Wanyi Wang 0

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ALCOHOLIC LIVER DISEASE: CIRRHOSIS

Wanyi Wang, Dietetic Intern

Pepperdine University

05/20/18

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The liver is responsible for processing alcohol once it gets into the body system. Alcohol

is the leading cause of liver disease in Western nations. Alcohol consumed in small amounts is

relatively harmless, however; in excess, over time, can lead to serious liver problems. Alcoholic

liver disease (ALD) is one of the major cause of morbidity and mortality worldwide.

The clinical spectrum of ALD includes steatosis, fibrosis, alcoholic hepatitis (AH),

cirrhosis, and hepatocellular carcinoma (HCC) (figure 1) [1]. This case study will first discuss

about pathophysiology of ALD, and then focus on the study of cirrhosis in its clinical complication,

genetic factors, signs and symptoms, diagnosis, treatment plan and modern nutrition therapies,

using the most recent 5 years literature.

In addition, the patient, who will be referred to as “Patient A”. Patient A has PMH of ALD

and cirrhosis and was readmitted to the hospital for GI bleed with dark bloody emesis multiple

times and N/V x 3 days, as well as melena.

Epidemiology

According to the CDC, chronic liver disease was ranked 9th as one of leading cause of death

in California. Within the United State in 2015, there were 21,028 deaths attributed to alcoholic

liver disease. Worldwide, there were 493,330 deaths related to liver cirrhosis in 2010 [30]. In a

recent analysis, however, Mayo Clinic researchers showed that liver disease-related mortality in

the United States has been underestimated during the past two decades, and the figure was closer

to 66,000 deaths annually [2].

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Genetics

Besides one’s individual choice to become a habitual drinker or alcoholic, genotype also

plays a significant role in increasing one’s vulnerability to liver damage. [3].

In a recent research study in 2016, two polymorphisms rs26907 in RASGRF2 gene and

rs61764370 polymorphism in the KRAS gene were studied about their susceptibility and

association to alcoholic liver disease. So, 301 male patients were recruited that have been identified

as an alcoholic (103 were diagnosed with liver cirrhosis) and 156 healthy male volunteers. A

TaqMan PCR assay was used to analyze the SNPs KRAS 3377 and RASGRF2. This study found

that single nucleotide polymorphism, RASGRF2 Gene, has been shown to be linked to alcoholic

liver cirrhosis in men [3].

Pathophysiology

Ethanol and the products of its metabolism have toxic effects on the liver. Once in the liver

cells or hepatocytes, there are three pathways [1] shown in Figure 2. The first pathway involves

an enzyme called alcohol dehydrogenase (ADH). Alcohol dehydrogenase first oxidized ethanol to

acetaldehyde, and this takes place in the cytosol of the cell

Another pathway that is involved in ethanol metabolism is the microsomal ethanol

oxidizing system (MEOS) constituted by the cytochrome P450 (CYP) enzymes [6]. In

physiological conditions, only a small amount of ethanol, about 10%, is oxidized to acetaldehyde

by cytochrome P450 2E1 CYP2E1 but during chronic alcohol abuse, there is an induction of

microsomal system and an increase in CYP2E1 protein expression. CYP2E1 catalyzes the

oxidation of ethanol to acetaldehyde and it can catalyze the oxidation of the latter to acetate. Apart

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from generating acetaldehyde, CYP2E1 also contributes of oxidative damage by the formation of

reactive oxygen species (ROS) [[7, 8].

Additional metabolic pathway involved Peroxisome catalase in ethanol oxidation. Catalase

is a heme-containing enzyme that catalyzes the removal of hydrogen peroxide (H2O2 ) but it can

catalyze the oxidation of alcohol to acetaldehyde [9] .

All three of these pathways lead to the conversion of alcohol to acetaldehyde. Acetaldehyde

is known to be toxic to the liver. It impairs cellular functions and gene expression by forming

adducts with proteins and DNA. Acetaldehyde can bind to macromolecules, enzymes, and the cell

membranes to produce protein adducts by interacting with the epsilon amino group of lysine, or

the α amino group of N-terminal amino acids [10]. Stable acetaldehyde adducts alter the structure

and function of proteins, including enzymes. For example, acetaldehyde adducts formed with the

O6-methylguanine methyltransferase, impair DNA repair mechanisms, which could mediate

carcinogenesis [10].

In addition, acetaldehyde accumulated in three pathways will be further oxidized to acetate

by aldehyde dehydrogenase. During this process, and reactive oxygen species (ROS) such as

superoxide (O− ₂), hydrogen peroxide (H2O2), hydroxyl radical (OH.), hydroxyl ion (OH-), and

nitric oxide (NO) are formed. These species are unstable and rapidly react with additional electrons

and protons. What’s more, ROS generates radicals, including superoxide anion and hydroxyethyl

radical (HER), are highly reactive and form adducts with lipids, proteins, and DNA. Although

most of these ROS are converted to water before they can damage cells, a small proportion can

generate toxic effects as lipid peroxidation, enzyme inactivation, DNA mutation, and destruction

of cell membranes [1].

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Cirrhosis

Cirrhosis is the final outcome of all chronic liver disease which results from progressive

fibrosis. It is among the ten leading causes of death in the United States. Cirrhosis is characterized

by extensive fibrosis with nodule formation and disruption of the liver architecture. When cells

are injured or damaged and die off, usually the dead tissue that was previously full of living cells

becomes fibrotic, meaning that it becomes thickened with irregular scarring from protein and

forms permanent scar tissue surrounding and between hepatocytes known as fibrosis.

Hepatic fibrosis is a major histological feature associated with the progression of the

chronic liver disease to cirrhosis; it is characterized by increased deposition of components of the

extracellular matrix (ECM), in particular, fibrillar collagens types I and III. Hepatic myofibroblasts

are the major source of collagen Type I in fibrotic liver.

This process is associated with an upheaval of hepatic architecture, decreased number of

endothelial cell fenestrations, and portal hypertension. The key event in hepatic fibrogenesis is

hepatic stellate cell (HSC) activation during which they lose their characteristic vitamin A and

lipid stores and obtain a myofibroblastic phenotype [10].

Liver fibrosis is generally reversible. Sequential liver biopsies from the patient with liver

fibrosis have demonstrated that removing underlying cause may reverse hepatic fibrosis in patients

with secondary biliary fibrosis, Hepatitis C, Hepatitis B, nonalcoholic steatohepatitis (NASH), and

autoimmune hepatitis. After the removal of the suppression or removal of inflammatory stimuli

(e.g. HBV, HCV) that drives the development of fibrosis, it results in a decrease in pro-

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inflammatory and fibrogenic cytokines, increased collagenase activity, decreased ECM production

and the disappearance of activated myofibroblast.

Clinical Complications:

Cirrhosis can lead to many complications, including portal hypertension, hepatic

encephalopathy, ascites, and many other diseases.

As the central veins and sinusoids become compressed and pushed on the fluid inside, their

pressure starts to build up, leading to intrasinusoidal or portal hypertension (portal HTN), which

is this higher pressure in the portal vein. Higher portal vein pressure means that fluid in blood

vessels is more likely to get pushed into tissues and across tissues into large open spaces like the

peritoneal cavity [11].

Ultimately, cirrhosis can lead to excess peritoneal fluid, also known as ascites and can

result in other complications like congestive splenomegaly and hypersplenism, where the spleen

becomes enlarged due to all this fluid and blood that can’t get into the liver and gets back up into

the spleen. In the same way, the circulatory system starts diverting blood away from the liver

because of the high liver pressure (aka portosystemic shunt). When this happens, blood flow will

follow the path of least resistance and shunt away from the portal system and towards the systemic

system of circulation.

Hepatic encephalopathy is another complication observed in patients with cirrhosis, after

exclusion of brain disease [12-14]. Hepatic encephalopathy is characterized by personality

changes, intellectual impairment, and a depressed level of consciousness. Subtle signs of hepatic

encephalopathy are observed in nearly 70% of patients with cirrhosis, and overt hepatic

encephalopathy(OHE) occurs in about 30-40% of patients with cirrhosis. Approximately 30% of

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patients dying of end-stage liver disease experience significant encephalopathy, approaching coma

[15]. One of the theories proposed to explain the development of hepatic encephalopathy in

patients with cirrhosis are that neurotoxic substances, including ammonia, may gain entry into the

brain in the setting of liver failure. Ammonia is a normal by-product of processing nitrogen in the

body and is excreted as waste in the urine, in healthy people. However, elevated blood ammonia

levels can occur when the kidneys or liver are not working properly, allowing this waste to remain

in the bloodstream, which can be poisonous to your cells.

Signs and symptoms

The general symptoms of cirrhosis can be broken down into two stages. The early stage

when there is a small amount of scarring and fibrosis is called the compensated cirrhosis. The liver

is still able to do a lot of its jobs. During this stage, the patient might not experience any symptoms

or only have non-specific symptoms such as weight loss, general weakness, or fatigue.

If cirrhosis is left undiagnosed, it progresses into the later stage with extensive fibrosis.

The liver will progress to decompensated cirrhosis, which the liver can’t function normally

anymore. At this stage, many of the described symptoms start to develop such as jaundice, ascites,

itchy skin, hepatic encephalopathy leading to confusion, and easy bruising from low coagulation

factors, as shown in table 1 [16].

In addition, increased unconjugated bilirubin in the blood can also lead to jaundice. As a

result, yellowing of the skin and whites of the eyes and darkening of the urine. Portal hypertension

can cause blood to be redirected to smaller veins, causing them to increase in size and become

varices. Strained by the extra load, these smaller veins can burst, causing serious bleeding. Life-

threatening bleeding most commonly occurs when veins in the lower esophagus (esophageal

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varices) or stomach (gastric varices) rupture. Portal hypertension can also cause fluid to

accumulate in the legs (edema) and in the abdomen (ascites).

The liver helps in making clotting factors or protein that coagulate the blood. So, when the

liver is not producing these coagulation factors, you can get bruising easily.

Diagnosis

The diagnosis of the alcoholic liver disease can be based on clinical and laboratory tests.

The diagnostic tests include serum aspartate aminotransferase/alanine aminotransferase

(AST/ALT). If the AST: ALT ratio is greater than 2, it can be utilized as an indicator that the liver

disease is associated with alcohol. The gamma-glutamytranspeptidase (GGT) can also be elevated

[16]. In addition to the blood labs, ultrasonography to computed tomography imaging, magnetic

resonance imaging (MRI) tool is also utilized to detect for cirrhosis, as well as the signs of portal

HTN. The most cost-effective choices might be the ultrasound compared to MRI and MR

spectroscopy.

Liver biopsy is considered the gold-standard diagnostic method to confirm the diagnosis

and to determine the extent of the liver injury and the prognosis of cirrhosis. Biopsy helps rule out

other coexisting conditions such as hepatitis C, hemochromatosis, or Wilson’s disease.

Furthermore, according to a recent study of patients with alcoholic cirrhosis, early liver biopsy has

been very helpful in providing insights to help assess the stage of the liver disease[17].

After liver disease or cirrhosis has been diagnosed, it’s essential to be able to assess the

severity of the disease in order to determine the best treatment plan and to predict the mortality

rate. Since 1978, the Maddrey discriminant function (DF) has been in use to help predict the

mortality rate of the disease. A DF value > 32 is an indicator of a high -risk morality and the patient

will likely to be prescribed with corticosteroid therapy [16]. A more recent predictive model used

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is Model for End-stage Liver Disease (MELD) score created by the Mayo Clinic, which involves

serum bilirubin, creatinine, and INR. Another clinical tool that has been widely used to determine

the diagnosis cirrhosis in the patient is the Child-Turcotte-Pugh (CTP), which is based on bilirubin,

albumin, an International Normalized Ratio (INR), and grade of encephalopathy and ascites [16].

Treatment

It’s important to prevent continued liver damage by identifying the underlying cause and

the treatment. In the past cirrhosis was generally thought to be irreversible but recent studies have

shown that treatments aimed at the underlying cause especially in earlier stages of the disease can

improve or even reverse fibrosis [18]. Overall, the first line of treatment for cirrhosis is abstention

from alcohol and treating the underlining etiologies of cirrhosis.

Ascites is the most common complication of cirrhosis. The mainstays of first-line treatment

of patients with cirrhosis and ascites include (1) education regarding dietary sodium restriction

(2000 mg per day [88 mmol per day]) and (2) oral diuretics. More stringent dietary sodium

restriction can speed mobilization of ascites but is not recommended because it is less palatable

and may further worsen the malnutrition that is usually present in these patients. Fluid loss and

weight change are directly related to sodium balance in patients with portal hypertension-related

ascites. It is sodium restriction, not a fluid restriction, which results in weight loss, as fluid follows

sodium passive. Oral diuretics (spironolactone and furosemide are commonly used) and non-

steroidal anti-inflammatory drugs (NSAIDs) can also be part of the treatment plan.

Another complication of cirrhosis is GI bleeding, which is the second admission diagnosis

for case study patient A. Cirrhotic patient with GI bleeding should receive spontaneous bacterial

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peritonitis (SBP) antibiotic prophylaxis combined with either intravenous or oral ceftriaxone for a

period of 7 days to prevent infection in patients with variceal hemorrhage [19].

In addition, hepatic encephalopathy, elevated ammonia level, accompanied with mental

confusion, asterixis is another complication of cirrhosis. The neuropsychiatric disturbance that can

be corrected with the proper treatment. Lactulose, a non-absorbable disaccharide cathartic and/or

with Rifaximin therapy can help reduce the nitrogenous load in the gut, thus reduce the ammonia

level production. In a double-blind, randomized, controlled trial of lactulose (3 times per day and

titrated to produce 3 soft stools per day) with or without Rifaximin (400 mg 3 times per day) in

120 patients with overt HE, this research studied found that mortality was reduced significantly

with combination therapy, which may be due to the antimicrobial properties of Rifaximin and the

resulting lower rates of sepsis. So, Lactulose plus Rifaximin is superior to lactulose alone in

reversing hepatic encephalopathy [18].

If the cirrhosis has progressed to the end-stage and to the point that it could not function,

then liver transplantation will be needed. Total counts of liver transplants in 2017 is 8,082

according to the U.S. Department of Health & Human Services. And the number of liver

transplants increased by 20.7% between 2007 and 2016 according to the data from Organ

Procurement and Transplantation Network (OPTN) and Scientific Registry of Transplant

Recipients (SRTR) 2016 Annual Data Report [20].

Nutrition Therapy

Patient with cirrhosis and alcoholic hepatitis have increased nutritional demands, but many

have an average of daily intake of <50% of the recommended calorie intake. Acute Nutritional

intervention in cirrhotic patients should aim to support hepatic regeneration, prevent or correct

malnutrition and prevent and/or treat the complications associated with cirrhosis.

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Despite alcohol having relatively higher kcal per gram (2.3-18 kcal/g) than carbohydrate

(4.1 kcal/g) in average, patients are still observed with primary or secondary malnutrition. A

common nutrition diagnosis for a patient with cirrhosis is protein-energy malnutrition or

inadequate protein-energy intake. The contributing factors includes: (1) low dietary intake due to

imbalanced diet pattern or replacement of food calories by the heavy alcohol consumption giving

the false conception that they are full; (2) poor appetite related to dysguesia, esophagitis, gastritis,

and poor dental condition; (3) alteration in sense of taste and smell; (4) malabsorption of nutrient

secondary to diarrhea, nausea and vomiting, exogenous pancreatic insufficiency; (5) clinical

complications secondary to liver disease such as ascites, hepatic encephalopathy [22-24].

Fat soluble vitamin deficiencies are common manifestations of malnutrition and liver

disease. Vitamin A (retinol) is implicated in ocular retinoid metabolism, tissue repair, and

immunity, and is principally stored in hepatic stellate cells. As stellate cells become activated, they

lose their vitamin A stores and are then capable of producing collagen and subsequent fibrosis

The chronic liver disease commonly results in vitamin D deficiency. It was postulated that

a key mechanism responsible for the low serum 25-hydroxy-vitamin D levels in patients with the

end-stage liver disease may relate to the decreased hepatic production of vitamin D binding protein.

Vitamin E deficiency has been well documented in alcoholic liver disease. However, the beneficial

effects of vitamin E supplementation in liver disease are dependent upon the nature of the disorder.

For example, vitamin E supplementation in ambulatory patients with decompensated alcoholic

cirrhosis was not beneficial at 1-year follow-up [25] .

Deficiencies in pyridoxine (vitamin B6), folate (vitamin B9) and cobalamin (vitamin B12)

may develop rapidly in chronic liver disease due to diminished hepatic storage. An original study

showed that 80% of 70 chronic alcoholics that were admitted to a large U.S. urban hospital had

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low serum folate levels, including 44% with serum folate levels in the severely deficient range. In

general, the three main cause of the folate deficiency in the patient with ALD is reduced folate

absorption by the small intestine, Abnormal liver uptake and low folate storage, and increased

urinary folate excretion [1].

Many works of literature such as the American Association for the Study of Liver Disease

(AASLD) and American College of Gastroenterology (ACG) recommend nutritional therapy in

cirrhosis when the patient is undernourished and cannot meet the calculated daily nutritional

demand of 35-40 kcal/kg and protein intake 1.2-1.5 kg/day. Also, small frequent meals are

encouraged, emphasizing breakfast and nighttime snack ([23] [24] [27] [28]).

Enteral is recommended as the route of administration considering the risk of

complications when given parentally[26, 27] according to the European Society of Clinical

Nutrition and Metabolism (ESPEN). Some benefits of enteral nutrition have been shown in

patients with alcoholic hepatitis, malnourished patients with cirrhosis and patients with liver

transplantation[28], where glycogen stores may be depleted after overnight fast and metabolic

conditions resemble prolonged starvation in healthy individuals.

Current Research

The intestinal dysbiosis is common in chronic liver disease and can induce inflammatory

responses and mediate the collagen deposition in the liver. A research was conducted in 2017, to

evaluate the probiotic Lactobacillus rhamnosus GG (LGG) for the treatment of liver fibrosis in a

model of chronic cholestatic liver disease in rats. Lactobacillus rhamnosus GG (LGG) is a

commensal Gram-positive bacterium widely used as a probiotic strain because of its beneficial

effects on the intestinal barrier and inflammatory profile. This study suggests that LGG can be a

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promising therapy for adjuvant treatment of hepatic fibrosis. There were 29 rats in the study, one

group (n=17) have bile duct-ligated and another group (n=17), have sham-operated. Two group

are randomly assigned to receive the (LGG) or phosphate buffered saline for 14 days. Researchers

found the treatment with probiotic LGG was able to reduce liver fibrosis and hepatic gene

expression of IL-6 in cholestatic liver disease rats [29].

Case study: Patient A

Patient A is a Hispanic 44-year-old and was readmitted to the ICU unit due to an altered

level of consciousness, acute GI bleeds with dark emesis, with nausea and vomiting for three days,

as well as melena. According to the patient medical record, he was first admitted in January to the

hospital for a GI bleed and a long history of heavy alcohol abuse, alcoholic liver cirrhosis. During

the recent admission, in a GI doctor consult, it was revealed the patient had a probable cirrhosis.

The patient was employed and lived at home. After admission, the patient was NPO, except

medication for GI rest. Patient A was given octreotide drip IV therapy and later a Banana bag with

multivitamin, thiamine, folic acid and dextrose 5% + 0.45% sodium chloride were infused to the

patient. The rationale behind ordering banana bags for these patients is relatively simple–

alcoholics are likely to have nutritional deficiencies related to their dietary preferences for alcohol

over nutrient-dense foods, putting them at risk for complications. Furthermore, the administration

of fluids is conventionally believed to help speed up sobriety. The patient also received a blood

transfusion after proper screening and cross-matching due to the anemia as shown in Table 3. After

the EKG was done, Patient continued with amlodipine, Aldactone, hydromorphone, and Protonix

as shown in table 1 with further details [29].

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On day 2 of stay, the patient was advanced to a clear liquid. The banana bag IV was

discontinued and 0.45% sodium chloride was infused to the patient because patient’s condition has

stabilized.

On Day 3, Patient A underwent esophagogastroduodenoscopy (EGD) with band ligation

of varices per anesthesia and propofol. Patient A was then transferred to the recovery room unit in

a stable condition. During the hospital stay, the patient was provided reality orientation and

supportive psychotherapy.

On day 4 of stay, the nutrition department received a consult for Patient A at risk for

malnutrition at level 2 and above, and nausea, vomiting, diarrhea greater than 3 days. Patient A’s

BMI upon this hospital admission was 22 kg/m2 (Normal) [29], using his admission weight of 67.5

kg (148.5 pounds) and 175.2 cm (68.9 inches). During the assessment the patient was unarousable

and the nurse-reported patient was unable to consume the clear liquid due to mental status. Nurse

further reported that the patient has not had an episode of vomiting, diarrhea or constipation after

the admission. The nutrition department diagnosed the patient with inadequate oral intake related

to mental status as evidenced by the patient was not alert enough to consume the clear liquid diet

as reported by the nurse. Later in the day, an NG placement was ordered to provide adequate

nutrition intake. The nutrition department calculated the estimated energy needed by using MSJ x

1.2-1.3 activity factor (25-30 kcal/kg). The patient’s energy needs were calculated out to be 1866-

2022 kcal, protein with 0.8-1 gm/kg, a range of 54-67 gm. The patient’s fluid needs were based on

the RDA method of 1 mL of fluid/calorie range of estimated needs computed out to 1800-2000 ml.

Therefore, an NG tube feeding formula, Jevity 1.5 kcal was selected because it peptide-

based advanced formula with ingredients to help manage inflammation and promote GI tolerance.

The goal rate of 60 ml/hr. was recommended to provide 1980 kcal, 269 gm carbohydrate, 83 gm

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protein, free water 1003 ml, and meeting 132% of RDI. and meets 100% of estimated calorie needs

and 100% of estimated protein needs. Although the tube feeding goal was at 60 ml/hr., the nutrition

department recommended starting the feeding at 20ml/hr. as tolerated then advance to the goal rate.

The recommended nutrition therapy for the patient was discussed with the medical doctor who

agreed with the plan. The recommended tube feeding was started the next day. Lastly, the

department scheduled a follow-up assessment for 2 days later to assess patient’s tolerance of the

tube feeding rate and formulate (Table 4).

On the day of 6, during the follow-up visit, the tube feeding was discontinued, patient A

had already started the GI soft diet and tolerated it well with no nausea, vomiting, diarrhea or

chewing/ swallowing difficulty. The patient discharged from the hospital on day 7 of his stay.

According to the physician discharge summary note, patient’s discharge diagnosis was: alcoholic

cirrhosis of the liver without ascites, portal hypertension, gastric varices, dehydration, and severe

protein-calorie malnutrition. The condition upon discharge was hemodynamically stable and

improved and the recommended discharge diet was cardiac diet. In sum, Patient A went through

a series of diet changes, He began with NPO, then, went from clear liquid to NG tube due to altered

in the level of mental status. After patient’s condition stabilized, the patient was on GI soft diet.

The goal of the nutrition department in Patient A’s stay in the hospital was to improve his nutrition

status and provide adequate oral nutrition intake to prevent or avoid further damage to the liver.

Risk Associated in the Role of RDN in Patient Care

According to the physician discharged summary note, one of the patient’s discharge

diagnosis was severe protein-calorie malnutrition. However, upon the review of all the chart notes

since the first admission in January until the recent admission, there was not a nutrition intervention

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provided to improve the protein-calorie energy intake via supplementations. There was also no

history of nutrition education provided to patient A documented in the chart notes. It would be

beneficial to the patient if the nutrition department communicates and collaborates with the doctors

to encourage nutrition education consult before patient gets discharged. In addition, the dietitian

can monitor all the nutritional related labs with emphasis on vitamins and mineral levels to ensure

the patient is not deficient in certain vitamins and minerals such as fat-soluble vitamins and vitamin

B complex.

In addition, the patient will be benefited if dietitian follows a standard nutrition assessment

guide when assessing the calorie and protein needed. According to the Morrison’s Nutrition

Assessment Guide, a patient with uncomplicated cirrhosis, the estimated energy need should range

from 30-35 kcal/kg (RMR x1.2-1.4), and estimated protein needs range from 1-1.2 g/kg., whereas,

Patient’s A, the calculated estimated energy needs was at 25-30 g/kg and protein needs at 0.8-1.0

g/kg. Thus, the estimated needs for Patient A was likely to be not enough to improve his nutrition

status. Also, the guideline mentions the need to evaluate vitamin D and thiamine for

supplementation due to the decreased hepatic production of vitamin D binding protein and

depletion of liver thiamine stores. (Morrison Nutrition Assessment Guide 2014)

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Supplementary Material

Figure 1: The progression for alcoholic liver injury to steatosis with scarring, inflammation and architectural distortion leading to cirrhosis. As a complication of cirrhosis, hepatocellular carcinoma may occur. However, only a minority of patients with alcoholic steatosis progress to severe liver injury.

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Figure 2: Hepatic metabolism of ethanol by enzymes ADH, CYP2E1 and catalase. Each enzyme generates acetaldehyde, a toxic and mutagenic metabolite of ethanol. While ADH is metabolically stable regardless of the alcohol challenge and catalase is irrelevant with respect to its role in hepatic alcohol degradation, CYP2E1 is inducible and contributes most to acetaldehyde production during heavy alcohol consumption.

Table 1: Clinical features of hepatitis or chronic liver disease

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Table 2: List of medication patient was on after admission.

Medication Uses Drug/ Nutrition Interaction

Amlodipine Lower the blood pressure by relaxing the blood vessels so the heart does not have to pump as hard.

The consumption of grapefruit juice may slightly increase plasma concentrations of amlodipine.

Aldactone Spironolactone, is an oral diuretic and is also used to treat low potassium levels

Avoid a diet high in salt. Too much salt will cause your body to retain water and can make this medication less effective. Do not use salt substitutes or low-sodium milk products that contain potassium. These products could cause your potassium levels to get too high while you are taking spironolactone.

Lactulose Ammonia reducer and

laxative

Side effects: nausea, vomiting, mild diarrhea

Potassium

Chloride

Used to treat or prevent low amounts of potassium in the blood.

Upset stomach, nausea, vomiting, gas, or diarrhea may occur as side effects.

Sodium

Chloride

Used to treat or prevent sodium loss caused by dehydration, excessive sweating.

Side effects: nausea, vomiting, stomach pain.

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Table 3: Laboratory values

Laboratory Assay

Reference Range

Day 1

(4/15)

Day 2

(4/16)

Day 3

(4/17)

Day 4

(4/18)

Day 5

(4/19)

Day 6

(4/20)

Day 7

(4/21)

Day 8

(4/23)

Red blood cell count

4.7-6.1

million/L

2.33

(L)

2.17

(L)

2.47

(L)

2.79

(L)

2.16

(L)

2.22

(L)

2.21

(L)

2.57

(L)

Hemoglobin 13.5-17.5

g/dL

8.7

(L)

7.9

(L)

7.9

(L)

8.8

(L)

8.0

(L)

8.4

(L)

8.5

(L)

9.7

(L)

Hematocrit 42-52% 25

(L)

22.5

(L)

25.2

(L)

28.4

(L)

22.6

(L)

23.5

(L)

23.7

(L)

27.6

(L)

MCV 80-95 fL 107.6

(H)

103.8

(H)

104.4

(H)

101.6

(H)

104.6

(H)

106.2

(H)

107.6

(H)

107.6

(H)

Platelet count

150-350x103 µm3

56

(L)

34

(L)

38

(L)

37 (

L)

38

(L)

46

(L)

36

(L)

47

(L)

sodium 136-145

mEq/L

WNL WNL 135

(L)

132

(L)

WNL 135

(L)

134

(L)

Potassium 3.5-5.0

mEq/L

WNL WNL 3.1

(L)

3.2

(L)

3.2

(L)

3.3

(L)

3.3

(L)

WNL

Glucose 74-106

mg/dL

152

(H)

151

(H)

145

(H)

122

(H)

WNL WNL 108

(H)

WLN

-Empty boxes represent unreceived blood samples -MCV: Mean corpuscular volume - Range values for laboratory Assay: Interpretation were adapted from the Manual and

Laboratory Test [28].

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Table 4: Overview of Nutrition Care Process

Day of Stay

Reason for visit

Diet Nutrition Diagnosis

Nutrition Intervention

Nutrition Monitoring/Evaluation

1

(4/15)

Octreotide IV drip

+ Banana Bag

2

(4/16)

NPO

4

(4/18)

Nutrition Consult: Risk for malnutrition at level ³2 and N/V, diarrhea greater than 3 days

Clear Liquid

Inadequate oral intake related to mental status as evidence by patient is not alert enough to consume the clear liquid diet as reported by nurse

Recommend to start the NG TF at 20 ml/hr. Increase gradually to the goal rate of 60 ml/hr. as patient tolerated. TF at goal rate provides 976 ml total volume, 1980 kcal, 83g protein, 216g CHO, 760 ml free water meet 100% of estimated energy and protein needs and meets 132% of RDI. Nutrition education inappropriate at this time.

Assess need for water flush at follow-up visit (noted Sodium 135, is low at this time). Monitor PO intakes, GI function, nutrition related labs and skin integrity. Follow-up 2x/week

5

(4/19)

NG tube feeding at 20 ml/hr.

Dinner

time: GI Soft diet

6

(4/20)

Follow-up GI soft diet

No nutritional diagnosis identified at this time.

Continue the GI diet as tolerated. Nutrition education inappropriate at this time as patient due to patient was asleep.

Monitor PO intakes, GI function, nutrition related labs and skin integrity. Follow-up 1x/week

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