presence of esophageal varies without further complication. Stages three and

four are considered decompensated cirrhosis; these are the stages in which cirrhosis is generally

diagnosed, as the symptoms become more distinctive. Stage three cirrhosis is characterized by

the presence of ascites, and stage four cirrhosis by the presence of gastrointestinal bleeding.8

Ascites is the most common complication of cirrhosis, caused by extreme vasodilation of the

arteries in the abdomen. Scarring of the liver leads to shutting off of some hepatic blood vessels,

resulting in portal hypertension and formation of collateral veins to compensate for the loss of

others. Blood that builds up in the decompensated liver begins to be shunted to the systemic

circulation and nitric oxide is produced by nearby cells to help dilate blood vessels in the area,

both mechanisms intended to help relieve portal hypertension. The vasodilation caused by nitric

oxide becomes extreme as cirrhosis worsens and portal hypertension increases, affecting not just

the portal vessels but also the neighboring splanchnic arteries. Arterial pressure in these vessels

falls dramatically, and mechanisms such as sodium and fluid retention are activated in an effort

to maintain blood pressure. Retained fluid is eventually pushed into the abdominal cavity, where

it can accumulate in massive volumes.4

Another complication related to portal hypertension is splenomegaly. The increased blood

pressure in the portal vein, to which blood from the spleen flows, causes increased blood

pressure in the spleen and enlargement of the spleen. This back-up of blood can lead to a

decrease in the number of red and white blood cells, as well as platelets, in the systemic

circulation. The bone marrow blood cell production mechanism may also be suppressed by

alcohol intake and hepatitis viruses, which may contribute to low peripheral blood cell count in

many patients with cirrhosis.6

Important laboratory values to watch in cirrhosis patients include the liver function tests,

such as bilirubin, prothrombin time, albumin, and ALT/AST; electrolytes and glucose; hepatitis

marker like BUN and glucose; blood counts and clotting factors; protein levels like albumin,

prealbumin, and transferrin (as disease indicators, not indicators of protein status); and vitamin

and mineral levels. The most validated test combination in the diagnosis and staging of cirrhosis

is a high ALT/AST ratio, low albumin, extended prothrombin time, and thrombocytopenia.8 The

AST/ALT ratio was studied in patients with and without cirrhosis by Nyblom et al, whose

experimentally determined normal range of 0.5-1.0 is used in this research paper.10 Electrolyte

labs such as sodium are important in order to diagnose hyponatremia. Glucose monitoring is

important to catch and treat hypoglycemia and hyperglycemia. Vitamin and mineral levels are

also vital to check to ensure that the patient’s micronutrients needs are being met.1 When

cirrhosis patients with ascites undergo paracentesis, a procedure in which a needle is inserted

into the abdominal cavity and used to draw out the trapped fluid, the collected fluid should be

analyzed in the lab for presence of infection and any other remarkable fluid abnormalities.4

Another important lab test in cirrhosis evaluation is hepatitis B and C testing, since both are

potential causes of cirrhosis. Serum creatinine and urine protein are other important lab values to

monitor, as abnormalities could point to hepatorenal syndrome. Regular screening for

hepatocellular carcinoma is also important for cirrhosis patients.8

Treating the cirrhosis patient based on the underlying etiology of their disease is important in

ensuring the best outcome. For example, treatment of hepatitis B and C when they are the cause,

and drinking cessation when alcoholism is the cause, greatly improve complications like ascites,

and can improve therapeutic outcomes.7 The long-term treatment for cirrhosis is generally liver

transplantation when patients reach decompensated cirrhosis. Patients with ascites tend to have

poor prognosis without transplant, so they are often given priority on liver transplant lists.4

Patients who are diagnosed with compensated cirrhosis can live up to 20 years without

experiencing symptoms; however, following diagnosis with decompensated cirrhosis, patients

generally live less than two years.8

Nutrition therapy for cirrhosis patients includes meeting basal energy and nutrient needs and

then providing the extra nutrients needed in the hypermetabolic state. Energy needs may be

increased, with estimated needs ranging from 25-40 kilocalories per kilogram dry body weight

per day,13 or basal energy expenditure, calculated using dry weight, plus twenty percent.1 Excess

calorie intake, however, should be avoided to prevent fat accumulation in the liver.5 Protein

needs may also be increased, estimated at 0.8-1.5 grams per kilogram dry body weight per day,

due to disease-induced protein loss and muscle protein breakdown. 1, 13 Patients with liver disease

were at one time encouraged to restrict protein, but it is now believed that it is more important to

prevent muscle catabolism than to rest the liver. Patients with hepatic encephalopathy should

take in normalized amounts of protein with each meal to meet protein needs.5 Branched chain

amino acids are encouraged, since they are processed by the muscles and theoretically do not

significantly add to the liver’s workload. They show promise in improving muscle mass, but

have not yet been proven to improve hepatic encephalopathy.11

Carbohydrate intake and blood glucose should be monitored, as there is potential for both

hypoglycemia and hyperglycemia in patients with cirrhosis due to decreased liver glycogen

stores, decreased gluconeogenesis, and insulin resistance.13 If insulin resistance worsens to the

point of a diabetes mellitus diagnosis, the patient should be managed with a diabetic dietary plan

and diabetic medications such as metformin. Fat intake should also be modified and limited to

less than 30 percent of total calories if the patient experiences steatorrhea due to bile acid

deficiency. Total fat intake should be decreased and intake of medium-chain triglycerides should

be considered to maximize absorption.13

Sodium intake should be restricted if fluid retention is evident, as in ascites, to 2000 mg per

day. However, according to Nusrat, restrictions under two grams per day “are not recommended

because they are less palatable and create the potential to reduce food intake and worsen the co-

existing malnutrition.” 9 Research in this patient population has found that mortality rate is

significantly higher in patients with low serum sodium concentrations. In the same study, low

serum sodium was also associated with presence of ascites, but not associated with other

common complications such as hepatic encephalopathy.15 Fluid intake goals should generally be

30-40 ml per kilogram per day, but for patients with serum sodium levels under 128 mEq per

liter, fluid intake should be restricted to 1200-1500 ml per day, and for patients with serum

sodium below 125 mEq per liter, restricted to 1000-1200 ml per day.1

Lactulose, a nonabsorbable (prebiotic) disaccharide which traps and prevents absorption of

ammonia in the colon, has been a widely accepted therapy for decades. However, it is being

reexamined, as some recent studies have shown no more improvement in patients on Lactulose

as opposed to a placebo.11 Other new therapies are emerging, however. Probiotic therapy shows

some potential in decreasing total ammonia in the portal circulation, reducing inflammation in

the liver, and decreasing toxin uptake in the gastrointestinal tract. Several studies have been done

to demonstrate its efficacy, one including fructo-oligosaccharides (prebiotics) along with the

probiotic Bifidobacterium and one with just probiotics. More studies need to be done, but

probiotics plus fructo-oligosaccharides are a potential future treatment recommendation for

cirrhosis patients in preventing and improving hepatic encephalopathy.5, 11

According to the Nutrition Care Manual, “The vast majority of patients with cirrhosis will be

at risk for nutritional compromise because of their liver disease and its symptoms.” 1 Nutrition

status is often moderate or severely compromised in patients with decompensated cirrhosis due

to hypermetabolism, decreased oral intake, decreased nutrient absorption and increased nutrient

losses, and decreased nutrient synthesis, secretion, and storage capacity.13 Weight loss, especially

loss of lean body mass even as fluid weight is accumulated, is common and often severe.

Malnutrition is a common sequela of cirrhosis, especially decompensated cirrhosis such as

cirrhosis with ascites. According to Johnson et al, “those with tense ascites generally have the

lowest protein energy intake and most compromised status.” 5 Liver disease can cause

malabsorption, dysmetabolism, and inadequate storage of vitamins and minerals. Liver disease

patients tend to have inadequate oral intake due to anorexia, abdominal distention and pain,

dysgeusia, nausea and vomiting, alcohol intake, encephalopathy, decreased gastric emptying, a

limited and less appetizing diet due to prescribed dietary restrictions, and increases in leptin

levels causing early satiety. Cirrhosis is also associated with low socioeconomic status and

alcoholism, both of which can lead to decreased dietary intake and decreased nutritional value of

intake,5 and, according to Singal et al, “the prevalence and severity of malnutrition are also high,

with increasing amounts of alcohol use, lower socioeconomic status, and lack if employment.” 13

It is therefore likely that many patients are already malnourished who become cirrhotic, and then

the cirrhosis further worsens their malnutrition, leading to worsened outcomes.

Deficiencies of the fat-soluble vitamins A, D, E, and K are very common, which can lead to

symptoms such as night blindness and scaly skin, osteopenic bone disease, neuropathy, and

increased bleeding, respectively. They are important to supplement in many liver disease

patients. Vitamin A deficiency also “promotes fibrosis and collagen deposition” in the liver,

worsening cirrhosis.13 Vitamin E is thought to play an interesting role in cirrhosis patients,

possibly reducing liver oxidative stress and thus discouraging inflammation. Deficiency may

lead to hemolytic anemia and increased red blood cell lysis.5 Iron deficiency can also lead to

anemia, but iron should not be supplemented unleash the patient is deficient, as excess can be

hepatotoxic. Zinc, another common deficiency, can lead to nutritional issues, such as anorexia,

ageusia, and altered protein metabolism.5 Alcoholic liver disease can cause deficiency of the

water-soluble vitamins as well, especially folate, niacin, pyridoxine, cyanocobalamin, thiamine,

and Vitamin C.13

II. General Patient Information

Mr. D. B. is a 51 year old Caucasian man who was living alone in a motel in St. Petersburg

prior to admission to the Bay Pines VA. He was born in Michigan, and is a high school graduate.

He served in the army from 1981-1984, and subsequently worked as a carpenter. 10 years ago,

he suffered a traumatic brain injury during a fight, after which he began to experience memory

problems and suffer from a mood disorder. He has been unemployed for eight years and receives

$997 monthly from Social Security Disability Insurance. Mr. B. has been married and divorced

three times, and has one 13 year old daughter; however, the girl’s aunt has custody, and he does

not get to see her often. In his motel, he has a mini-fridge and a microwave, which is his primary

cooking method. Mr. B. has been dependent on alcohol at least since 2007. He has been treated

for substance abuse several times, and has sobered up at the hospital only to go home and start

drinking again.

This patient was selected for an in depth case study because of his complex disease state

including both alcohol use and viral hepatitis in the etiology of his cirrhosis, and the vital

importance of nutrition therapy in giving him the best possible outcome. He was nutritionally

compromised upon admission due to his disease and its complications and, likely, his alcohol

intake, which may be greater than reported. Nutrition therapy was vital for him, to assist in

decreasing further fluid accumulation, to replete his body protein stores, and to prevent and

correct vitamin and mineral deficiencies.

III. Present Admission and Status

Mr. B. presented at the Bay Pines VA Emergency Room on August 17, 2014 with tense

ascites for the second time. He was diagnosed with cirrhosis in July 2014. His medical history

also includes GERD, a cholecystectomy, hepatitis C, alcohol dependence, tobacco use disorder

(smokes a pack a day), mood disorder, anxiety disorder, depression, and a subdural hematoma.

In July 2014, Mr. B. was also first diagnosed with ascites, and underwent his first paracentesis.

He was prescribed lactulose to manage his hyperammonemia, but has been noncompliant with

the medication because of fear of not making it to the bathroom in time. The bathroom in his

hotel is down the hall, making it difficult for him to get there quickly enough. The admitting

physician, Dr. Maysa Ahmad, prescribed a dose of furosemide and spironolactone that evening

(August 17) and recommended paracentesis.

Mr. B. was transferred to ward 5B once he was stabilized. According to his attending

physician, Dr. Ira Azneer, Mr. B. complained of nausea, vomiting, shortness of breath, and

abdominal pain persisting for the past four days. Along with the ascites, he also had 2++ edema

in his extremities. Mr. B.’s MRSA screening test came back positive, so he was placed in an

infection control setting. Dr. Azneer scheduled the paracentesis for August 18. The procedure

removed seven liters (approximately 15 pounds) of fluid. He was continued on the diuretic

regimen of spironolactone and furosemide to flush out excess fluid accumulation in the rest of

his body.

Dr. Azneer also prescribed Mr. B. a potassium chloride supplement, a magnesium sulfate

supplement, a thiamine supplement, and a multivitamin/mineral supplement. Ondansetron was

administered multiple times during his hospital stay for nausea and vomiting. Mr. B. was already

on lactulose, a laxative designed to help him clear ammonia from his system more effectively

and prevent hepatic encephalopathy, omeprazole, a proton-pump inhibitor for his GERD, and

trazodone and paroxetine, antidepressants. The medications and their nutrition-related effects are

shown in more detail in the table below.

Medication Type/Use Nutrition-Related EffectsSpironolactone Potassium-sparing diuretic –

treats fluid retention and edema

Hyperkalemia (avoid excessive potassium intake), possible hyponatremia. Can cause nausea, vomiting, and diarrhea.

Furosemide Loop diuretic – treats fluid retention and edema

Hyponatremia, hypokalemia, hypomagnesemia. Can also cause decreased serum chloride and calcium, and increased serum glucose. Need to increase the potassium and magnesium in the diet, and decrease caloric intake. Avoid natural licorice.

Lactulose Laxative – to treat hyperammonemia

High fiber diet with 1500-2000 mL liquid. Drug increases absorption of calcium and magnesium; supplementation with these is generally not recommended.

Omeprazole Proton pump inhibitor – anti-GERD

Decreases gastric acid secretion, increases gastric pH. Avoid alcohol. Can cause diarrhea. My decrease absorption of iron, vitamin B12, and calcium. Calcium citrate supplement recommended. Avoid gingko and St. John’s Wort.

Ondansetron Anti-emetic, anti-nauseant Can cause abdominal pain, constipation, and diarrhea.

Potassium Chloride Electrolyte, mineral supplement

Do not take with salt substitutes.

Magnesium Sulfate Mineral supplement, antacid, laxative.

May cause chalky taste and diarrhea. Do not take with high fiber, oxalate, or phytate food.

Thiamine B Complex Vitamin – prevent Wernicke/Korsakoff syndrome due to chronic alcohol abuse

Alcohol inhibits absorption.

Multivitamin/mineral Supplement – contains vitamin A, D, E, folic acid, niacin, pantothenic acid, riboflavin,Iron, calcium, magnesium, manganese,

Possible vitamin/mineral toxicities

After paracentesis, Mr. B.’s peritoneal fluid was assessed in the laboratory for bacteria and

white blood cells. Bacteria were not found, indicating that no infection of the peritoneal cavity

was present. White blood cells were found in normal amounts. The most important lab values in

monitoring cirrhosis and ascites are reported in the table below.6, 12

Normal values

August 17 August 19 August 20 August 21

Glucose 74-118 mg/dL 91 105 92 94Sodium 136-144

mEq/L133 (low) 136 136 137

Potassium 3.6-5.1 mEq/L 3.8 3.7 (low) 3.9 4.0Magnesium 1.8-2.4 mEq/L 1.7 (low) 1.8 1.8Calcium 8.9-10.3 8.2 (low) 7.7 (low) 7.8 (low) 7.8 (low)Prothrombin time

9.6-12.5 sec 17 (high) 19.6 (high) 18.6 (high) 18.9 (high)

BUN 8-20 mg/dL 6 (low) 7 (low) 4 (low) 7 (low)Albumin 3.5-4.8 g/dL 2 (low) 1.5 (low)Ammonia 9-33 umol/L 16Bilirubin 0.2-1.3 mg/dL 3.6 (high) 2.3 (high)AST/ALT ratio 0.5-1.1 2.84 (high) 2.63 (high)RBC 4.23-5.75

M/uL3.67 (low) 3.09 (low) 3.23 (low) 3.24 (low)

Hemoglobin 12.8-17 g/dL 12.7 (low) 10.6 (low) 11.2 (low) 11.1 (low)WBC 4.0-10.6 5.3 3.3 (low) 3.3 (low) 3.9 (low)Platelet 160-410 K/uL 98 (low) 57 (low) 65 (low) 72 (low)

During this hospital admission, Mr. B. had a consult with the Paracentesis Team on August

18, in which they compiled his labs and determined that he was eligible for the therapeutic and

diagnostic paracentesis procedure. He also had a consult with the Palliative Care Team to discuss

his quality of life and goals on August 18. Mr. B. expressed that he was not ready for hospice,

but wanted to be discharged to a skilled nursing facility where he could be rehabilitated to return

to living on his own. This request was granted upon discharge on August 21. He told the

Palliative Care consultant that he was going to stop drinking, but on August 20, when a consult

was sent for Outpatient Substance Abuse, he declined to complete their assessment and left with

a card with their contact information.

IV. Medical Nutrition Therapy

Though Mr. B. claims he has adequate access to healthy foods, financial troubles are evident,

as he lives in a motel and is unemployed. Mr. B.’s usual diet consists of ramen noodles and beef

stew from Dollar General, which he says he likes especially because it has carrots. He reports

that one can of soup and one package of noodles, mixed and cooked in the microwave, are

enough to feed him two to three days. He has a history of alcohol abuse; prior to his admission in

July, he typically drank a quarter of a gallon of vodka daily. After his hospitalization in July, he

reports that he decreased his alcohol consumption and now only drinks two to three four-packs

of beer a week, and claims that his drinking is mostly social while watching football with a

friend. He expressed intention to stop drinking, but consistently turned down counseling from the

substance abuse treatment program. He told the physician that he drinks to dull his abdominal

pain.

Mr. B. is 5’7” tall, and reports he usually weighs about 180 pounds, though he feels best

at 160 pounds. His ideal body weight is 148 pounds. Weight is not an accurate reflection of

nutritional status for patients with fluid alteration like Mr. B., but a chart is included below with

available recent weight history.

1/13/2014

1/21/2014

1/29/2014

2/6/2014

2/14/2014

2/22/2014

3/2/2014

3/10/2014

3/18/2014

3/26/2014

4/3/2014

4/11/2014

4/19/2014

4/27/2014

5/5/2014

5/13/2014

5/21/2014

5/29/2014

6/6/2014

6/14/2014

6/22/2014

6/30/2014

7/8/2014

7/16/2014

7/24/2014

8/1/2014

8/9/2014

8/17/2014

140

145

150

155

160

165

170

175

180

185

157.2

181.9

172175.4

Mr. B.'s WeightWeight

He was not weighed upon admission, but his estimated weight including accumulated fluid

was approximately 190 pounds. He was weighed on August 21, several days after paracentesis

and several days into his diuretic regimen, when he weighed 175.4 pounds. Assuming that this

was his dry body weight, Mr. B.’s BMI was roughly 27.5, which puts him into the overweight

category. However, considering this patient’s somewhat wasted physical appearance, including

evidence of moderate lipoatrophy in his triceps and evidence of severe temporal muscle wasting,

it is possible that this category could be misleading. His fluid status was greatly improved post

paracentesis, and Dr. Azneer’s notes indicate no edema at that time, but he likely had not reached

his dry body weight. The Veteran had another paracentesis procedure on September 2, 2014, and

following this procedure and further diuresis, the Veteran weighed 167 pounds. Unfortunately,

Mr. B. was not seen by a dietitian during this brief subsequent visit to ascertain if further lean

body mass loss had occurred along with further fluid loss.

Mr. B. had a good appetite after paracentesis on August 18, and reported consuming 75

percent of his dinner that evening and 75 percent of his breakfast the next morning. However, he

experienced nausea on the morning of August 19, and his appetite declined, eating only 50

percent of lunch and dinner that day and none of his breakfast the morning of August 20. He was

prescribed Ondansetron on August 20 to improve consumption. He has some trouble chewing

and reports he sometimes swallows large pieces of food because he is missing his top teeth but

finding it easier to eat without his top dentures. He has no trouble swallowing, and has no

problems with vomiting, constipation or diarrhea (aside from when he takes his Lactulose).

Using the VA Nutrition Status Classification guide, his poor appetite (score of three), his

increased metabolic stress (score of three), evidence of severe fluid alterations and moderately

altered body composition (score of four), Mr. B.’s overall rating is 10, putting him in the

moderately nutritionally compromised category.

Mr. B.’s nutrition diagnosis is:

Inadequate energy intake related to loss of appetite as evidenced by muscle and fat

wasting and diet recall.

In order to improve Mr. B.’s declining nutrition status, it is essential to increase his protein

and energy intake. Mr. B.’s hospital diet during his stay in August was the two gram sodium diet

due to his extreme fluid retention. His overall diet prescription includes calorie, protein, fluid,

sodium, alcohol, and vitamin/mineral recommendations. His nutrient needs are best estimated by

using his ideal body weight (148 pounds), since even diuresed and post-paracentesis, he does not

seem to have reached his dry body weight. His energy needs can be estimated by using the Harris

Benedict equation for basal energy expenditure times a stress factor of 1.2.1 This can be

calculated to 1790 kilocalories per day for Mr. B. The Nutrition Care Manual recommends

protein intake of 0.8 to 1.2 grams per kilogram ideal body weight, or 54 to 81 grams per day for

this patient.1 It is important for him to consume sufficient energy and protein, but not to

overconsume protein, as this will add excess stress to the liver.

It is also important for Mr. B., as a patient with repeated fluid retention and ascites, to restrict

his sodium intake to less than 2 grams a day. With his current diet, this may require major

changes from the canned and processed foods. A fluid restriction is currently not necessary for

hyponatremia according to the Nutrition Care Manual recommendations, as his sodium levels

have been consistently 133 milliequivalents per liter or above;1 however, the physician did order

a fluid restriction of 1200 milliliters per day along with the two gram sodium restriction as his

discharge diet.

Mr. B. also requires increased vitamin and mineral intake. Supplementation is recommended

by the Nutrition Care Manual with water-soluble forms of vitamins A, D, and E, folate, thiamine,

calcium, and zinc, all of which are included in the multivitamin/mineral supplement he was

prescribed. The physician prescribed magnesium and potassium supplements, though these

supplements are actually contraindicated by his medication regimen (potassium supplement with

a potassium-sparing diuretic, though he is simultaneously taking a potassium-losing loop

diuretic, and magnesium supplementation while taking Lactulose).12 It is important to monitor

these labs closely to ensure that he does not retain too much of the supplements and become

hypermagnesemic or hyperkalemic. His lab data indicates anemia, marked by low red blood cell

count, white blood cell count, hemoglobin, hematocrit, and platelet count. This looks like

aplastic anemia caused by his hepatitis C, or low peripheral blood cell count due to possible

splenomegaly, but tests should be done to ensure that it is not caused by a micronutrient

deficiency.6 It also appears that his serum calcium is consistently low, and his diet recall is

significantly calcium and vitamin D-deficient, which could warrant increased intake as well as a

higher dose calcium and vitamin D supplement (both are contained in modest amounts in the

prescribed multivitamin/mineral) to prevent osteopenic bone disease. A DEXA bone scan would

be a better way to check his bone mass and get a better idea of what his body stores are like.

Due to his anorexia and early satiety, eating four to six meals a day will assist with

optimizing energy intake. Daily physical activity may help in increasing hunger and preventing

loss of lean body mass.1 As a final important nutritional recommendation, it is essential for the

Veteran to stop drinking, as his alcohol intake is not only worsening his liver status and

promoting inadequate nutritional intake, but also causing increased vitamin and mineral losses.13

The Veteran’s reported pre-admission dietary intake of approximately half a package of

ramen noodles, half a can of beef stew, and one and a half beers (on average) per day does not

adhere to his calorie, protein, sodium, alcohol, or vitamin and mineral needs and restrictions.

Short-term nutritional goals for Mr. B. to move towards a better nutrition status during his

hospital stay include:

1) Improve intake by offering protein-rich supplements and foods between meals.

2) Consume more than 75 percent of meals and supplements provided.

In order to accomplish these goals during this admission, Boost Plus was provided as a

nourishment, providing 360 kilocalories and 14 grams of protein per serving. Making these

snacks available between meals may help the Veteran increase his intake by providing more

calories and protein throughout the day, allowing him to eat as much as he can whenever he gets

hungry.

On August 19, the Veteran was provided with education on nutrition in liver disease. This

education included limiting salt intake, increasing protein intake to meet needs, eating smaller,

more frequent meals to optimize intake, eliminating or significantly reducing alcohol

consumption, including why it will actually make his disease and his pain worse, and compliance

with medications such as Lactulose, including why he was on the medication and how it would

help him long-term. The Veteran was provided with a handout that reinforced these nutrition

messages. Mr. B. did not appear to be ready to change; though he reported to the dietetic intern

that he had significantly reduced his alcohol consumption following his previous paracentesis, it

is not clear if this really has occurred. He was receptive to education, but expected compliance

upon discharge was uncertain.

Long-term nutritional goals for the Veteran after discharge include:

1) Reduce sodium intake by replacing canned and packaged foods with low-sodium

versions.

2) Eliminate alcohol from the diet.

Since it was determined that Mr. B. would be discharged to Bay Pointe Nursing, a skilled

nursing facility, they were informed of his two gram sodium, 1200 milliliter fluid diet. Mr. B.’s

nurse at Bay Pointe indicated that the Veteran has been compliant with the sodium restriction

since his food is provided; however, he has not been compliant with the fluid restriction, as he

has continued to drink alcohol daily. He had a third paracentesis on September 2, and a fourth on

September 19. He is clearly worsening, and continues to need nutritional intervention. Follow-

ups should be done at least each time he is admitted for paracentesis, with continued education

on alcohol’s contribution to his liver failure. He has significant barriers to disease management

and compliance, including his mood and cognitive disorders, socioeconomic status, and

dependence on alcohol as a painkiller. However, at a skilled nursing facility and with help from

the substance abuse treatment program (if he will participate), these barriers can be overcome.

Mr. B. should continue to be monitored for further muscle and fat wasting, fluid status (both

edema and ascites), adequate protein and energy intake, consumption of alcohol, vitamin and

mineral status indicators, and liver function labs.

V. Summary

According to Dr. Azneer, the attending physician, Mr. B.’s prognosis is grave. Based on the

Model for End-Stage Liver Disease (MELD),7 Dr. Azneer estimated he has approximately three

months to live. Though he is currently in a skilled nursing facility and wishes to be rehabilitated

so he can go back to living on his own, the serious nature of his disease will more likely

necessitate his admission to hospice. Sadly, his health and nutrition status did not improve during

his hospital admission. His nurse at Bay Pointe reported no problems with his appetite and

consumption of 100 percent of his meals on September 17, which is a big change in a positive

direction. With optimal nutritional intake, sodium and fluid restriction, vitamin and mineral

supplementation, and alcohol cessation, Mr. B.’s nutritional status could conceivably improve,

which could improve his short-term survival.2 However, real improvement in his status is

unlikely due to his severe disease state and unwillingness to stop drinking. It is possible that if

his pain were better controlled in general, he would be more likely to stop drinking, but from his

past history with alcohol, complete cessation seems, sadly, unlikely. The only real treatment for

cirrhosis that has advanced to Mr. B.’s state is liver transplant, a treatment they are unlikely to do

on someone with his poor nutritional status, due to increased mortality risk.2

In retrospect, Mr. B.’s cognitive impairments and alcoholism were certainly bigger barriers

to change than it seemed at the time of education. While Mr. B. was agreeable and responsive to

learning about his nutrition care plan, and it seemed that he was making positive change in his

life already (such as decreasing the amount of alcohol he drank), his true self-efficacy and

readiness to change was likely very low. His underlying issues have taken a long time to develop

and could take a lot of time and multidisciplinary effort, as well as his buy-in, to repair. Nutrition

counseling is designed to create buy-in and bring patients from Mr. B.’s precontemplation stage

of change to readiness for action. Mr. B. might have benefited from implementation of the

Health Belief Model, which recommends health education on a personalized, applicable way.

The model is designed to focus on disease prevention, but can be expanded to prevent worsening

of disease. The dimensions of the Health Belief Model are perceived susceptibility to a disease,

perceived severity of the disease, perceived benefits of engaging in healthy behavior, and cues to

action, or stimuli that promote the healthy behavior.14 In Mr. B.’s case, this would have involved

spending more time with Mr. B. explaining the disease process, why his actions (especially

drinking alcohol, consuming too much sodium, and not eating enough) were exacerbating his

health problems and how following his nutrition prescription would help alleviate disease

symptoms and prevent his cirrhosis from worsening as quickly. It would also have involved

addressing the barriers of alcoholism, severe pain, early satiety, and food insecurity, and

acknowledging how they would affect his ability to comply with the nutrition prescription, as

well as creating plans for how to overcome the barriers. The barrier of alcoholism likely requires

professional guidance, such as from SATP, to overcome, but the barrier of food insecurity was at

least temporarily overcome when he was admitted to the skilled nursing facility. Establishing

clear, achievable goals for overcoming barriers will help in building Mr. B.’s self-efficacy and

thus making the change sustainable. Finally, his cues to action, such as abdominal pain cuing

him to take pain medication and stay away from alcohol, rather than drinking to numb the pain.

Application of this counseling method, as well as incorporating motivational interviewing,

building self-efficacy, and using the teachback method to ensure comprehension and to promote

information retention, are important in working with patients like Mr. B. with significant health

concerns and significant barriers to overcome. No patient is a lost cause, and with

multidisciplinary support and compassionate care, Mr. B.’s quality of life can still be

significantly improved.

VI. APPENDIX

a. Nutrition assessment (CPRS)

b. Estimated nutrient needs

c. Handouts provided to patient

d. References

D. References

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