1 Stephanie Ensign March 7, 2012 Clinical Nutrition Liver Disease INTRODUCTION The liver is one the most important organs in the body. A person cannot survive without a liver because it is vital for so many important functions in the body (1). These functions include the metabolization of carbohydrate, protein, and fat, the storage and activation of vitamins and minerals, the formation and excretion of bile which is then used to digest and absorb fat and fat- soluble vitamins, the conversion of ammonia to urea, the metabolization of steroids, and the detoxification of drugs and alcohol. However, a person doesn’t need all of their liver to survive. In fact, only 10% to 20% of the functioning liver is needed to sustain life (1). However, it is important that the liver is functioning properly so that it can perform all of the functions it is supposed to. Therefore, any disease of the liver is concerning and can potentially lead to many complications and even death. DISEASE DESCRIPTION Liver disease is defined as any disease that reduces the function of the liver, and it can be classified as being either acute or chronic and inherited or acquired (1). There are many different diseases of the liver, including acute viral hepatitis, fulminant hepatitis, chronic hepatitis, and many others. Chronic liver disease and cirrhosis is the tenth leading cause of death in the United States as of 1998, and the number of liver-related deaths from viral hepatitis and hepatic malignancies have been steadily increasing (2). About one in 679 people in the United States have either chronic liver disease or cirrhosis, and the number has been steadily climbing (3). It is important that people understand the adverse effects of alcohol on the liver so that the rates of liver disease can start to decline.
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1
Stephanie Ensign
March 7, 2012
Clinical Nutrition
Liver Disease
INTRODUCTION
The liver is one the most important organs in the body. A person cannot survive without a
liver because it is vital for so many important functions in the body (1). These functions include
the metabolization of carbohydrate, protein, and fat, the storage and activation of vitamins and
minerals, the formation and excretion of bile which is then used to digest and absorb fat and fat-
soluble vitamins, the conversion of ammonia to urea, the metabolization of steroids, and the
detoxification of drugs and alcohol. However, a person doesn’t need all of their liver to survive.
In fact, only 10% to 20% of the functioning liver is needed to sustain life (1). However, it is
important that the liver is functioning properly so that it can perform all of the functions it is
supposed to. Therefore, any disease of the liver is concerning and can potentially lead to many
complications and even death.
DISEASE DESCRIPTION
Liver disease is defined as any disease that reduces the function of the liver, and it can be
classified as being either acute or chronic and inherited or acquired (1). There are many different
diseases of the liver, including acute viral hepatitis, fulminant hepatitis, chronic hepatitis, and
many others. Chronic liver disease and cirrhosis is the tenth leading cause of death in the United
States as of 1998, and the number of liver-related deaths from viral hepatitis and hepatic
malignancies have been steadily increasing (2). About one in 679 people in the United States
have either chronic liver disease or cirrhosis, and the number has been steadily climbing (3). It is
important that people understand the adverse effects of alcohol on the liver so that the rates of
liver disease can start to decline.
2
ETIOLOGY
There are many different kinds of liver disease, and they all have different causes. Some
of the general causes of liver failure include different hepatitides, cytomegalovirus, human
Becker U, Bendtsen F. Long term prognosis of fatty liver: Risk of chronic liver disease
and death. Gut. 2004;53(5):750-755.
8/24/2012
Liver Function
Martha Ellsworth
Julie Loveland
Stephanie Ensign
Ashlee Whipple
Normal Liver Functions
Physiology
● The liver is able to regenerate itself
● Only 10% to 20% of the functioning liver is needed to sustain life
● Metabolizes carbohydrate, protein, and fat
● Stores and activates vitamins and minerals: all fat-soluble vitamins, B12, Zn, Fe, Cu, Mg
● Forms and excretes bile which is used to digest and absorb fat and fat-soluble vitamins
Physiology
• Converts ammonia to urea
• Metabolizes steroids: inactivates and excretes aldosterone, glucocorticoids, estrogen, progesterone, and testosterone
• Detoxifies drugs and alcohol
• Filter and flood chamber: removes bacteria and debris by action of Kupffer cells
Carbohydrate Metabolism
● Galactose and fructose are converted into glucose in the hepatocyte or liver cell
● The liver stores glucose as glycogen (glycogenesis) and then returns it to the blood when blood glucose levels are low (glycogenolysis)
● Gluconeogenesis from lactic acid, glycogenic amino acids, and intermediates of tricarboxylic acid
Protein Metabolism
● Transamination and oxidative deamination convert amino acids to substrates that are used in energy and glucose production, and in creating nonessential amino acids
● Forms serum proteins: albumin, α-globulin, β-globulin, transferrin, ceruloplasm, lipoproteins
Fat Metabolism
● Fatty acids are converted to acetyl-coenzyme A to produce energy
● Ketone bodies produced
● Synthesizes and hydrolyzes triglycerides, phospholipids, cholesterol, and lipoproteins
Pathophysiology of Different Liver Diseases
● Liver disease can be classified as:
– Acute or chronic
– Inherited or acquired
● Various kinds of liver diseases:
– Acute viral hepatitis
– Fulminant hepatitis
– Chronic hepatitis
– Other liver diseases
• Various kinds of liver diseases:
• Non-alcoholic steatohepatitis (NASH)
• Alcoholic hepatitis
• Cirrhosis
• Cholestatic liver diseases
• Inherited disorders
End Stage Liver Disease (ESLD)
● Liver failure
● Caused by cirrhosis
● Damages the liver tissue and keeps it from working like it should
● If the damage is not stopped, the liver gradually loses its ability to carry out its normal functions
HAV and HEV→ Acute Hepatitis •Vaccine created for prevention
HBV/HDV and HCV→ Chronic Hepatitis→ Cirrhosis→ Liver failure
Type of Hepatitis Virus Transmission
Hepatitis A (HAV) Picornaviridae hepatovirus Fecal-oral routes
Hepatitis B (HBV) Hepadnaviridae orthohepadnavirus
Blood, body-fluid contact, vertical transmission (mother to child)
● Found in other body tissues but highest in the liver
– ↑’d with liver cell damage
● Aspartate aminotransferase (AST)
– In cytosol and mitochondria of hepatocyte
● Also in cardiac and skeletal muscle, brain, pancreas, kidney, leukocytes
– ↑’d with liver cell damage
Hepatic Enzymes
• Serum lactic dehydrogenase
• In liver, RBCs, cardiac muscle, kidney
• ↑’s with liver disease
• Lacks sensitivity and specificity because found in most other body tissues
Serum Proteins ● Serum Albumin
• Main export protein made in liver; important in oncotic pressure
• ↓’d synthesis with liver dysfunction
● Can also be a sign of other dysfunctions
● Serum Globulin
• Synthesized in the liver
• ↑’d with chronic liver disease
• Limited diagnostic use in hepatobiliary disease
●Conjugation of Bilirubin ● Heme breaks down from hemeoglobin, myoglobin, and etc. to form
unconjugated bilirubin
● Not soluble in water
● Bound to albumin and goes to the liver
● In liver, bilirubin is conjugated
● Water soluble
● Most is bound to bile and secreted out with the feces
– Gives the stool its dark color
● Reabsorbed bile goes back to the liver
● Some is secreted back into the SI and some is excreted into the urine
– Gives urine its characteristic yellow color
Other Tests ● Total Serum Bilirubin
● If ↑’d may indicate bilirubin overproduction or a defect in hepatic uptake on conjugation
● Indirect Serum Bilirubin
● Unconjugated bilirubin
● ↑’d with excessive bilirubin production (hemolysis), immaturity of enzyme systems, inherited defects, drug effects
● Direct Serum Bilirubin
● Conjugated bilirubin
● ↑’d with depressed bilirubin excretion, hepatobiliary disease, intrahepatic or extrahepatic cholestasis, benign postoperative jaundice and sepsis, and congenital conjugated hyperbilirubinemia
●Other Tests—Cont’d ● Urine Bilirubin
● More sensitive than total serum bilirubin
● Confirms if liver disease is cause by jaundice
● Urine Urobilirubin
● Objective jaundice is expected—rarely used
● Serum Bile Acids
● Reflects efficacy of ileal resorption and hepatic extraction of bile acids from portal circulation
● ↑’d with liver disease
● Has little clinical use
● Ammonium
● Liver converts ammonia to urea
● May ↑ with hepatic failure and portal-systemic shunts
Acute Liver Failure
● Also known as fulminant hepatic failure.
● The liver rapidly loses its ability to function.
● Can develop in a matter of days.
● Complications include excessive bleeding and increasing pressure in the brain.
● S/S: jaundice, pain in the upper right of abdomen, nausea, vomiting, a general sense of not feeling well, difficulty concentrating, disorientation and confusion, and sleepiness.
Acute Viral Hepatitis
•Widespread inflammation of the liver
•Caused by hepatitis viruses A,B,C,D, and E as well as Epstein-Barr virus, cytomegalovirus, herpes simplex, yellow fever, and rubella
Chronic Hepatitis
•To be defined as chronic hepatitis, a patient must have at least a 6-month course of hepatitis or have biochemical and clinical evidence of liver disease with confirmatory biopsy findings of unresolving hepatic inflammation.
•Clinical symptoms are usually nonspecific, occur intermittently, and are mild.
Fulminant Hepatitis
•Severe liver dysfunction is accompanied by hepatic encepholopathy.
–Characterized by impaired mentation, neuromuscular disturbances, and altered consciousness.
Absence of pre-existing liver disease.
Extrahepatic complications:
●Cerebral edema
●Coagulopathy and bleeding
●Cardiovascular abnormalities
●Renal failure
●Pulmonary complications
●Acid-base disturbances
●Electrolyte imbalances
●Sepsis
●Pancreatits
Fulminant Hepatitis
Caused by:
●Viral hepatitis (75% of cases)
●Chemical toxicity
–Acetaminophen
–Drug reactions
–Poisonous mushrooms
–Industrial poisons
Other causes
–Wilson’s disease
–Fatty liver of pregnancy
–Reye’s syndrome
–Hepatic ischemia
–Hepatic vein obstruction
–Disseminated malignancies
Nonalcoholic Fatty Liver Disease (NAFLD)
•Refers to a large spectrum of liver disease.
•3 stages:
–Simple fatty liver (steatosis)
–Nonalcoholic steatohepatitis (NASH)
–Cirrhosis
•The accumulation of fat (fatty infiltration) in the liver cells (hepatocytes).
•Occurs in individuals who don’t drink alcohol.
NASH
● Intermediate stage of NAFLD.
● Defined as the accumulation of fat droplets in the hepatocytes, which are surrounded by acute and chronic inflammatory cells.
● It resembles alcoholic liver disease but isn’t caused by alcohol.
● Occurs most often in people who are overweight or obese.
•Causes:
–Drugs
–Inborn errors of metabolism
–Acquired metabolic disorders
•Type 2 diabetes
•Lipodystrophy
•Jejunal ileal bypass
•Obesity
•Malnutrition
NASH
•Treatments include weight loss and the use of insulin-sensitizing drugs.
Alcoholic Liver Disease
● Most common liver disease in the US.
● Damage to mitochondrial membrane structure and function caused by acetaldehyde.
● 3 stages:
– Hepatic steatosis
– Alcoholic hepatitis
– Cirrhosis
• Predisposing factors: • Genetic polymorphism of alcohol-metabolizing enzymes
• Gender (female)
• Simultaneous exposure to other drugs
• Infections with hepatotropic viruses
• Immunologic factors
• Poor nutrition status
Alcoholic Liver Disease
Alcohol Liver Disease
● Acetaldehyde, a toxic by product of alcohol metabolism, causes damage to mitochondrial membrane structure and function
● Develops in three stages:
● Hepatic steatosis
• ↑ in mobilization of FA from adipose tissue
• ↑ in hepatic synthesis of FA
• ↓ in FA oxidation
• ↑ in TGA production
• Trapping of TGA in liver
• Reversible with abstinence from alcohol
Alcohol Liver Disease- Cont’d
● Alcoholic Hepatitis
● Hepatomegaly
● Modest elevation in transaminase levels
● ↑ serum bilirubin concentrations
● Normal or depressed serum albumin concentrations
● Anemia
● May resolve if with discontinued use of alcohol but usually progresses to third stage
• Alcoholic Cirrhosis
• S/S may be like stage two
• GI bleeding
• Hepatic encephalopathy
• Portal Hypertension (elevated BP in portal venous system caused by obstruction of blood flow through liver)
• Ascites
Alcohol Liver Disease- Cont’d
Cholestatic Liver Diseases
● Primary biliary cirrhosis (PBC): caused by progressive destruction of small and intermediate-size intrahepatic bile ducts.
– Extrahepatic biliary tree and larger intrahepatic ducts are normal
– Slow progressing disease that eventually results in cirrhosis, portal hypertension, liver transplantation, or death
●Wilson's disease – ↑ Cu excretion, ↑ Cu in organs, ↓ Serum Cu
–Calcium, Magnesium, Zinc malabsorbed
•RDI level supplement
● Herbal supplements
– Milk thistle – viral hepatitis/alcoholic liver
– Reduces free radicals?
– S-adenosyl-L-methionine (SAMe)
– Methyl donator?
●Diuretic + Albumin
● In a controlled study, patients whose ascites/edema in cirrhosis did not regress after bed rest and sodium restriction were given a diuretic or diuretic + albumin
● Diuretic + albumin
● More responsive
● Decreased Hospital Stay
● Decreased recurrence of edema
● Lower cumulative probability of developing ascites
Complications of Liver Disease
● Portal hypertension
– Nodules and scar tissue compress veins in liver causing high BP
– Increased collateral blood flow, results in varices in GI tract, which can lead to bleeding
– If NPO > 5 days, treated by Parenteral Nutrition
● Ascites
– Fluid retention in the abdominal cavity caused by high pressures forcing fluid out of blood vessels in the liver
– Treated by paracentesis and/or diuretic therapy
● Na+ restriction
– 2 g/day
– Watch protein needs
• Hyponatremia
• Caused by a decreased ability to excrete water from Na+ restriction, anti-diuretics, paracentesis
• Fluid restricted to 1-1.5 L/day
• Glucose alterations
• 66% Cirrhosis patients develop this
• Insulin resistance in peripheral tissue
• Decreased availability of glucose from glycogen
• Fasting hypoglycemia – acute liver disease
• Fat malabsorption
• Decreased bile salt secretion, pancreatic enzyme deficiency.
• Stools are greasy, floating, or light or clay colored • MCT replacement for LCT • Low fat diet may resolve diarrhea
•Hepatorenal syndrome • Renal failure associated with severe liver disease
• No intrinsic kidney abnormalities
• Urine sodium level < 10 mEq/L
• Dialysis required if conservative therapies fail
● Osteopenia
• Hemochromatosis causes depressed osteoblastic function and osteoporosis
• Long term treatment of corticosteriods
• Weight maintenance
• Adequate protein
• 1500 mg calcium
• 400-800 units Vitamin D
Hepatic Encephalopathy
●AKA Portal systemic encephalopathy ●Characterized by impaired mentation, neuromuscular disturbances and altered consciousness ●Multiple causes, multiple theories of etiology
–Ammonia theory –Dietary protein –Altered neurotransmitter theory
Four stages: I. Mild confusion, agitation, irritability, sleep disturbance, decreased attention
II. Lethargy, disorientation, inappropriate behavior, drowsiness
III. Somnolent but arousable, incomprehensible speech, confused, aggressive behavior when awake
IV. Coma
Hepatic Encephalopathy
Hepatic Encephalopathy
●Ammonia theory ●Liver unable to convert ammonia to urea ●Sources of ammonia: protein metabolism, breakdown of bacteria and blood from GI bleeding ●Ammonia collects in body as a cerebral toxin –Ammonia levels in serum and cerebrospinal fluid do not correlate with severity of disease.
–Glutamine and α-ketoglutarate correlate with disease
●Treatments - Lactulose & Neomycin –Lactulose retains ammonium ion in colon by acidifying colonic contents
–Neomycin decreases ammonia production
MNT - Hepatic Encephalopathy
● Tradition – protein restriction ● But, 95% of patients have inadequate protein ● Studies vary as to the effectiveness of BCAA-
enriched formulas. ● Vegetable and Casein proteins
● Higher in BCAAs, lower in AAAs ● Fiber benefit
● Probiotics and synbiotics ● Reduces ammonia, decrease inflammation and oxidative
stress
●Hepatic Encephalopathy
●Dietary Protein? ●Dietary protein → increases ammonia levels → hepatic encephalopathy ●Not proven ●Higher protein intakes correlated with lower blood urea and creatinine levels
●Hepatic Encephalopathy
●Altered Neurotransmitter theory ●In ESLD, Branched-chain AAs ↓, Aromatic AAs↑ ●BCAAs provide 30% of energy when gluconeogenesis and ketogenesis fail. ●Serum BCAAs ↓, Serum AAAs ↑ from muscle proteolysis ●AAAs compete BCAAs for carrier-mediated transport at the Blood-brain barrier.
●MNT - Hepatic Encephalopathy
●Tradition – protein restriction ●But, 95% of patients have inadequate protein ●Studies vary as to the effectiveness of BCAA-enriched formulas. ●Vegetable and Casein proteins ●Higher in BCAAs, lower in AAAs ●Fiber benefit
●Probiotics and synbiotics ●Reduces ammonia, decrease inflammation and oxidative stress
Immune Response to Cirrhosis
•Primary biliary cirrhosis is immune-mediated
–Destruction of small and intermediate-size intrahepatic biles ducts
–Reduced hepatic phagocytosis results in increased antigenic stimulation to the spleen
–Increased immune responses to thymus independent antigens
–Endotoxin is accumulated which enhances IgM responses
–IgA is increased in alcoholic-induced cirrhosis
–Mild elevation of liver enzymes
At Risk Populations for Liver Disease
•Alcohol consumption
•Genetics (ability to metabolize alcohol, increased risk for alcohol abuse, etc.)
•Gender (women)
•General health status (malnourished)
•Mental health
•Age (elderly)
•Social and economic circumstances
Treatments
General
•Goal: prevent further liver damage and reduce complications.
•Maintain a healthy lifestyle
•Limit salt in the diet
•Avoid raw shellfish
•Stop drinking alcohol
Treatments for Complications
•Bleeding varices -- upper endoscopy with banding and sclerosis, transjugular intrahepatic portosystemic shunt (TIPS)
•Excess abdominal fluid (ascites) -- take diuretics, restrict fluid and salt, and remove fluid (paracentesis)
Treatments for Complications
•Coagulopathy -- blood products or vitamin K
•Confusion or encephalopathy -- lactulose medication and antibiotics
•Infections -- antibiotics
•End-stage liver disease and failure– liver transplant
Bleeding Esophogeal Varices
•Swollen veins in walls of the lower part of the esophagus that start to bleed
•Scarring from cirrhosis causes the veins to balloon outward
•Severe bleeding results from rupture
•Evidenced by black, tarry stools, bloody stools, vomiting blood
Treatment- Stop Bleeding
•Directly inject varices with a clotting medicine or place rubber band around bleeding veins using an endoscope
•Insert tube into stomach through the nose and inflate with air to create balloon tamponade
•Place patient on ventilator to protect airways and prevent blood from going into lungs if massive bleeding occurs
Complications and Prevention
•Encophalopathy
•Esophageal stricture
•Hypovolemic shock
•Infection (pneumonia, peritonitis)
•Return of bleeding
•Give propranolol or nadolol (beta blockers) to reduce risk of bleeding
•Transjugular intrahepatic portosystemic shunt (TIPS): creates new connections between blood vessels in the liver to decrease vein pressure and prevent future bleeding
TIPS
•When the liver is damaged, blood coming from the esophagus, stomach and intestines to the liver cannot flow very easily, leading to portal hypertension. This can lead to :
–Bleeding from veins in stomach, esophagus, intestines (variceal bleeding)
–Buildup of fluid in abdomen (ascites)
–Buildup of fluid in chest (hydrothorax)
–Clotting in vein carrying blood from liver to heart (Budd-Chiari syndrome)
•Creates new connections between blood vessels in the liver to decrease vein pressure and prevent future bleeding
TIPS Procedure:
-A catheter is placed through the skin of the neck into a vein
-Using x-ray, the catheter is guided into a vein in the liver
-The balloon is blown up to place the stent
-The stent connects the portal vein to one of the hepatic veins
-60-90 minute procedure
-The new pathway allows for better flowing of blood. It eases pressure on veins in the stomach, esophagus, intestines, and liver
TIPS Complications and Prognosis •Damage to blood vessels
•Fever
•Infection, bruising, or bleeding
•Reactions to medicines or the contrast dye
•Stiffness, bruising, or soreness in the neck
•Bleeding in the belly
•Blockage in the stent
•Cutting of the blood vessels of the liver
•Heart problems or abnormal heart rhythms
•Infection of the stent
-Effective in 80-90% of portal hypertension cases
-Safer than surgery; requires no cutting or stitches
Liver Transplant
•Needed when the liver fails from cirrhosis
•Over 6,000 transplants a year in the US
•Transplant surgery takes between four and twelve hours
•Patients remain in hospital up to three weeks after surgery
Transplant Eligibility
•Doctor refers the patient to a transplant center
• Transplant team evaluates the physical health, mental health, ability to pay for expenses, emotional support from family and friends and decides if the person is eligible
•If determined eligible, the name of the patient is added to the national transplant waiting list by the center, with the people in the most critical condition prioritized to be at the top of the list
Liver Availability
•The waiting list has over 16,000 names. The wait differs from person to person, depending on how critical their condition is
•Livers can come from living or non-living donors
•Most donated livers are from people who recently died with healthy livers who agreed to be organ donors, or their families decide after they pass
•The donor’s liver is split into two parts. One part is removed for the transplant. The surgeon then closes the wound with sutures or staples.
•The remaining liver begins to heal and grow new tissue.
• It takes about 6 to 8 weeks for the liver to grow back to normal size in the donor and recipient
Prognosis
•Most return to their regular lifestyle six months to a year after the transplant
•75% of patients are alive five years later
•Sometimes the disease they had before the transplant returns and they may need to receive another transplant
Transplant Rejection
•Rejection occurs in 60-70% of patients
•Signs of rejection
•Fever above 100 degrees
•Swelling or tenderness over the new liver
•Flu-like feelings
•Clay-colored stools
•Dark, tea-colored urine
•Jaundice (yellow skin or eyes - late sign)
Transplant Rejection
- Rejection can happen at any time, so it’s important to keep up with liver function blood tests to detect signs of rejection
- If caught early, it is generally very treatable
Medications
•Initially 10-15 medications one to four times a day
•By one year, two to six a day
•Immunosuppressive medications -- help prevent rejection of the new liver; taken for life
•Nntibiotics/antivirals -- first 3-6 months after surgery when immunosuppression is highest to prevent viral/bacterial infections
•Antacids -- prevent upset stomach
•Antihypertensives -- may be prescribed to lower blood pressure
•Diuretics-- may be needed to remove fluid
Medications
•Multivitamins, calcium, and vitamin D
•Insulin -- occasionally needed to treat diabetes caused by the prednisone or other immunosuppressive medications
•Cholesterol-lowering drugs -- may be started later high cholesterol occurs
•Iron --prescribed in some cases for low blood counts
•Aspirin -- may be prescribed for narrowing or blood clots in blood vessels supplying the liver
● Inadequate oral intake related to decreased appetite as evidenced by significant weight loss
● Intervention:
● Soft, high protein, high-kcal foods
●One-day Sample Diet
● Breakfast
● 1 cup Hash browns, frozen potatoes
● 1 cup Milk, fat free (skim)
● 2 medium Pancakes, plain
● 3 tablespoon Syrup
• Dinner
• 1 cup Chili beef soup
• 1 piece Cornbread
• Lunch
• 2 regular slice Bread, 100% whole wheat
• ¾ cup canned green beans
• 3 slices Ham
• 1 tablespoon Light Mayonnaise
• ½ slice (1 oz) Cheese, Cheddar or Colby, low fat
• Snacks
• 1 cup, sauce Applesauce, unsweetened
• 1 medium Banana, raw
• 6 oz yogurt, fruit, light
References
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•Judd AM. Lecture slides. Pathophysiology, Brigham Young University, September 20, 2011.
•Gentilini P, Casini-Raggi V, Di Fiore G, Romanelli RG, Buzzelli G, Pinzani M, La Villa G, Laffi G. Albumin improves the response to diuretics in patients with cirrhosis and ascites: results of a randomized, controlled trial. J Hepatology. 1999;30(4):639-645.
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•Hep C Connection. Common Q&A. Available at http://www.hepc-connection.org/default.asp?page=1161. Accessed March 3, 2012.
●References ● The American Liver Foundation. Liver Transplants. Available at http://www.liverfoundation.org/abouttheliver/info/transplant/.
Accessed February 29, 2012.
● The University Hospital. After the Transplant. Available at http://www.theuniversityhospital.com /livertransplant /html/transplantprocess/afterthetransplant.htm. Accessed February 29, 2012.
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● Medline Plus. Bleeding Esophageal Varies. Available at http://www.nlm.nih.gov/medlineplus/ency/article/000268.htm. Accessed March 3, 2012.
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