Lewis: Medical-Surgical Nursing, 7th Edition
Answer Guidelines for Case Studies in Textbook
Chapter 44: Nursing Management: Liver, Pancreas, and Biliary Tract
Problems
Cirrhosis of the Liver
1. Possible causes of cirrhosis include alcohol abuse, complication of hepatitis, chronic biliary
obstruction and infection, and long-standing severe, right-sided heart failure. Mr. Begay’s
cirrhosis is likely the result of his 20-year history of heavy drinking. Based on this history Mr.
Begay’s cirrhosis is alcoholic (previously called Laënnec’s), which is also called portal or
nutritional cirrhosis.
2. The first change in the liver from excessive alcohol intake is an accumulation of fat in the liver
cells. The liver cells attempt to regenerate, but the regenerative process is disorganized, resulting
in abnormal blood vessel and bile duct architecture. The overgrowth of new and fibrous
connective tissue distorts the liver’s normal lobular structure, resulting in lobules of irregular size
and shape with impeded blood flow. Eventually, irregular, disorganized regeneration; poor
cellular nutrition; and hypoxia caused by inadequate blood flow and scar tissue result in
decreased functioning of the liver.
Uncomplicated fatty changes in the liver are potentially reversible if the person stops drinking
alcohol. If the alcohol abuse continues, widespread scar tissue formation occurs throughout the
liver.
3.
• A thin and malnourished state in liver failure results from the anorexia, dyspepsia, and nausea
and vomiting caused by altered metabolism of carbohydrates, fats, and protein by the liver.

Ascites and peripheral edema develop as a result of several mechanisms. Portal
hypertension causes leakage of proteins from the blood vessels into the lymph
spaces in the liver tissue. When the lymphatic system is unable to carry off the
excess proteins and water, they leak through the liver capsule into the peritoneal
cavity. The osmotic pressure of the proteins pulls additional fluid into the
peritoneal cavity, creating ascites.

Hypoalbuminemia resulting from impaired liver synthesis of albumin also
contributes to ascites and peripheral edema by decreasing colloidal osmotic
pressure.
Copyright © 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Answer Guidelines for Case Studies in Textbook

44-2
Hyperaldosteronism resulting from impaired liver metabolism of aldosterone also
contributes to ascites and edema by causing increased sodium reabsorption by the
renal tubules. The retention of sodium, as well as an increase in antidiuretic
hormone (ADH), causes additional water retention in the patient with liver
failure.

Jaundice of the sclera and skin results from functional derangement of liver cells
and compression of bile ducts by connective tissue growth that impairs the ability
of the liver to conjugate and excrete bilirubin.

Hepatomegaly occurs from the fatty infiltration, inflammatory reactions, and
scarring of the liver that occurs with cirrhosis, whereas splenomegaly occurs as a
result of portal hypertension and congestion of the spleen.
4.

Mr. Begay’s total bilirubin is 15 mg/dl (257 mmol/L). Total (conjugated and
unconjugated) bilirubin increases as a result of the liver’s altered ability to take
up bilirubin from the blood or to conjugate or excrete it.

His serum ammonia level is 220 mcg/dl (122 mmol/L). A major source of
ammonia is the bacterial and enzymatic deamination of amino acids in the
intestines. The ammonia that results from this deamination process normally goes
to the liver via the portal circulation and is converted to urea, which is then
excreted by the kidneys. When the blood is shunted past the liver via the
collateral anastomoses or the liver is unable to convert ammonia to urea, large
quantities of ammonia remain in the systemic circulation.

The laboratory value for his AST is 190 U/L (3.2
U/L (3.5
μkat/L) and his ALT is 210
kat/L). Enzyme levels, including alkaline phosphatase, AST, ALT,
and GGT are elevated because of the release of these enzymes from damaged
liver cells.
5. Clinical manifestations of encephalopathy are changes in neurologic and mental
responsiveness, ranging from lethargy to deep coma. Changes may occur suddenly because of an
increase in ammonia in response to bleeding varices or gradually as blood ammonia levels slowly
increase. In the early stages, manifestations include euphoria, depression, apathy, irritability,
memory loss, confusion, yawning, drowsiness, insomnia, agitation, slow and slurred speech,
emotional lability, impaired judgment, hiccups, slow and deep respirations, hyperactive reflexes,
and a positive Babinski reflex. Clinical manifestations of impending coma include disorientation
as to time, place, or person. A characteristic symptom is asterixis, or flapping tremors (liver flap).
Copyright © 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Answer Guidelines for Case Studies in Textbook
44-3
This may take several forms, the most common involving the arms and hands. Other signs
include hyperventilation, hypothermia, grimacing, and grasping reflexes.
The goal in managing hepatic encephalopathy is to reduce ammonia formation. Several measures
to reduce ammonia formation in the intestines are used. Lactulose (Cephulac) may also be used to
treat hepatic encephalopathy. In the colon, it is split into lactic acid and acetic acid, which
decreases the pH from 7.0 to 5.0. The acidic environment discourages bacterial growth. The
lactulose traps the ammonia in the gut, and the laxative effect of the drug expels the ammonia
from the colon. It is usually given orally but may be given as a retention enema or via NG tube.
Sterilization of the intestines with antibiotics such as neomycin sulfate, which are poorly
absorbed from the GI tract, is another method. Neomycin can be given orally or rectally. This
reduces the bacterial flora of the colon. Bacterial action on protein in the feces results in ammonia
production. Cathartics and enemas are also used to decrease bacterial action. Constipation should
be prevented.
Control of hepatic encephalopathy also involves treatment of precipitating causes. This
involves controlling GI hemorrhage and removing the blood from the GI tract to decrease the
protein in the intestine. Electrolyte and acid-base imbalances and infections should also be
treated.
6. Esophageal varices are a common complication, occurring in 66% to 75% of patients with
cirrhosis. These collateral vessels contain little elastic tissue and are quite fragile. They have poor
tolerance for the high pressure, and the result is distended, tortuous veins that bleed easily. Large
varices are more likely to bleed. In addition, because of compromised liver function, there are
alterations in normal blood clotting mechanisms.
7. Health promotion for cirrhosis depends on the cause of the cirrhosis. Patients need to be urged
to avoid alcohol ingestion and their efforts must be supported. Adequate nutrition, especially for
the alcoholic and other individuals at risk for cirrhosis, is essential to promote liver regeneration.
Hepatitis must be identified and treated early so that it does not progress to chronic hepatitis.
Drugs that are potentially toxic to liver cells should also be avoided. Biliary disease must be
treated so that the stones do not cause obstruction and infection. The underlying cause (e.g.,
chronic lung disease) of right-sided heart failure must be treated so that the heart failure does not
lead to cirrhosis.
8. Nursing diagnoses: nausea, imbalanced nutrition: less than body requirements, impaired skin
integrity, disturbed sensory perception
Collaborative problems: anorexia, malnourishment, esophageal varices, hepatic encephalopathy
Copyright © 2007 by Mosby, Inc., an affiliate of Elsevier Inc.