Introduction
Injury to the cellular structure of the liver causes fibrosis due to chronic inflamma-
tion and necrotic changes, resulting in cirrhosis. There are nodular changes to the
liver. The bile ducts and blood vessels through the liver may become blocked due
to both the nodular changes and fibrosis. These changes to the liver cause enlarge-
ment of the organ and change in texture. There is increased pressure within the
portal vein. This causes resistance to blood flow throughout the venous system in
the liver and also backs up venous blood to the spleen, causing enlargement of this
organ also. Damage to the liver may be reversible if the cause if identified early and
removed. The most common causes of cirrhosis include chronic alcohol use, liver
damage secondary to exposure to drugs or toxins, viral hepatitis (especially hepati-
tis B, hepatitis C, and hepatitis D in those already infected with hepatitis B), fatty
liver (steatohepatitis), autoimmune hepatitis, cystic fibrosis, metabolic disorders
(excess iron storage—hemachromatosis), or genetic causes.
PROGNOSIS
As cirrhosis progresses, the patient may develop encephalopathy and coma. Early
signs and symptoms of encephalopathy include altered level of consciousness,
neuromuscular changes, and elevated serum ammonia levels.
SIGNS AND SYMPTOMS
• Initially asymptomatic
• Weakness, fatigue due to chronic disease
• Muscle cramps
• Weight loss
• Anorexia
• Nausea with possible vomiting
• Ascites—the accumulation of fluid within the abdominal cavity due to por-
tal hypertension
• Abdominal pain
• Portal hypertension
• Pruritus (itching)
• Ecchymosis (bruises) or petechiae (small, pinpoint, round, reddish purple
marks)
• Coagulation defects due to problems with vitamin K absorption, causing
problems with production of clotting factors
• Amenorrhea
• Impotence due to inactivity of hormones
• Gynecomastia
• Jaundice due to problems with excretion of bilirubin
• Hepatomegaly (enlarged liver) in over one-half of the patients
TREATMENT
• Low-sodium diet; adequate calorie intake.
• Restrict fluid intake if hyponatremic (low serum sodium) or fluid overloaded.
• Restrict alcohol intake to prevent further damage.
• Administer vitamin supplements—folate, thiamine, multivitamin.
• Administer diuretics to reduce excess fluids:
• furosemide
• spironolactone
• Paracentesis to remove ascitic fluid.
• Monitor electrolytes for imbalance.
• Monitor coagulation profile (PT, PTT, INR).
• Administer lactulose to promote removal of ammonia in the gut.
• Administer antibiotics to destroy the normal GI flora which decreases pro-
tein breakdown and the rate of ammonia production:
• neomycin sulfate
• metronidazole
• Shunt placement:
• Peritoneovenous—moves ascitic fluid from abdomen to superior vena
cava.
• Portocaval—diverts venous blood flow from liver to decrease portal and
esophageal pressures.
• Transjugular intrahepatic portal systemic—nonsurgical procedure per-
formed in interventional radiology—sheath placed into jugular and hepatic
vein; needle threaded through sheath and pushed into portal vein through
the liver; balloon enlarges the tract and stent maintains.
• Gastric lavage.
• Esophagogastgric balloon tamponade for control of bleeding from esophageal
varices.
• Administer blood products as needed for patients with bleeding esophageal
varices.
• Sclerotherapy for esophageal variceal bleeding.
NURSING DIAGNOSES
• Ineffective breathing pattern
• Excess fluid volume
• Risk for infection
NURSING INTERVENTION
• Monitor intake and output.
• Monitor vital signs.
• Weigh patient daily.
• Measure abdominal girth—making sure to measure at level of umbilicus for
consistency; marks are typically made at sides of abdomen to align tape meas-
ure on subsequent days.
• Assess peripheral edema.
• Assess heart and lung sounds for excess fluid.
• Elevate head of bed 30 degrees or greater to ease breathing.
• Elevate feet to decrease peripheral edema.
• Monitor for signs of bleeding or bruising.
• Monitor level of consciousness, orientation, recent and remote memory, be-
havior, mood, and affect.
Injury to the cellular structure of the liver causes fibrosis due to chronic inflamma-
tion and necrotic changes, resulting in cirrhosis. There are nodular changes to the
liver. The bile ducts and blood vessels through the liver may become blocked due
to both the nodular changes and fibrosis. These changes to the liver cause enlarge-
ment of the organ and change in texture. There is increased pressure within the
portal vein. This causes resistance to blood flow throughout the venous system in
the liver and also backs up venous blood to the spleen, causing enlargement of this
organ also. Damage to the liver may be reversible if the cause if identified early and
removed. The most common causes of cirrhosis include chronic alcohol use, liver
damage secondary to exposure to drugs or toxins, viral hepatitis (especially hepati-
tis B, hepatitis C, and hepatitis D in those already infected with hepatitis B), fatty
liver (steatohepatitis), autoimmune hepatitis, cystic fibrosis, metabolic disorders
(excess iron storage—hemachromatosis), or genetic causes.
PROGNOSIS
As cirrhosis progresses, the patient may develop encephalopathy and coma. Early
signs and symptoms of encephalopathy include altered level of consciousness,
neuromuscular changes, and elevated serum ammonia levels.
SIGNS AND SYMPTOMS
• Initially asymptomatic
• Weakness, fatigue due to chronic disease
• Muscle cramps
• Weight loss
• Anorexia
• Nausea with possible vomiting
• Ascites—the accumulation of fluid within the abdominal cavity due to por-
tal hypertension
• Abdominal pain
• Portal hypertension
• Pruritus (itching)
• Ecchymosis (bruises) or petechiae (small, pinpoint, round, reddish purple
marks)
• Coagulation defects due to problems with vitamin K absorption, causing
problems with production of clotting factors
• Amenorrhea
• Impotence due to inactivity of hormones
• Gynecomastia
• Jaundice due to problems with excretion of bilirubin
• Hepatomegaly (enlarged liver) in over one-half of the patients
TREATMENT
• Low-sodium diet; adequate calorie intake.
• Restrict fluid intake if hyponatremic (low serum sodium) or fluid overloaded.
• Restrict alcohol intake to prevent further damage.
• Administer vitamin supplements—folate, thiamine, multivitamin.
• Administer diuretics to reduce excess fluids:
• furosemide
• spironolactone
• Paracentesis to remove ascitic fluid.
• Monitor electrolytes for imbalance.
• Monitor coagulation profile (PT, PTT, INR).
• Administer lactulose to promote removal of ammonia in the gut.
• Administer antibiotics to destroy the normal GI flora which decreases pro-
tein breakdown and the rate of ammonia production:
• neomycin sulfate
• metronidazole
• Shunt placement:
• Peritoneovenous—moves ascitic fluid from abdomen to superior vena
cava.
• Portocaval—diverts venous blood flow from liver to decrease portal and
esophageal pressures.
• Transjugular intrahepatic portal systemic—nonsurgical procedure per-
formed in interventional radiology—sheath placed into jugular and hepatic
vein; needle threaded through sheath and pushed into portal vein through
the liver; balloon enlarges the tract and stent maintains.
• Gastric lavage.
• Esophagogastgric balloon tamponade for control of bleeding from esophageal
varices.
• Administer blood products as needed for patients with bleeding esophageal
varices.
• Sclerotherapy for esophageal variceal bleeding.
NURSING DIAGNOSES
• Ineffective breathing pattern
• Excess fluid volume
• Risk for infection
NURSING INTERVENTION
• Monitor intake and output.
• Monitor vital signs.
• Weigh patient daily.
• Measure abdominal girth—making sure to measure at level of umbilicus for
consistency; marks are typically made at sides of abdomen to align tape meas-
ure on subsequent days.
• Assess peripheral edema.
• Assess heart and lung sounds for excess fluid.
• Elevate head of bed 30 degrees or greater to ease breathing.
• Elevate feet to decrease peripheral edema.
• Monitor for signs of bleeding or bruising.
• Monitor level of consciousness, orientation, recent and remote memory, be-
havior, mood, and affect.
