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I. INTRODUCTION
Present History
Leonida Malto, a 67 year-old mother of four, was admitted at BRTTH last July 1, 2011 at the
Gastro Unit of Medical Ward. She currently resides at Guinobatan, Albay together with thefamily of his third son, and occupies herself as a street vendor to help the family financially. The
written medical diagnosis is T/C Liver Cirrhosis, decompensated, not in PSE. On my interview,
his son claims that the mother is a non-drinker and a non-smoker; but declares that she used to
have her regular diet with high sodium content. This might have been the predisposing factor to
her current diagnosis. Their low financial stability concludes the fact that they cannot afford to
have a balanced-diet, or nutritious meal, everyday. She, being a vendor at day and a care-taker of
her grandchildren at night, may also be the reason why she failed to have achieved a healthier
lifestyle.
In patients with previously stable cirrhosis, decompensation may occur due to various causes,such as constipation, infection, increased alcohol intake, medication, bleeding from esophageal
varices or dehydration. It may take the form of any of the complications of cirrhosis listed above.
Patients with decompensated cirrhosis generally require admission to hospital, with close
monitoring of the fluid balance, mental status, and emphasis on adequate nutrition and medical
treatment - often with diuretics, antibiotics, laxatives and/or enemas, thiamine , and steroids.
Administration of saline is generally avoided as it would add to the already high total body
sodium content that typically occurs in cirrhosis.
Cirrhosis of the liver is a chronic disease that causes cell destruction and fibrosis (scarring) of
hepatic tissue. Fibrosis alters normal liver structure and vasculature, impairing blood and lymph
flow and resulting in hepatic insufficiency and hypertension in the portal vein. Complications
include hyponatremia, water retention, bleeding esophageal varices, Coagulopathy, spontaneous
bacterial peritonitis, and hepatic encephalopathy.
Cirrhosis is a potentially life-threatening condition that occurs when scarring damages the liver.
This scarring replaces healthy tissue and prevents the liver from working normally. Cirrhosis
usually develops after years of liver inflammation. When chronic diseases cause the liver to
become permanently injured and scarred, the condition is called Cirrhosis. Cirrhosis harms the
structure of the liver and blocks the flow of blood. The loss of normal liver tissue slows the
processing of nutrients, hormones, drugs, and toxins by the liver. Also, the production of proteins
and other substances made by the liver is suppressed. People with cirrhosis often have few
symptoms at first. The person may experience fatigue, weakness, and exhaustion. Loss of
appetite is usual, often with nausea and weight loss. As liver function declines, water may
accumulate in the legs and the abdomen (ascites). A decrease in proteins needed for blood
clotting makes it easy for the person to bruise, bleeding or infection. In the later stages of
cirrhosis, jaundice (yellow skin) may occur, caused by the buildup of bile pigment that is passed
by the liver into the intestines. The liver of a person with cirrhosis also has trouble removing
toxins, which may build up in the blood. Drugs taken usually are filtered out by the liver, and
this cleansing process also is slowed down by cirrhosis. People with cirrhosis often are very
sensitive to medications and their side effects. The doctor often can diagnose cirrhosis from the
patient’s symptoms and from laboratory tests. During a physical exam, the doctor could notice a
change in how your liver feels or how large it is. If the doctor suspects Cirrhosis, you will be
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given blood tests. The purpose of these tests is to find out if liver disease is present. In some
cases, other tests that take pictures of the liver are performed such as the computerized axial
tomography (CAT) scan, and ultrasound. The doctor may decide to confirm the diagnosis by
putting a needle through the skin (biopsy) to take a sample of tissue from the liver. In some
cases, cirrhosis is diagnosed during surgery when the doctor is able to see the entire liver.
Development History
Medical History
Upon interview, his son stated that her mother had already been admitted at their district hospital
with the same diagnosis several weeks ago with complaints of onset symptoms like loss of
appetite, weakness, and jaundice. Her mother had stayed for less than a month in the district
hospital before they were advised to transfer to BRTTH.
Social History
On Mrs. Malto’s stay at the Medical Ward, her third son, who was also my interviewee, is the
one who used to stay with her in the hospital even before she was admitted at BRTTH. At times,
her son’s wife took care of her alternately.
II. ANATOMY AND PHYSIOLOGY
The liver is located in the upper right-hand portion of
the abdominal cavity, beneath the diaphragm and on top
of the stomach, right kidney and intestines. The liver, a
dark reddish-brown organ that weighs about 3 pounds,
has multiple functions.
There are two distinct sources that supply blood to the
liver:
oxygenated blood flows in from the hepatic artery
nutrient-rich blood flows in from the portal vein
The liver holds about one pint (13 percent) of the body’s
blood supply at any given moment.
The liver consists of two main lobes, both of which are
made up of thousands of lobules. These lobules are
connected to small ducts that connect with larger ducts to ultimately form the hepatic duct. The
hepatic duct transports the bile produced by the liver cells to the gallbladder and duodenum (the
first part of the small intestine).
The liver regulates most chemical levels in the blood and excretes a product called ―bile,‖ which
helps carry away waste products from the liver. All the blood leaving the stomach and intestines
passes through the liver. The liver processes this blood and breaks down the nutrients and drugs
into forms that are easier to use for the rest of the body. More than 500 vital functions have been
identified with the liver. Some of the more well-known functions include the following:
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Production of bile, which helps carry away waste and break down fats in the small intestine
during digestion.
Production of certain proteins for blood plasma.
Production of cholesterol and special proteins to help carry fats through the body.
Conversion of excess glucose into glycogen for storage. (This glycogen can later beconverted back to glucose for energy.)
Regulation of blood levels of amino acids, which form the building blocks of proteins.
Processing of hemoglobin for use of its iron content. (The liver stores iron.)
Conversion of poisonous ammonia to urea. (Urea is one of the end products of protein
metabolism that is excreted in the urine.)
Clearing the blood of drugs and other poisonous substances.
Regulating blood clotting.
Resisting infections by producing immune factors and removing bacteria from the blood
stream.
When the liver has broken down harmful substances, its by-products are excreted into the bile or
blood. Bile by-products enter the intestine and ultimately leave the body in the feces. Blood by-
products are filtered out by the kidneys, and leave the body in the form of urine.
III. PATHOPHYSIOLOGY
Cirrhosis is characterized by diffuse fibrotic bands of connective tissue that distort the liver’snormal architecture. Inflammation caused by either toxins or disease results in extensive
degeneration and destruction of hepatocytes (liver cells). As cirrhosis develops, the tissue
becomes nodular. These nodules can block lile ducts and normal blood flow throughout the liver.
Flow alterations in the vascular system and lymphatic bile duct channels result from compression
caused by the proliferation of fibrous tissue. In early disease, the liver is usually enlarged, firm
and hard. As the pathologic process continues, the liver shrinks in size.
The liver plays a vital role in synthesis of proteins (e.g., albumin, clotting
factors and complement), detoxification and storage (e.g., vitamin A). In addition, it participates
in the metabolism of lipids and carbohydrates.
Cirrhosis is often preceded by hepatitis and fatty liver (steatosis), independent of the cause. If the
cause is removed at this stage, the changes are still fully reversible.
The pathological hallmark of cirrhosis is the development of scar tissue that replaces
normal parenchyma, blocking the portal flow of blood through the organ and disturbing normal
function. Recent research shows the pivotal role of the stellate cell, a cell type that normally
storesvitamin A, in the development of cirrhosis. Damage to the hepatic parenchyma leads to
activation of the stellate cell, which becomes contractile (called myofibroblast) and obstructs
blood flow in the circulation. In addition, it secretes TGF-β1, which leads to a fibrotic response
and proliferation of connective tissue. Furthermore, it secretes TIMP 1 and 2, naturally occurring
inhibitors of matrix metalloproteinases, which prevents them from breaking down fibrotic
material in the extracellular matrix.
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The fibrous tissue bands (septa) separate hepatocyte nodules, which eventually replace the entire
liver architecture, leading to decreased blood flow throughout. The spleen becomes congested,
which leads to hypersplenism and increased sequestration of platelets. Portal hypertension is
responsible for most severe complications of cirrhosis.
IV. DIAGNOSTIC EVALUATIONS/LABORATORY EXAMS
Liver biopsy – detects destruction and fibrosis of hepatic tissue.
Liver scan – shows abdominal thickening and a liver mass.
CT scan – determines the size of the liver and its irregular nodular surface.
Esophagoscopy – to determine esophageal varices.
Paracentesis – to examine ascetic fluid for cell, protein, and bacterial counts. PTC – differentiates extrahepatic from intrahepatic obstructive jaundice.
Laparoscopy and liver biopsy – permit direct visualization of the liver.
Serum liver function test – results are elevated.
The following findings are typical in cirrhosis:
Aminotransferases - AST and ALT are moderately elevated, with AST > ALT. However,
normal aminotransferases do not preclude cirrhosis.
Alkaline phosphatase - usually slightly elevated.
Gamma-glutamyl transferase – correlates with AP levels. Typically much higher in chronic
liver disease from alcohol.
Bilirubin - may elevate as cirrhosis progresses.
Albumin - levels fall as the synthetic function of the liver declines with worsening cirrhosis
since albumin is exclusively synthesized in the liver
Prothrombin time - increases since the liver synthesizes clotting factors.
Globulins - increased due to shunting of bacterial antigens away from the liver to lymphoid
tissue.
Serum sodium - hyponatremia due to inability to excrete free water resulting from high
levels of ADH and aldosterone.
Thrombocytopenia - due to both congestive splenomegaly as well as
decreased thrombopoietin from the liver. However, this rarely results in platelet count <
50,000/mL.
Leukopenia and neutropenia - due to splenomegaly with splenic margination.
Coagulation defects - the liver produces most of the coagulation factors and thus
coagulopathy correlates with worsening liver disease.
There is now a validated and patented combination of 6 of these markers as non-invasive
biomarker of fibrosis (and so of cirrhosis):FibroTest.
Other laboratory studies performed in newly diagnosed cirrhosis may include:
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Serology for hepatitis viruses, autoantibodies (ANA, anti-smooth muscle, anti-mitochondria,
anti-LKM)
Ferritin and transferrin saturation (markers of iron
overload), copper and ceruloplasmin (markers of copper overload)
Immunoglobulin levels (IgG, IgM, IgA) - these are non-specific but may assist in
distinguishing various causes
Cholesterol and glucose
Alpha 1-antitrypsin
V. MEDICAL AND EVALUATION TREATMENT
VI. DRUG STUDY
Antiviral Medications:
Ribavirin – for treatment of chronic hepatitis C in adult patients
Lamivudine – for treatment of patients with chronic hepatitis B and evidence of hepatitisB virus replication
Entecavir (Baraclude) – for treatment of chronic hepatitis B virus infection in adults with
evidence of active liver inflammation Telbivudine (Sebivo) – for treatment of chronic hepatitis B with evidence of viral
replication and active viral disease
Chronic viral hepatitis B and C may respond to treatment with antiviral medications. These may
include interferon (for hepatitis B and C) or a combination of interferon and ribavirin (hepatitis
C).
For hepatitis C, combination therapy consistently yields higher rates of sustained response than
treatment with just one drug. At present, use of interferon alone is generally reserved for people
who should not use ribavirin. Interferon is given subcutaneously (injected beneath the skin) once
every week. Treatment of hepatitis C usually lasts for 24-48 weeks depending on the HCVgenotype. Ribavirin is an oral antiviral agent that is given twice a day.
Lamivudine, adnovir, entecavir, telbivudine is used to treat hepatitis B infection. It is usually
provided in an oral form that is taken once a day for a year or more. Sometimes these drugs are
combined with interferon.
Possible side effects associated with antiviral use include:
Abdominal or stomach pain (severe)
Feeling of fullness
Nausea
Tingling, burning, numbness, or pain in the hands, arms, feet, or legs
Flu-like symptoms (fever, body aches, chills)
Anti-inflammatory Medications (Corticosteroids)
Azathioprine (Imuran) – to reduce the corticosteroid requirements of renal transplantrecipients, treatment of auto-immune chronic active hepatitis
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Metal Chelating Agent
Deferoxamine (Desferal) – treatment for aldosterone overload for patients with ESRF(under maintenance with dialysis encephalopathy)
Vitamin K
Phytonadione (AquaMEPHYTON, Mephyton)
Bleeding abnormalities are common in cirrhosis. Vitamin K plays an important role in bloodclotting. Because your liver metabolizes this vitamin, liver diseases can affect vitamin K levels
and its ability to function, and thereby alter clotting ability.
Possible side effects associated with vitamin K use include:
Flushing of the face
Redness, pain, or swelling at the site of injection
Unusual taste
Diuretics
*―Loop‖ diuretics:
Bumetanide (Bumex)
Furosemide (Lasix)
*Thiazide diuretics:
Hydrochlorothiazide (HydroDIURIL, Esidrix)
Chlorothiazide (Diuril)
*Potassium-sparing diuretics:
Amiloride (Midamor)
Triamterene (Dyrenium)
Diuretics are used to treat the buildup of excess fluid in the body that occurs with cirrhosis (as
well as other diseases). These drugs act on the kidneys to increase urine output, which reducesthe amount of fluid in the bloodstream. This can help reduce portal vein hypertension and help
alleviate some of the symptoms of cirrhosis, such as fluid accumulation in the abdomen and
legs.
Possible side effects associated with diuretic use include:
Loss of appetite
Nausea and vomiting
Dizziness
Headache
Lethargy
Low or high blood potassium level
Low sodium level
Bleeding from Varices
Octreotide (Sandostatin, Sandostatin LAR)
This drug is often used with endoscopic treatment to treat bleeding from esophageal varices. It
reduces the pressure in the varices. Once started, it is continued five days after bleeding.
Possible side effects associated with the use of this drug include:
Abdominal cramps
Nausea
Vomiting
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Diarrhea
Constipation
Slow heart rate
Hypothyroidism
Greasy stools
Upset stomach
Antihypertensives (Beta-Blockers)
Atenolol (Tenormin)
Metoprolol (Lopressor)
Nadolol (Corgard)
Propranolol (Inderal)
Timolol (Blocadren)
In cirrhosis, these are used to reduce venous blood pressure in the abdomen (called portalhypertension) and thereby reduce the risk of esophageal variceal bleeding and other
complications. These drugs come in capsule, tablet, liquid, and injectable forms.
Possible side effects associated with beta-blocker use include:
Drowsiness and dizziness
Cold sensitivity
Sleep disorders
Laxatives
Beta-galactosidofructose (Lactulose)
Although laxatives are usually prescribed to treat constipation, they can help treat cirrhosis by
absorbing or binding toxins, such as ammonia, in the intestine and remove them from the body.
Not all laxatives are equally effective, and your doctor may be more likely to prescribe beta-
galactosidofructose (Lactulose).
Possible side effects associated with laxative use include:
Diarrhea
Abdominal cramping, flatulence, and bloating
Dehydration and weakness
Multivitamin/Mineral Supplements
Centrum
This may be recommended to help correct any nutrient deficiencies may have developed if dietary intake was reduced because of liver disease. It will also promote healing of damaged
liver tissue.
VII. NURSING CARE MANAGEMENT
Ongoing Assessment
1. Measure I&O, noting positive balance — intake in excess of output. Weigh daily and note
gain more than 0.5 kg/day.
2. Monitor BP and CVP, if available. Note JVD and abdominal vein distention.
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3. Assess respiratory status, noting increased respiratory rate and dyspnea.
4. Auscultate lungs, noting diminished or absent breath sounds and developing adventitious
sounds — crackles.
5. Monitor for cardiac dysrhythmias.
6. Assess degree of peripheral and dependent edema.
7. Measure abdominal girth.
8. Encourage bedrest when ascites is present.
9. Monitor serum albumin and electrolytes, particularly potassium and sodium.
Diet
1. Provide frequent mouth care and occasional ice chips, particularly if NPO; schedule fluid
intake around the clock.
2. Advice to have Soft diet as ordered, taking egg whites in particular.
Possible Complications
The most serious complications are those associated with so-called decompensation, which occur
when cirrhosis progresses. They include the following:
Bleeding and fluid buildup (ascites).
Infections.
Damage to the brain (encephalopathy). Impaired brain function occurs when the liver cannot
detoxify harmful substances.
Liver cancer is also a long-term risk with cirrhosis. Cirrhosis is irreversible, but the rate of
progression can be very slow, depending on its cause and other factors. Five-year survival rates
are about 85% and can be lower or higher depending on severity.
For example, alcoholics with cirrhosis who abstain can have a 5-year or more survival rate of
as high as 85%. For those who continue drinking, the chance for living beyond 5 years is no
higher than 60%.
In patients with hepatitis B or C, the 5-year survival rate after a diagnosis of cirrhosis ranges
between 71 – 85%.
About two-thirds of patients with primary biliary cirrhosis never develop symptoms and can
have a normal life span. Once symptoms of liver damage, such as jaundice, occur, however,
the average survival time declines. In one study of women diagnosed with primary biliary
cirrhosis, about 36% developed symptoms over an 11-year period, and 11% either died or
required liver transplantation.
1. Portal Hypertension
In cirrhosis, liver cell damage slows down blood flow. This causes a backup of blood through the
portal vein, a condition called portal hypertension. The effects of portal hypertension can be
widespread and serious, including fluid buildup and bleeding.
2. Ascites and Fluid Buildup
Ascites is fluid buildup in the abdomen. It is uncomfortable and can reduce breathing function
and urination. Ascites is usually caused by portal hypertension, but it can result from other
conditions. Swelling can also occur in the arms and legs and in the spleen. Although ascites itself
is not fatal, it is a marker for severe progression. Once ascites occurs, only half of patients
survive after 2 years. In fact, some experts refer to the phases of cirrhosis aspreascitic and ascitic.
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Some doctors even believe that ascites signals the need for liver transplantation, particularly in
alcoholic cirrhosis.
3. Variceal Bleeding
One of the most serious repercussions of portal hypertension is the development of varices,which are blood vessels that enlarge to provide an alternative pathway for blood diverted from
the liver. In about two-thirds of patients they form in esophagus. Varices pose a high risk for
rupture and bleeding because of the following characteristics:
They are thin-walled.
They are often twisted.
They are subject to high pressure.
Internal bleeding from these varices (variceal bleeding) occurs in 20 – 30% of patients with
cirrhosis. The risk of death from a single episode can reach 70%.
Bleeding commonly recurs within 2 weeks of the first episode, but after 6 weeks, the risk for
recurrence is the same as for patients who have not had a bleeding event.
Factors that predict variceal bleeding include:
Ascites.
Encephalopathy.
Large veins.
Factors that can increase the danger for a bleeding episode in high-risk individuals include the
following: Moderate to intense exercise.
Bacterial infection.
Certain times of the day. Eating increases portal pressure, and there is a greater risk for
bleeding in the evening. A lesser but still significant risk occurs in the early morning.
It is important for patients to be screened for esophageal varices and treated with preventive beta
blockers if they show signs of risk. Between 30 – 40% of patients with cirrhosis experience
bleeding. This complication has a mortality rate of 20 – 35%. Some experts recommend that all
newly diagnosed patients be screened using endoscopy. Screening should also be considered for
all previously diagnosed patients who have not been screened but would benefit from preventive
treatments.
4. Kidney Failure
Portal hypertension can cause several secondary complications, including kidney failure. Non-
steroidal anti-inflammatory drugs (NSAIDs), such as naproxen, may increase the risk for kidney
failure.
5. Gastrointestinal Bleeding
Gastrointestinal (GI) bleeding can occur from abnormal blood clotting, which can be result of a
combination of complications associated with cirrhosis. They include vitamin K deficiencies and
thrombocytopenia — a drop in platelets (the blood cells that normally initiate the clotting
process). Some research now suggests that thrombocytopenia itself may be associated with more
advanced liver failure.
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6. Infections
Bacterial infections are very common in advanced cirrhosis, and may even increase the risk for
bleeding. Most bacterial infections, including those in the urinary, respiratory, or gastrointestinal
tracts, develop when patients are in the hospital. Abdominal infections are a particular problem
in cirrhosis and occur in up to 25% of patients with cirrhosis within a year of diagnosis.
7. Mental Impairment and Encephalopathy
Mental impairment is a common event in advanced cirrhosis. In severe cases, the disease
causes encephalopathy (damage to the brain), with mental symptoms that range from confusion
to coma and death. A combination of conditions associated with cirrhosis causes this serious
complication:
Buildup in the blood of harmful intestinal toxins, particularly ammonia.
An imbalance of amino acids that affect the central nervous system.
Encephalopathy is often triggered by certain conditions, including:
Gastrointestinal bleeding
Constipation
Excessive dietary protein
Infection
Surgery
Dehydration
Alcoholics with cirrhosis are believed to be at higher risk for this complication than arenonalcoholic cirrhosis, but one study suggested that alcoholics simply tend to have more severe
cirrhosis. Even minimal hepatic encephalopathy (MHE) can have detrimental effects on
functional ability. One study suggested that MHE impairs the ability to safely drive a car, and
that all patients with cirrhosis be tested for MHE.
8. Symptoms of Encephalopathy
Early symptoms of hepatic encephalopathy include forgetfulness, unresponsiveness, and trouble
in concentrating. Sudden changes in the patient’s mental state, including agitation or confusion,
may indicate an emergency condition. Other symptoms include bad fruity-smelling breath and
tremor. Late stage symptoms of encephalopathy are stupor and eventually coma.
9. Hepatorenal Syndrome
Hepatorenal syndrome occurs if the kidneys drastically reduce their own blood flow in response
to the altered blood flow in the liver. It is a life-threatening complication of late-stage liver
disease that occurs in patients with ascites. Symptoms include dark colored urine and a reduction
in volume, yellowish skin, abdominal swelling, mental changes (delirium, confusion), jerking or
coarse muscle movement, nausea, and vomiting.
10. Liver Cancer
Cirrhosis greatly increases the risk for liver cancer, regardless of the cause of cirrhosis. Although
few studies have been conducted on the risk for liver cancer in patients with primary biliary
cirrhosis, one study reported an incidence of 2.3%. About 4% of patients with cirrhosis caused
byhepatitis C develop liver cancer. In Asia about 15% of people who have chronic hepatitis B
develop liver cancer, but this high rate is not seen in other parts of the world. (One Italian study
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that followed a group of hepatitis B patients for 11 years found no liver cancer over that period
of time.)
11. Osteoporosis
About 30% of patients with chronic liver disease develop osteoporosis (loss of bone density),which is twice the usual incidence. Patients with primary biliary cirrhosis have a particularly
high risk for osteoporosis. Treating osteoporosis in patients with cirrhosis can be complicated.
One study found that calcitriol (a form of vitamin D) is especially helpful in preventing bone loss
in patients with cirrhosis.
Osteoporosis is a condition characterized by progressive loss of bone density, thinning of bone
tissue, and increased vulnerability to fractures. Osteoporosis may result from disease, dietary or
hormonal deficiency, or advanced age. Regular exercise and vitamin and mineral supplements
may reduce and even reverse loss of bone density.
12. Insulin Resistance
Nearly all patients with cirrhosis are insulin resistant. Insulin resistance is a primary feature in
type 2 diabetes and occurs when the body is unable to use insulin. This hormone is important for
delivering blood sugar and amino acids into cells and helps determine whether these nutrients
will be burned for energy or stored for future use.
VIII. NCP DISCHARGE PLAN
Medications
Client was advised to take medications regularly at home. Also, not altering the dosage and
schedule of medications was highly emphasized. Having a regular check-up was also
encouraged.
Exercise
In order to promote activity tolerance, Mrs. Malto was encouraged to do alternating periods of
rest and ambulation. Maintaining some periods of bed rest with legs elevated to mobilize edemaand ascites, and, was encouraged to be assisted with gradually increasing periods of exercise.
Health education
To better protect the skin integrity of the client, I advised his son to note and record the degree of
jaundice of skin and sclera and the scratches on her body as well. Also, having frequent skin
care, bathing without soap, and to keep fingernails short were also emphasized.
In connection with her health maintenance, his son was asked to provide written dietaryinstructions; to encourage her daily weighing for self-monitoring of fluid retention depletion;
discussed the adverse effects of diuretic therapy; emphasized the importance of rest, a sensible
lifestyle, and an adequate, well-balanced diet; to be involved to the person closest to the patient
because recovery usually is not easy and relapses are common; and lastly, gave importance of
having continued follow – up for laboratory test and evaluation by a health care provider.
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Diet
To improving nutritional status of the client, patient was encouraged to eat high calorie,
moderate protein meal and to have supplementary feedings. Taking small, frequent feedings andattractive meals in an aesthetically pleasing setting at meal time was also suggested.
IX. REFERENCES
Brunner and Suddarth. Textbook of Medical-Surgical Nursing 12th
Edition.
Cales P, Masliah C, Bernard B, Garnier PP et al. Early Administration of Vapreotide forvariceal Bleeding in Patients with Cirrhosis. New E J Med. 2001;344:23-28 .
Heidelbaugh JJ, Bruderly M: Cirrhosis and Chronic Liver Failure. Part I. Diabnosis and
Evaluation. Am Fam Phy. 2006;74:756-62. Miniño AM, Heron MP, Murphy SL, Kochanek KD. Deaths: Final data for 2004. Centers
for Disease Control and Prevention Web site
National Digestive Diseases Information Clearinghouse
http:/ /www.digestive.niddk.nih.gov
http:/ /www.google.com
http:/ /www.nurseslab.com
http://www.cdc.gov/nchs/data/nvsr/nvsr55/nvsr55_19.pdf
http://www.liverfoundation.org/ . Accessed March 8, 2006.