Liver

Cirrhosis
Irish Nicole Dela Cruz
Gessel Ann Boguen

LEARNING OBJECTIVES:
After discussion, the students will be able to:
1. Define liver Cirrhosis
2. Enumerate the different types of liver
cirrhosis
3. Enumerate the predisposing/ contributing
factors of liver cirrhosis
4. Discuss the pathophysiological changes and
clinical manifestations of patients with liver
cirrhosis
5. Discuss the Complications of Liver Cirrhosis
6. Discuss the Nursing Interventions for patients
with Liver Cirrhosis

ANATOMY

Liver
The liver is the largest organ in the body
It consists of 2 lobes and it lies in the upper
quadrant of the abdomen, just below the
diaphragm.
The hepatic artery supplies the liver with about
one third of its blood, while the portal vein
supplies the other two thirds.
The hepatic artery carries oxygenated blood
while the portal vein carries deoxygenated blood.

 The portal vein carries nutrients, metabolites,

and toxins from the digestive organs to the liver
for processing, detoxification, or assimilation.
The vasculature of the liver has been called the
antechamber of the heart
Any process impeding blood flow through the
right atrium of the heart causes liver
engorgement.
Any process impeding blood flow through the
liver causes engorgement of vessels draining
the digestive organs.

 The functional unit of the liver is the liver

lobule, with the hepatocyte being the major
cell.
Each lobule is composed of multiple plates of
hepatic cells. Between the individual cells of
the cellular plate is a venous sinusoid, which
receives blood from the branches of the portal
vein and hepatic artery.
The sinusoids are lined with phagocytic cells
of the reticuloendothelial system (Kupffer
cells). These cells cleanse the blood of
bacteria and other foreign products.
The blood from the venous sinusoids empties
into the central vein and then into the hepatic
vein. The hepatic vein empties into the inferior
vena cava.

LIVER

LIVER FUNCTIONS:

CARBOHYDRATE METABOLISM

Glycogenesis
Glycogenolysis
Storage of glycogen
Conversion of galactose
and fructose to glucose.
Gluconeogenesis
Lipogenesis

 LIPID (FAT) METABOLISM

Oxidation of fatty acids for energy

Formation of most lipoproteins
Synthesis of cholesterol and
phospholipids
Synthesis of fat from proteins and
carbohydrates

 PROTEIN METABOLISM

Deamination of amino acids

Formation of urea for the removal
of ammonia from the body
Formation of plasma proteins
The liver also synthesizes plasma
proteins, such as albumin,
prothrombin, fibrinogen, and
clotting proteins (factors V, VI, VII,
and X).
Biotransformation of substance,
hormones, drugs, and other
chemicals.

 BILE PRODUCTION
The liver normally produces and secretes between
600 and 1200 ml of bile each day.
The basic components of bile are:
Water
Bile salts
Bilirubin
Cholesterol
Fatty acids
Lecithin
Sodium
Potassium
Calcium
Chloride
Bicarbonate ion

 Water is the most abundant

component of bile, followed by bile
salts.
Because bile is concentrated in the
gall bladder, this water and a large
portion of the electrolytes are
reabsorbed
by
the
gallbladder
mucosa.
Bile salts are produced by the liver in
a quantity of about 0.5 g a day. The
precursor of these bile salts is
cholesterol, supplied either by the
diet or synthesized by the liver
through fat metabolism.

 Bile salts function in two ways:

They function in emulsifying
or detergent function,
They help in the absorption of
fatty acids, monoglycerides,
cholesterol, and other lipids
from the intestine.

 The next most abundant component

of bile is bilirubin. Bilirubin, an
orange-yellow or greenish yellow
pigment in the bile, is the product of
hemoglobin breakdown.
Cholesterol, a precursor of bile acid,
may precipitate unless enough bile
salts are present to keep it in
suspension. When the balance of
cholesterol, lecithin, and bile salts is
disturbed, cholesterol or other
components may precipitate and form
gallstones.

 The liver continuously secretes bile, which

is then stored in the gallbladder until it is
needed in the duodenum for digestion. The
bladder can hold only 20 to 60 ml of bile at
a time; however, up to 450 ml is produced
in about 12 hours. The gallbladder can
manage this amount because water, Na,
chloride and most small electrolytes are
reabsorbed by the gallbladder mucosa. This
process concentrates the bile from 5 to 20
times.
The gallbladder continues to store the bile
until fatty foods enter the small intestine and
stimulate the release of cholecystokinin.

The sphincter of Oddi must relax

completely if adequate emptying is to occur.
There are three mechanisms that help this
occur:
Cholecystokinin has a weak relaxant
effect on the sphincter
Rhythmic contractions of the gallbladder
wall transmit peristaltic waves down the
common bile duct to the sphincter,
leading to partial relaxation.
Relaxation phases of intestinal peristaltic
waves cause the greatest relaxation of
the sphincter and the intestinal wall.

Bilirubin Metabolism
Bilirubin is a byproduct of the heme portion of red blood
cells and is released when these cells are destroyed.
The released bilirubin is not water soluble
(unconjugated). Unconjugated bilirubin is carried in
the blood bound to albumin and other proteins.
The liver extracts the unconjugated bilirubin from the
blood and combines it with glucoronide into a water
soluble form (conjugated).
The conjugated bilirubin is secreted into the bile and
then enters the duodenum. In the GI tract, bilirubin is
metabolized to urobilinogen.
Urobilinogen is excreted in feces as stercobilin, giving
feces its brown color, or it is reabsorbed. Most of the
reabsorbed urobilinogen is extracted from the body by
the liver and recycled; some is excreted in the urine.

 BLOOD
RESERVOIR/CIRCULATORY
FUNCTION
THE liver processes more than 1000 ml of
blood a minute circulating through its
sinusoids from the portal vein, and more than
350 ml of blood a minute from the hepatic
artery.
Blockage within the portal venous system, often
caused by cirrhosis, leads to increased
pressures within the system, called portal
hypertension. The result is an increase in
pressure in the venous system draining into the
liver, with subsequent distention and a decrease
in the flow of blood from the liver to the heart.

 DETOXIFICATION
Steroid hormones (estrogen, progesterone,
testosterone, and aldosterone) are inactivated by
the liver. Liver disease may depress this
inactivation, resulting in pathologic levels of these
hormones.
The liver detoxifies many drugs; all barbiturates
(except Phenobarbital and barbital) and many
sedatives are inactivated by the liver.
The status of the liver has an important role in the
effectiveness or toxicity of these and other drugs.

Cirrhosis of
the liver

 Cirrhosis of the liver is the term applied to

chronic disease of the liver characterized
by diffuse inflammation and fibrosis of
the liver resulting in drastic structural
changes and significant loss of liver
function.
The basic changes in cirrhosis are liver
cells death and replacement of normal
tissue by regeneration of cell mass and
scar tissue that results in nodules of
normal liver parenchyma surrounded by
fibrous tissue. These changes result in
loss of function and distortion of the
structures with a resultant obstruction of
hepatic blood flow.

TYPE

ETIOLOGY

DESCRIPTION

LAENNECS CIRRHOSIS Alcoholism

(nutritional,
portal,
or Malnutrition
alcoholic cirrhosis)

Massive collagen formation; liver

in early fatty stage is large and
firm; in late state it is small and
nodular

POSTNECROTIC
CIRRHOSIS

Massive necrosis from

hepatotoxins, usually viral
hepatitis

Liver is decreased in size with

nodules and fibrous tissue

BILIARY CIRRHOSIS

Biliary obstruction in liver and Chronic impairment of bile

CBD
drainage; liver is first large then
becomes firm and nodular;
jaundice is major symptom

CARDIAC CIRRHOSIS

Right-sided CHF

NONSPECIFIC,
METABOLIC CIRRHOSIS

Metabolic problems,
diseases, GI diseases

Liver is swollen and changes are

reversible if CHF is treated
effectively; some fibrosis occurs
with long standing CHF
infectious Portal and liver fibrosis may
develop; liver is enlarged and
firm.

Pathophysiology
Lannecs
Cirrhosis

Alcohol
Abuse
Malnutrition

Destruction of
Hepatocytes
Postnecrotic
Postnecrotic
Cirrhosis
Cirrhosis

Infection
Drugs

Fibrosis/scarring
Biliary
Cirrhosis

Cardiac
Cirrhosis

Biliary
Obstruction

Right sided
heart failure

Obstruction of blood flow

Increased pressure in the venous
and sinusoidal channels

PORTAL HYPERTENSION
Hepatosplenomegaly
Caput medusae
Spider Angioma
Palmar erythema
Ascites

RELATIONSHIP BETWEEN NORMAL LIVER

FUNCTIONS AND ALTERED FUNCTIONS
ASSOCIATED WITH LIVER:
NORMAL FUNCTION OF THE LIVER:
Maintenance of normal size and drainage of
blood from GI tract
Liver inflammation venous congestion of GI
tract altered GI functions GI symptoms
Metabolism of CHO
Increased glycogenesis and decreased
glycogenolysis and gluconeogenesis altered
glucose metabolism decreased energy

 Metabolism of fats

Increased fatty acid and

triglyceride synthesis and
decreased fatty acid oxidation
and triglyceride release 1.
Fatty liver hepatomegaly
2. Decreased energy
production; weight loss

 Protein metabolism
Decreased production of albumin
decreased colloidal osmotic pressure
edema and ascites
Decreased production of clotting factors
altered clotting studies bleeding
tendencies blood loss anemia
Decreased protein synthesis in general
alteration in immune function and alteration
in healing.

Bile production
Obstruction to bile flow decreased fat
absorption decreased vitamin K absorption
decreased clotting factors bleeding/blood
loss

Bilirubin metabolism
Decreased uptake of bilirubin from circulation
increased unconjugated bilirubin jaundice,
pruritus, scratching, and skin lesions
Decreased conjugated and release of bilirubin
increased conjugated bilirubin and increased
urine bilirubin jaundice, pruritus, scratching,
and skin lesions
Decreased excretion of bilirubin to bowel light
colored stools (clay or grayish-white)
Decreased reuptake of urobilinogen urine
urobilinogen dark urine

Clinical
Manifestations

ASSESSMENT

PATHOPHYSIOLOGIC BASES

Emaciation, ascites

Malnutrition, portal hypertension,

hypoalbuminemia, and hyperaldosteronism

Splenomegaly
Lower leg edema

Portal hypertension
Hypoalbuminemia, hyperaldosteronism,
and pressure of massive ascites
obstructing venous return from legs

Prominent abdominal wall veins (caput

medusae)

Collateral vessels bypass scarred liver to

carry portal blood to superior vena cava;
portal hypertension causes dilation

Internal hemorrhoids

Superior rectal veins dilate with pressure of

portal hypertension

Palmar erythema, spider nevi, altered hair

distribution; amenorrhea, atrophy of
testicles, gynecomastia
Bleeding tendency, especially
gastrointestinal

Probably decreased hormone metabolism

in liver, resulting in manifestations of
estrogen excess
Hypoprothrombinemia, thrombocytopenia;
portal hypertension and esophageal
varices; peptic ulcers common in
alcoholism

Anemia

GI blood losses; erythrocyte

destruction in enlarged spleen; folic
acid deficiency due to inadequate diet

Renal failure

Rapidly failing hepatic function;

occasionally precipitated by volume
depletion; hepatorenal syndrome

Infections

Leukopenia due to enlarged, overactive

spleen; bacteria in portal blood bypass
liver, so not removed by Kupffer cells
Ammonia, no longer removed by liver,
accumulates to levels toxic to brain

Encephalopathy

Chronic viral, toxic, or alcoholic

hepatitis progressing to cirrhosis may
have inflammatory exacerbations

Initial or recurrent symptoms of

hepatitis (jaundice)
Esophageal varices

Collateral veins in esophagus bypass

scarred liver to carry portal blood to
superior vena cava; portal hypertension
causes dilation

DIAGNOSTIC TESTS

The patient with cirrhosis will have

various abnormalities in blood and urine
laboratory data, such as:
Increased levels of total, unconjugated and
conjugated bilirubin
Increased urine bilirubin
Increased urine urobilinogen
Increased prothrombin time
Decreased platelets, WBC and RBCs
Decreased serum albumin and serum
glucose
Hypokalemia
Hyponatremia
Elevated levels of serum enzymes (ALT, AST,
LDH, and alkaline phosphatase)

 Other studies such as liver biopsy, CT

scan, endoscopy, barium contrast,
angiography, and so on may be done if the
clinical manifestations are vague or
inconsistent.

MEDICAL MANAGEMENT:

THREE goals guide the medical

management of a client with cirrhosis:
Maximization of liver function
Prevention of infection:
Control of disabling complications:

Therapy will depend on the signs and

symptoms the patient exhibits and
may include the following:

Antihistamines
Potassium
Diuretics
Folic acid, thiamine, and other vitamins and
minerals

Sodium and fluids are also usually

restricted.
Occasionally albumin may be given
for hypoalbuminemia, however its
effects last only a short time.
If ascites causes severe distress,
paracentesis may be done.

NURSING
INTERVENTIONS

 SUPPORTING RESPIRATION
The patient with cirrhosis has decreased resistance
to infection and may be particularly prone to
respiratory infection, because of the presence of a
hydrothorax and/or shallow breathing. The patient
may experience dyspnea because of pressure on
the diaphragm from ascites.
A high fowlers position may assist respiratory
exchange.
The patient who is in bed rest should be
encouraged to turn frequently and to take deep
breaths to prevent stasis of secretion
Hydrothorax is sometimes treated with
thoracentesis. The nurse should prepare the patient
for this pressure, assist with the procedure, and
monitor the patients response during the procedure
and afterwards.

 CONTROLLING FATIGUE
Patients with cirrhosis will have various levels of
fatigue. The amount and type of activity encouraged
will depend on the individuals energy level, level of
consciousness and coordination, and whether any
sequelae to cirrhosis are present.
If the patient has severe fluid excess and ascites or
signs and symptoms of other sequelae, bed rest is
required. When bed rest is required, special attention
to skin care is necessary, particularly if the patient
also has severe peripheral edema.
If bedrest is not required, the patient should be
gotten up and ambulated within the room or hall as
tolerated. Level of tolerance is based on the patients
statement about the level of fatigue and pulse
changes (pulse should not increase by more than 10
beats above baseline).

 MAINTAINING FLUID AND ELECTROLYTE

BALANCE
Potassium
replacement
will
be
given
for
hypokalemia. It is usually given orally, and the nurse
should monitor the patients serum potassium value
to verify that the patient is not developing
hyperkalemia. Some patients with cirrhosis have
decreased renal function, which impairs the excretion
of potassium and can develop hyperkalemia quite
rapidly.
Sodium imbalance and ascites are treated in several
ways. Restriction of sodium aids greatly in limiting the
formation of ascitic fluid. The basis for determining
the amount of dietary restriction necessary to reduce
sodium and water retention may initially be a
collection of urine for 24 hours to determine sodium
loss. Sodium is generally restricted to 1 g daily. The
sodium restriction along with bed rest may be enough
to relieve the ascites and edema.

 If bed rest and sodium restriction do not improve

ascites, diuretics may be used. Spironolactone is
frequently used.
Fluid restriction will be used if hyponatremia
secondary to fluid retention is present. Fluid
restriction is monitored closely because it may
lead to decreased output and the hepatorenal
syndrome. When fluids are restricted, the nurse
must work with the patient to provide fluids that
are tolerated best and to spread the allotted fluids
throughout the total 24 hours.
Daily weights are required.
Measurement of abdominal girth assists in
determining the gross amount of abdominal
swelling. Patients need to be taught the
importance of monitoring and reporting weight
gain or rapid increase in abdominal girth after
discharge.

 ASSISTING THE PATIENT TO AVOID

ALCOHOL
A major nursing focus for many patients is
helping them to deal with alcoholism.
Helping the patient cope with alcohol requires
that the patient trust that the health team is
interested in their well-being.

 PREVENTING INFECTION
Proper handwashing.
Observing sterile technique with all invasive
procedures, respiratory preventive care, and
avoidance of contact with persons with
infections.
The patient must be monitored carefully for
presence of infection, and any increase in
temperature should be reported immediately
so that appropriate measures can be taken.

 PREVENTING BLEEDING AND FALLS

Nursing care should focus on monitoring for the presence of
bleeding and instituting measures that decrease the risk of
bleeding from trauma or injury to vertices.

Monitoring to detect bleeding:

Monitor urine and stool for blood
Checks the patients body daily for purpura, hematomas,
and petechiae
Check mouth, especially gums, carefully for signs of
bleeding
Check vital signs at least every 4 hours
Monitor prothrombin time, partial thromboplastin time, and
thrombocyte count frequently.

 Measures to decrease risk of bleeding in persons

with cirrhosis:
Avoid all IM and SQ injections, if possible.
Use the smallest gauge needle possible when giving
an injection
Apply pressure to injection sites and venous puncture
sites for at least 5 minutes and to arterial sites for at
least 10 minutes
Give vitamin K as ordered
Use or instruct patient to use a soft-bristled
toothbrush or cotton swabs for oral hygiene.
Instruct patient not to strain at stool and to avoid
vigorous blowing of nose or coughing.
Instruct patient to avoid foods that can traumatize
esophageal varices
Provide assistance to avoid falls
Make sure that room is free of clutter, that floors are
dry, and that shoes or slippers are worn to avoid
injuries.

 PROMOTING NUTRITION
Most patients with cirrhosis will require a wellbalanced high protein, high-CHO diet with
adequate vitamins to provide nutrients for
repair of the liver.
When nausea is problem, antiemetics should
be given 30 minutes before meals to help
increase food tolerance.
Frequent oral hygiene and a pleasant
environment should be provided to help
increase food intake.
The patients food preference should be
incorporated into the diet.
Foods should be served in small, frequent
amounts.

 CONTROLLING PRURITIS
Use of cool, light, nonrestrictive clothing and
avoidance of clothes or blankets made of wool.
Use a soft, dry, clean bedding; use of warm,
not hot, tub baths
Application of emollient creams and lotions to
dry skin.
Avoidance of activities that promote sweating
and increase body temperature.
Maintenance of cool environment
Administration of antihistamines as ordered
Use of diversional activities such as reading,
television, and radio to reduce the patients
perception of pruritus.

 PROMOTING A POSITIVE SELF

ESTEEM
Involving the patient in goal setting. Allowing
the patient to make as many decisions as
possible
Giving positive feedback for accomplishments
Supporting the patient in times of failure
whatever the failure mig8ht be, including
conflicts with family of friends or participation
in drinking
Helping the patient recall past
accomplishments
Helping significant others provide positive
feedback

 PROVIDING SKIN CARE

Because of pruritus, malnutrition, and the
edema often associated with cirrhosis, the
patient is prone to skin lesions and decubitus
formation.
Preventive nursing care to avoid skin
breakdown, such as mattresses, frequent
turning, backrubs, and massage of bony
prominences should be instituted.

PORTAL HYPERTENSION:
Structural damage
Portal vascular system may become
obstructed
Rise in portal venous pressure
hypertension.

portal

splenomegaly
ascites
Cause the development of collateral channels of
circulation that bypass the obstruction. Collateral
channels are most likely to occur in the paraumbilical
and the hemorrhoidal veins, and at the cardia of
stomach extending into the esophagus.

MANAGEMENT:
The nursing and medical
management of portal hypertension is
directed first to treatment of the
consequence of portal hypertension;
ascites and esophageal varices.
The only way to achieve permanent
lowering of portal pressure is surgical
treatment to reduce blood flow
through the obstructed portion of the
portal system.

DECOMPRESSION OPERATIONS FOR

PORTAL HYPERTENSION:
End-to-side portacaval shunt
Splenorenal shunt
Distal splenorenal shunt

Ascites
abnormal intraperitoneal
accumulation of watery
fluid containing small
amounts of protein
due to:

intravascular colloidal
pressure
capillary hydrostatic
pressure
Na and H2O retention
Failure of the liver to
metabolize aldosterone

Ascites
S/sx:
abdominal enlargement, wt.
fatigue
abdominal discomfort, respiratory
difficulty
Med. Mgt. (depending on severity of
ascites)
Na+ & fluid restriction (500-1000 ml/day)
diuretic therapy (furosemide/
spironolactone)
Paracentesis for diagnosis or when fluid
volume compromise comfort & breathing

Ascites
Nursing Interventions to ascites & increase/promote
comfort
maintain on bed rest
fluid & Na restriction
monitor I/O, daily wt.
measure abd. girth every shift
maintain on high-Fowlers for max. respiration
support abdomen with pillows
administer diuretics, salt-poor albumin IV as
ordered
- monitor for signs of CHF, pulmonary
edema, dehydration,
electrolyte imbalance, hypersensitivity reaction
Assist with Paracentesis
have the client void before the procedure
high fowlers position during the procedure
monitor pt. for hypovolemia & electrolyte imbalance
observe puncture wound for leakage & signs of
infection

Complications of Liver
Cirrhosis
Hepatic Encephalopathy

cerebral dysfunction assoc. with

severe liver disease
inability of the liver to metabolize
substances that can be toxic to
the brain such as ammonia, which
is produced by the breakdown of
protein in the intestinal tract

Hepatic
Encephalopathy
S/Sx:
Asterixis- flapping hand tremors ---early sign
LOC lethargy progressing to coma
mental status, confusion, disorientation
dullness, slurred speech
behavioral changes, lack of interest in grooming/
appearance
twitching, muscular incoordination, tremors
Fetor hepaticus
elevated serum ammonia level

Hepatic
Encephalopathy
Interventions:
a. ) ammonia production
dietary protein to 20-40 g/day, maintain adequate
calories
ammonia formation in the intestine give laxative,
enema as ordered and Neomycin - bacterial
ammonia production
b.) Protect pt. from injury
side rails up
turning to side
assess mental status, LOC
proper positioning (semi-Fowlers)
prevent aspiration
c.) Prevent further episodes of encephalopathy
low protein diet
prescribed medications
avoid constipation ( to ammonia production by
bacteria in the GIT)
early signs of encephalopathy (restlessness, slurred
speech, dec. attention span)

Esophageal Varices
distention of the smaller blood vessels of the
esophagus as a result of portal hypertension
due to obstruction of venous circulation w/in
the damaged liver
the portal venous pressure causes blood to
be forced into these vessels become tortous
and fragile
blood vessel become prone to injury by
mechanical trauma from ingestion of coarse
food and acid pepsin erosion which may result
in bleeding
bleeding may also occur as a result of
coughing, vomiting, sneezing, straining at stool
or any physical exertion that abdominal
venous pressure

Esophageal
Varices
S/Sx:
upper GI bleeding
(hematemesis)
- melena
massive hemorrhage
signs/symptoms of
hypovolemic shock

Esophageal Varices
Medical Management:
find the source of bleeding esophagoscopy,
angiography
control bleeding
a. Gastric lavage, administration of antacid
via NGT
b. Surgical bypass procedures (splenorenal
shunt)
c. Variceal band ligation (esophageal
variceal ligation (EVL))
d. Endoscopic sclerotherapy or injection
sclerotherapy
e. Balloon tamponade

insertion of SengstakenBlakemore tube

with gastric and esophageal balloon that
are inflated to stop bleeding

Diagnostic Tests
These include routine liver function
tests such as serum enzymes,
bilirubin, and albumin to establish the
presence of cirrhosis and
esophagoscopy, angiography, or
barium studies to identify the
presence of esophageal varices.

Balloon tamponade

esophageal variceal ligation (EVL)

INTERVENTIONS
Medical Management
The first priority in medical management is to
establish the source of GI bleeding.
Esophagoscopy is the major diagnostic tool,
and if this isnt possible, angiography is used.
If severe hemorrhage is not present, barium
studies or scans may be used.
After diagnosis, the first line of therapy is to
control bleeding and replace blood volume.

 Bleeding may be controlled with:

Gastric lavage

If the hemorrhage is considered

to be minor, introduction of a
nasogastric tube by the nurse or
physician and administration of
an antacid through the tube may
be sufficient to control the
hemorrhage.
The NGT removes gastric
secretions, and antacids
neutralize gastric acid that may
irritate esophageal varices.

 Pharmacological management

Vasopressin is given intravenously

mixed in 120 or 200 ml of dextrose
either on an intermittent basis or
as a continuous infusion.
It lowers portal pressure by
causing splanchnic
vasoconstriction and can thus stop
or control esophageal bleeding.
Propranolol (inderal), a beta
adrenergic blocking agent, has
been shown to decrease
esophageal bleeding in some
patients.

 Injection sclerotherapy

For emergency treatment of varices and

longer-term control or for control and
prevention of rebleeding in patients who
may not be candidates for surgery,
injection sclerotherapy may be used.
In this procedure a fiberoptic endoscope
is introduced into the esophagus by the
physician; and once the bleeding is
identified, a sclerosing agent (sodium
morrhuate, 5 ml) is injected into the
varices.

 This agent causes thromboses

and sclerosis of the vessel and
should result in hemostasis in 3 to
5 minutes.
If hemostasis does not occur, a
second injection may be given.
Before the procedure the patient
and SO need an explanation of
the procedure, and the patient
should receive nothing by mouth
for at least 6 hours.
A mild sedative and a local
anesthetic will be given

 After the procedure the

nurse will monitor the patient
for complications
Perforated esophagus
Aspiration pneumonia
Pleural effusion
Worsening of ascites

 Balloon tamponade of varices

Surgery- ligation and shunts

Nursing care:

Explain procedure and provide

continued support to patient
during the procedure
Monitor v/s every 15 minutes
until blood pressure is stable
and then monitor hourly or
every 2 hours

Measure and record

pressures in the esophageal
balloon every hour; maintain
pressure at prescribed level
Ensure that patient does not
pull on the tube
Provide care to mouth and
nares every 1 to 2 hours

If iced solutions are used in the

balloons, report patient chilling to the
physician who may then order a
warming blanket.
Record intake and output; test GI
output for occult blood
Consult physician concerning
permissible patient movement;
passive ROM is usually allowed
Provide comfort measures(rub back,
change patients position)

Nsg. Interventions:
1.
2.
3.
4.
5.
6.

Promote rest
Diet
Skin Care
Prevent trauma/injury
Protect client from infection
Minimize shortness of breath due to
ascites
7. Relieve ascites
8. Prevent rupture of esophageal varices
9. Control Hemorrhage
-Beta adrenergic blocking agents
-Balloon tamponade
-Sclerotherapy
-Portasystemic shunt
10. Reduce Ammonia formation

THANK
YOU!