Liver

Cirrhosis
Ma. Tosca Cybil A.
Torres, RN, MAN

LEARNING OBJECTIVES:
After 2 hours of active lecture 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. Formulate possible nursing diagnoses applicable
for patients with liver cirrhosis
6. Enumerate nursing interventions applicable for
each identified nursing diagnosis
7. Integrate Christian Values in rendering nursing
care for clients with liver cirrhosis
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Liver
Cirrhosis
a chronic, degenerative
disease characterized by
replacement of normal liver
tissue with diffuse fibrosis
that disrupts the structure
and function of the liver

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Liver
Cirrhosis
Types:

a. Alcoholic Cirrhosis ( Laennecs Cirrhosis)

Most common type of liver cirrhosis

Caused by chronic alcoholism

b. Postnecrotic cirrhosis

Late result of a previous bout of acute viral

hepatitis

c. Biliary cirrhosis

Resulted from chronic biliary obstruction

and infection
Least common type

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Liver Cirrhosis
Predisposing/ Precipitating factors:
malnutrition
effects of alcohol abuse
chronic impairment of bile excretion
biliary obstruction in the liver and
common bile duct (gallbladder
stones)
necrosis from hepatotoxins or viral
hepatitis
Congestive heart failure

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Liver Cirrhosis
Pathophysiology:

liver cell damage result in

inflammation & hepatomegaly
attempts at regeneration eventually
result to fibrosis and a small nodular
liver
hepatic function is slowly impaired
obstruction of venous channels
blocks hepatic blood flow and cause
portal hypertension

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Assessment:
Clinical Manifestations

S/Sx - early:

anorexia, nausea, indigestion

aching or heaviness in right
upper quadrant
weakness & fatigue

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Clinical
Manifestations
Late signs:

abnormal liver function tests:

bilirubin (N=0-0.9mg/dl),
AST (N=4.8-19U/L)
ALT (N= 2.4-17U/L)
Serum alkaline phosphatase (N=30-40U/L)
Ammonia (plasma) (N= 15-45umol/L)
intermittent jaundice, pruritus
edema, ascites, prominent abdominal wall veins
Ecchymosis, bleeding tendencies
anemia
Infection
Gynecomastia, testicular atrophy
Neurologic changes
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Complications of Liver
Cirrhosis
1. 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
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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
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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
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infection

Complications of Liver
Cirrhosis
2. 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

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Pathogenesis of Hepatic
Encephalopathy
BRAIN

LIVER

Toxic N2 metabolites
From Intestines

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Encephalopa
thy
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

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Encephalopath
y

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
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speech, dec. attention span)

Complications of Liver
Cirrhosis
3. 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

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

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insertion of SengstakenBlakemore tube

with gastric and esophageal balloon that
are inflated to stop bleeding

Balloon tamponade

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esophageal variceal ligation (EVL)

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Possible Nursing Diagnoses

Activity intolerance R/T fatigue, lethargy, and

malaise
Imbalanced nutrition R/T abdominal distention and
discomfort, and anorexia
Impaired skin integrity R/T pruritus from jaundice
and edema
High risk for injury R/T altered clotting
mechanisms and altered LOC
Disturbed body image R/T changes in appearance,
sexual dysfunction, and role function
Chronic pain R/T enlarged tender liver and ascites
Fluid volume excess R/T ascites and edema
formation
Ineffective breathing pattern R/T restriction of
thoracic excursion secondary to ascites and
abdominal distention
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Nsg. Interventions:
1. Reduce metabolic demands on the liver
provide bed rest
eliminate
ingestion
of
toxic
substances to the liver: sedatives
opiates, alcohol, acetaminophen
activities

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Nsg. Interventions:
2. Provide adequate nutrition & hydration
Low protein, high-carbohydrate, high
calorie, sodium- restricted diet
multiple vitamin therapy
restrict fluids & sodium if there is edema
or ascites
provide mouth care before meals
monitor I/O, daily wt.
3. Prevent infection
encourage good personal hygiene
reverse isolation
assess for signs of infection esp. urinary
encourage deep breathing/position changes
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Nsg. Interventions:
4. Protect pt. from bleeding

monitor urine, stool, gums, skin for signs of

bleeding/ bruising
avoid
injections,
apply
pressure
to
venipuncture sites for at least 5 mins.
Monitor prothrombin time, bleeding time
Teach pt. to use soft toothbrush, avoid
constipation
Prevent scratching from pruritus, proper
skin care
Administer Vit. K as ordered

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Questions?????
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ASSIGNMENT:
Answer situation #4 in critical
thinking exercises, Brunner &
Suddarths Textbook of MedicalSurgical Nursing, 11th Edition,
2009 Page 1341
WRITE your answers in a
whole sheet of yellow paper

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Thank you...