jJ
objectives After studying this chapter, the learner should be able to:
1 Describe the normal anatomy and physiology of the liver.
2 Describe the role of the liver in metabolism and maintenance of energy balance.
3 Explain the basis for subjective and objective data that must be collected to identify problems of
the hepatic system.
4 Relate the various laboratory and diagnostic tests used in identifying the pathophysiological
states of the liver.
5 Synthesize a plan of care for patients undergoing the radiological
diagnosing hepatic dysfunction.
The liver is the largest gland in the body and has 500 identi-
fied functions. Of primary importance is its role in metabo-
lism and the maintenance of normal energy stores. Because
the liver has so many functions, pathological conditions in the
liver can cause a variety of problems that have an impact on
the entire body.
ANATOMY ANO PHYSIOLOGY
ANATOMY
The liver is one of the most complex organs in the body and
weighs approximately 1.3 to 1.8 kg. The falciform ligament di-
vides the liver into right and left lobes and provides attach-
ment to the anterior abdominal wall (Figure 36-1).
The round ligament is a remnant of the umbilical vein and
extends from the umbilicus to the inferior surface of the tiver.
Glisson capsule, a fibroelastic capsule containing blood ves-
sels, lymphatics, and nerves, covers the liver.
Anatomically, the liver extends up under the ribs and is 4 to
8 cm in height at the midsternalline and 6 to 12 cm in height
at the midclavicular line. The liver normally extends from the
fifth intercostal space.
The liver is served by two separate blood supplies, and at
any one time contains approximately 13% of the total blood
supply of the body. The hepatic artery supplies oxygenated
blood to the liver, and the portal vein carries nutrient-rich
blood from the stomach and intestines. Approximately 75% of
the blood flow is derived from the portal vein; thus the liver
receives mostly unoxygenated blood (Figure 36-2). The re-
maining 25% is derived from the hepatic artery, which is
highly oxygenated and supplies the hepatic cells.
The portal system is composed of veins, sinusoids, and he-
patic veins, which drain the blood from the abdominal area of
the digestive tract, spleen, pancreas, and gallbladder and carry
it to the tiver (Figure 36-3). Pressure in this system is normally
3mmHg.
,
•••
and special tests used in
The portal system empties into the inferior vena cava,
which delivers blood to the right atrium. Portal hypertension
is a rise in portal pressure to at least 10 mm Hg and can be
caused by any disorder that obstructs or impedes blood flow
through any portion of the portal system or vena cava. Ele-
vated pressures in the portal system cause collateral vessels to
open between the portal veins and the systemic veins, avoid-
ing the obstructed portal vessels. These collateral vessels may
develop in the esophagus, anterior abdominal wall, or rectum
(Figure 36-3).
The liver is innervated by the sympathetic and parasympa-
thetic nervous systems. Sympathetic fibers innervate the he-
patic artery branches and the bile ducts. Parasympathetic in-
nervation is supplied to the intrahepatic and extrahepatic
biliary tract system. Stimulation of the sympathetic and
parasympathetic nervous systems affects blood flow and the
flow of bile within the biliary tract, but the function of the he-
patic cells or parenchymal cells is not influenced.
The functional unit of the liver is the liver lobule (Fig-
ure 36-4). Each lobule is composed of multiple plates of
hepatic cells. Between the individual cells of the cellular plate
are biliary canaliculi, which empty into the bile ducts. The ter-
minal bile ducts join to form the hepatic duct, which merges
with the cystic duct of the gallbladder to form the common
bile duct. Each side of the cellular plate contains a venous
sinusoid, which receives blood from branches of the portal
vein and hepatic artery. As blood flows through the sinusoids,
substances can be exchanged between the hepatic cells and
the blood.
The sinusoids are lined with phagoeytic cells of the reticu-
loendothelial system (Kupffer cells). These cells remove bacte-
ria and other foreign substances from the blood. Because the
portal blood originates in the gastrointestinal (GI) tract, some
bacteria or other foreign substances need to be removed.
The blood from the venous sinusoids empties into the cen-
tral vein and then into the hepatic vein. The hepatic veinemp-
ties into the inferior vena cava.
1183
'1184 unit vii ALTERATIONS IN METABOLlSM

Inferior veno covo

RighI 1000 Folciform

ligamenl

figo 36-1 Gross structure of the liver, anterior view.

Inferior vena cava

RighI
lobe
Falciform proper
ligamenl
Hepalic
artery
Hepalic
partal vei
Common
hepalic duct

Quadrale lobe
Gallbladder
A

figo 36-2 Gross structure of the liver, inferior view.

PHYSIOLOGY metabolized into glycogen (glycogenesis) to replenish tiver

The liver can be thought of as a metabolic factory and a waste
disposal plantoAs should be evident from the anatomical de-
scription of the blood and bile flow, the liver is ideally struc-
tured to carry out its multiple metabolic and waste disposal
functions. The major functions of the liver are summarized in
Box 36-1. Each of these functions is presented in more detail
in the following sections.
Carbohydrate, Protein,
and Fat Metabolism
The liver has a significant role in the metabolism of each of
the three major nutrients. The liver either oxidizes these com-
ponents for energy, uses the nutrients to synthesize storage
forms of substances for future use, or uses the nutrients to
synthesize other essential compounds.
stores. If the diet ingested is low in carbohydrates, the liver
converts protein to glucose to replenish glycogen stores. If
more carbohydrate is ingested than is needed to replenish
glycogen stores or to supply energy, the excess carbohydrate is
converted to fat (lipogenesis). Between meals and during other
fasting states, the liver assists in maintaining the blood glucose
concentration. It does this by breaking down glycogen
(glycogenolysis) or forming new glucose (gluconeogenesis). The
new glucose is made from amino acids, glycerol, and lactic
acids. Through glycogenesis, lipogenesis, glycogenolysis, and
gluconeogenesis processes, which are under hormonal con-
trol, the liver helps to maintain a normal blood glucose level,
preventing high levelsimmediately after eating (postprandial)
and hypoglycemia between meals or during other periods
of fasting.

Carbohydrates Prote;ns
Immediately after meals, the liver extracts glucose, fruc- The liver is vital to normal protein metabolismo It provides
tose, and galactose from the blood. These simple sugars are needed amino acids through transamination. Transamination
 I
I1
Assessment of the Hepatic System chapter 36 1185 ,j
"

Azygos
Sinusoids Bile canaliculi
Esophageal varices Bile dud

Superior mesenteric
Inferior mesenteric

Hemorrhoidal
figo 36-3 Varices related to portal hypertension.
tai vein. its major tributaries. and the most impor-
tant collateral veins betvveen the portal and cavai
systems .
Branch of
hepatic artery
figo 36-4 Diagrammatical representation of a liver lob-
ule. A central vein is located in the center of the lobule
vvith plates of hepatic cells disposed radially. Branches
Por- of the portal vein and hepatic artery are located on the
periphery of the lobule. and blood from both perfuses
the sinusoids. Peripherally located bile ducts drain the
bile canaliculi that run betvveen the hepatocytes.

•••. j•. ,.,l!9j!lllij•••• Summary of Liver Functions

1. Carbohydrate, protein, and fat metabolism c. Fat metabolism

a. Carbohydrate metabolism (1) Oxidation of fatty acids for energy
(1) Glycogen formation and storage (2) Ketone formation
(2) Glucose formation from glycogen (glycogenolysis) (3) Synthesis of cholesterol and phospholipids
and from amino acids, lactic acids, and glycerol (4) Formation of triglycerides from dietary lipids and
(gluconeogenesis) excessive dietary carbohydrates and proteins
b. Protein metabolism (5) Formation of lipoproteins
(1) Protein catabolism 2. Production of bile salts
(2) Protein synthesis 3. Bilirubin metabolism
(a) Albumin 4. Detoxification of endogenous and exogenous substances
(b) Cl- and I3-Globulins a. Ammonia
(c) Clotting factors b. Steroids
(d) C-reactive protein C. Drugs
(e) Transferrin 5. Storage of minerais and vitamins
(f) Enzymes 6. Blood reservoir
(g) Ceruloplasmin
(3) Formation of needed amino acids

Ís the proeess of nitrogen metabolism in whieh the tiver trans-
fers an amino group (NH2) to form nonessential amino aeÍds.
The tiver also Ís the only souree of some of the major plasma
proteins. One of these major proteins Ís albumin, whÍeh Ís
neeessary for the maintenanee of a normal internal environ-
ment and for fluÍd and eleetrolyte balance. Albumin, pro-
dueed only in the tiver, Ís responsible for maintaining eolloid
osmotie pressure and thus the proper distribution of fluids
between the vascular and interstitial compartments.
The tiver Ís the souree of several clotting faetors. It pro-
duees fibrinogen (faetor I), prothrombin (faetor Il), faetor V
(proaeeelerin), faetor VII (serum prothrombin eonversion ae-
eelerator), faetor IX (Christmas faetor), and faetor X (Stuart
or Stuart-Prower faetor). The produetion of faetors lI, VII,

-
1186 unit vii ALTERATIONS IN METABOLlSM
IX, and X requires vitamin K. Vitamin K is a fat-soluble vita-
min and therefore requires adequate production and excre-
tion ofbile for its absorption. In addition to protein synthesis,
the liver catabolizes proteins as necessary for energy or glu-
cose production.
Fats
The liver is involved in multiple aspects of fat metabolismo
Triglycerides in the diet are absorbed in chylomicrons. The chy-
lomicrons are taken up by the liver, and the triglycerides are me-
tabolized to fatty acids. These fatty acids may be (1) oxidized and
utilized for energy by the liver and other body tissues; (2) me-
tabolized to ketones; (3) converted to phospholipids; (4) used to
combine with cholesterol, which is synthesized in the liver,
to form cholesterol esters; or (5) reesterified to triglycerides
and combined with protein, cholesterol, and phospholipids to
form lipoproteins. The liver also uses fatty acids released from
adipose tissue storage sites for these same processes.
Produetion of Bile Salts
Bile production is one of the major functions of the liver. Bile
is a complex compound composed of cholesterol, phospho-
lipids, bile salts, bile pigments (bilirubin), and very small
amounts of proteins and electrolytes. Ninety-seven percent of
bile is water. Metabolites of drugs and other substances that
need to be excreted may also be found in bile. Bile salts
are necessary for the absorption of fats, cholesterol, and fat-
soluble vitamins, particularly vitamin K. Bile is released from
the liver and concentrated and stored in the gallbladder. The
liver secretes approximately 700 ml of bile daily. The bile salts
released duiing each meal are reabsorbed into the enterohe-
patic circulation and recycled two or three times during a
meal. Bile is reabsorbed along the total intestinal tract, but the
terminal ileum has a major role in its active reabsorption. If
the terminal ileum is diseased or resected, reabsorption ofbile
does not occur and abnormal fat absorption results.
Bilirubin Metabolísm
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 se-
creted 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 ex-
tracted from the blood by the liver and recycled; some is ex-
creted in the urine.
Metabolie Detoxifieation
The liver has a prime role in metabolic detoxification or bio-
transformation of endogenous and exogenous substances.
Ammonia (NH3) is a major toxic produet processed by the
liver. Ammonia is produced in the gut and the liver from the
deamination of amino acids (the removal of the amino group
[NH2J from amino acids). Bacteria in the GI tract are respon-
l
sible for the ammonia formation in the gut. Peripheral blood
ammonia leveIs are kept very low because the ammonia from
the gut is extracted from the enterohepatic circulation by the
liver and it, along with the ammonia produced in the liver, is
detoxified by conversion into urea, which is then excreted by
the kidneys.
Steroids and hormones (estrogen, progesterone, testoster-
one, corticosterone, antidiuretic hormone, and aldosterone)
are inactivated by the liver. Liver diseases may depress this in-
activation, resulting in pathologicallevels of these hormones.
The liver detoxifies many àrugs; barbiturates (except pheno-
barbital and barbital), amphetamines, and many sedatives are
metabolized by the liver. Detoxification decreases intestinal or
renal tubular reabsorption of potentially harmful substances
and facilitates intestinal or renal excretion. Pathological states
of the liver may impair the effectiveness of detoxification.
Storage of Minerais and Vitamins
The liver stores reserves of various minerals and vitamins. This
storage prevents abnormal internallevels from occurring, al-
though the oral intake may be very irregular. Vitamins A, D,
and B12 are stored in sufficient quantities to prevent deficien-
cies for months. Vitamins E and K are also stored. lron in the
form of ferritin is stored and can be used to resupply iron for
hemoglobin formation as needed; copper is stored as well.
Blood Reservoir
The liver, because of its tremendous vascular supply and sinu-
soidal system, can act as a reservoir for blood. When the ve-
nous vascular volume becomes greater than can be handled by
the right side of the heart, the excess blood can be stored in the
liver. In the event of hemorrhage, the liver can release blood to
maintain systemic circulatory volume.
PHYSIOLOGICAL CHANGES WITH AGING
As the body ages, the number and size of hepatic cells de-
crease, which results in an overall decrease in the size and
weight of the liver. Conversely, the formation of fibrous tissue
within the liver increases, resulting in decreased protein syn-
thesis and possible changes in the production of enzymes that
assist in the metabolism of drugs, particularly anticonvul-
sants, psychotropic drugs, and oral anticoagulants. The nurse
should be alert to the signs and symptoms of drug toxicity
even when the drugs are administered in normal doses be-
cause the decreased metabolism in the liver can cause an ac-
cumulation of the drug. (See the Gerontological Assessment
Box). Although age-related changes in the hepatic system have
not been fully studied, the common liver function tests usu-
ally show normal results in elderly persons unless a patholog-
ical condition exists.
SUB.JECTIVE DATA
A thorough history is necessary to assess adequately the health
status of people with potential dysfunction of the hepatic sys-
tem. These data assist in identifying immediate nursing needs
and providing information necessary for helping patients to
 Assessment
live with chronic problems of the hepatic system. Assessment
focuses on comfort status; nutritional status; fluid and elec-
trolyte status; elimination pattems; energy level; perception,
motion, and cognition; and potential exposure to toxins, as
well as generalliving conditions and lifestyle.
COMFORT STATUS
Discomfort resulting from abdominal pain or pruritus (itch-
ing) may be one of the major problems of people with hepatic
dysfunction. The person may complain of continuous upper
abdominal discomfort or a dull ache in the upper right quad-
rant. The discomfort does not usually alter normal function-
ing, although it can cause ineffective breathing secondary to
the abdominal pain. The discomfort is most significant in that
it provides verification for the underlying pathological processo
Comfort status may be altered because of the general body
aching associated with acute viral infections of the hepatic sys-
tem. Most distressing to the patient is the pruritus usually as-
sociated with jaundice, which may cause significant discom-
fort. The elevated serum bilirubin that occurs with jaundice
causes capillary dilation in the skin, the source of the pruritus.
In addition, bilirubin is an irritating substance to the chemo-
sensitive area of the skin. The history should include an assess-
ment of factors that worsen itching and of measures that help
relieve it.
NUTRITIONAL STATUS
People with hepatic dysfunction often experience alterations
in nutritional status. Some hepatic problems result in
anorexia, nausea, and vomiting. The patient should be ques-
tioned about the occurrence of such episodes. Assessment
should include onset, precipitating factors, association with
food or alcohol intake, and measures that provide relief.
Poor nutritional habits and malnutrition resulting from
lifestyle pattems or food intolerances may be present. A useful
method to assess the patient's nutritional status is to ask the
patient what he or she has eaten in the past 24 hours and as-
certain whether this is the typical eating pattem.
Alcohol use should also be assessed. Alcohol, which pro-
vides calories but has no nutrient value, may hide weight loss
normally associated with malnutrition. In the case of chronic
alcohol use, muscle mass may have decreased while the over-
all weight remained stable. In addition, weight loss may be
masked by water retention.
People with chronic problems of the hepatic system of-
ten require treatment with special diets, such as low sodium,
altered protein intake, and water restriction. The history
should include information about food intolerances and food
preferences.
FLUIO ANO ELECTROLYTE STATUS
Hepatic dysfunction can be associated with volume deficit
from nausea and vomiting or from acute bleeding with cir-
rhosis. Fluid volume excess typically occurs in people with he-
patic dysfunction as a result of renal retention of sodium and
water that is initiated by peripheral vasodilation. This expan-
sion of the vascular space effectively decreases the circulating
blood volume, which results in the release of renin, an-
of the Hepatic System chapter 36 1187
gero~to~29ic~~ s se s_s1XlLe.D!
ASSESSMENT
Monitor Effects of Medications
• Older patients seem to have more problems with both
the therapeutic effects of medications and drug to xic-
ity. This may be due in part to the decrease in hepatic
circulation that accompanies aging as well as the de-
crease in the enzyme activity of the liver.
• Standard doses of medication published in a formulary
may be too high for elderly patients. Most drug dos-
ages are calculated for healthy white adult men.
• Polypharmacy occurs when the elderly patient receives
multi pie medications from multi pie prescribers.
Assess NutritionaI Status
• Because the liver has many functions that aim to main-
tain energy stores and metabolism, the elderly patient
may show signs of fatigue if liver function has dimin-
ished enough to limit the available energy needed to
support activities of daily living.
COMMON DISORDERS IN ELDERS
• Increased risk for drug toxicity
• Polypharmacy
• Malnutrition
giotensin, and aldosterone. These hormones increase sodium
and water retention.
Another factor causing fluid volume excess is the hypo-
albuminemia that is associated with liver disease. The hypoal-
buminemia decreases the osmotic pressure in the vasculature,
causing fluid to leave the vascular space and enter the intersti-
tial space, resulting in edema. Levels of electrolytes, particu-
larly sodium, potassium, hydrogen, and bicarbonate, can be
elevated or decreased.
To establish the patient's needs, the history collected
should include information about:
1. Normal fluid and food intake and output
2. Abnormal fluid and electrolyte losses, such as vomiting, di-
arrhea, or bleeding
3. Changes in weight, both losses and gains
4. Occurrence of signs and symptoms of fluid or electrolyte
deficit, such as weakness, dizziness, syncope, and weight
loss
5. Occurrence of signs and symptoms of fluid or electrolyte
excess, such as edema in hands, feet, and legs; an increase
in abdominal girth; and weight gain.
ELlMINATION PATTERNS
Intestinal and urinary elimination may be altered in people
with liver problems. If there is an obstruction of bile flow, the
person may give a history of grayish-white or clay-colored
stools and have dark amber, brown, or mahogany-colored
urine. Blood in the urine or stools may be present. The nurse
can test for occult blood in the urine by using a reagent strip
and test the stool by performing a Hematest or guaiac testo
A reported decrease in urine output or the occurrence of noc-
turia may result from sodium and water retention.
1188 unit vii ALTERATIONS IN METABOLlSM
ENERGY LEVEL
Because of altered nutrient intake, abnormal fluid and e!ec-
trolyte status, and increased metabolic needs, people with he-
patic problems often report an activity intolerance to normal
daily activities or simply fatigue. Weakness may be reported,
and nursing care should be adjusted to provide for the pa-
tient's safety. As the underlying liver condition resolves, the fa-
tigue and weakness may resolve. However, the patient and
family must understand that the energy leveI may take a long
time to return to normal.
PERCEPTION, MOTION, ANO COGNITION
Chronic health problems of the hepatic system can cause
changes in neurological functioning, particularly in re!ation
to the peripheral nervous system and higher cognitive func-
tions. The patient should be asked about alterations in sensa-
tion in extremities, any noticeable changes in memory,
episodes of forgetfulness or blackouts, and alterations in coor-
dination or in the ability to do fine motor tasks. The onset of
any alterations, pattern of changes (continuous or intermit-
tent), and duration of any changes should be determined.
EXPOSURE TO TOXINS
Hepatic dysfunction can be caused by various agents, such as
alcohol, drugs, industrial chemicals, and viruses. A history of
exposure to any toxins must be elicited. A drug and alcohol
history is necessary to determine whether the patient has been
exposed to these two hepatotoxins.
The drug history should focus on prescription, over-the-
counter, and street drugs. For example, acetaminophen is a
drug often used by adolescents to commit suicide and can
cause severe liver damage in doses 10 times greater than the
recommended dose. The liver damage is intensified by the
combination of acetaminophen and alcohol. The alcohol
history should focus on normal amount of intake and time
since last intake. An occupational history he!ps to identify
potential toxins in the work environment such as methylene
chloride solvents. An environmental/social history might
identify potential sources of viruses (see Box 36-2 for sig-
. . Health History Necessary
to Identify Exposure
• to Hepatitis Viruses
~AAi'f't%'!G'jI9!~~~~~~T.!'~~w
Contact with persons with jaundice
, Travei or visits to environments with poor sanitation
~ masses. The spleen often is enlarged in the patient with
.<1 (e.g., camping trips, travei to developing countries)
~. Ingestion of shellfish or raw fish
~ History of recent ear or body piercing or tattooing
~ History of recent blood transfusions
~ Intravenous drug abuse (sharing of contaminated
~ needles)
~. Occupational exposure (e.g., health service personnel
~. with frequent blood contact, personnel in daycare cen-
i" ters, personnel in centers of custodial care)
r History of hemodialysis
t~History of multi pie sex partners; male bisexual ar male
F homosexual lifestyle
f~~~~~'.j.~~~=~~_~~i~ ,,~
,
nificant sources of contact with the hepatitis viruses). The
environmental/social history also can he!p identify particular
persons, factors, or places associated with substance abuse, if
a problem exists. Data about persons, factors, or places asso-
ciated with substance abuse are needed for long-term man-
agement of drug and alcohol abuse (see Chapter 14).
OBJECTIVE DATA
To assess the functioning of the hepatic system completely, a
thorough assessment of the total body is required. First, ex-
amination of the overall appearance of the patient is neces-
sary. Does the patient appear chronically or acute!y ill? Is the
individual attentive, restless, or lethargic? Does the person ap-
pear nourished or malnourished? Is the skin jaundiced? Are
the sclerae yellow? In a darker-skinned person, are the palms
of the hands or soles of the feet jaundiced? Are the oral mu-
cous membranes yellow? Are there any other signs of hepatic
dysfunction, such as enlarged abdomen, palmar erythema,
change in secondary sexual characteristics, bruises, muscle
wasting, or edema? Petechiae and spider angiomas, usually on
the nose, cheeks, or upper thorax, may be present.
After the general inspection, the assessment should focus on
fluid status. Vital signs, including orthostatic changes, weight,
temperature, skin turgor, mucous membrane moisture, pres-
ence of edema, and behavior changes should be assessed. To
assess energy leve! and nutritional status, the patient's total
muscle mass and muscle strength should be examined.
While performing the assessment note the patient's mental
status, affect, and alertness. Note changes in facial expression,
responsiveness, leve! of consciousness, and affect. Are there
periods of confusion or disorientation? Is the affect appropri-
ate for this situation? Because handwriting or the ability to
draw a box, triangle, or square deteriorates with decreasing
liver function, a sample of handwriting or a drawing of a geo-
metric figure may be obtained from the patient.
After a general impression of the total patient is obtained,
the assessment should focus on the abdomen. The abdomen is
inspected for enlargement, presence of distended or dilated
periumbilical veins (caput medusae), and ascites. Ascites is
characterized by distention of the abdomen with tight, glis-
tening skin, protruding umbilicus, and bulging flanks. Palpate
or percuss the abdomen to ascertain the presence of a fluid
wave and shifting dullness, which are indicative of ascites. Pal-
•..'~;
pation and percussion are also used to assess for hepatic ten-
~. derness, size, and consistency and the presence of hepatic
j,
~.
~ chronic hepatic dysfunction and should be percussed to de-
[ termine the size and location; defer palpation because of the
i' fragility of the enlarged spleen. Last, measure abdominal
f' girth. Hemorrhoids caused by prolonged elevations in portal
~' system pressure may be present.
:
~.
DIAGNOSTIC TESTS
;;. Various tests he!p in assessing the status of the hepatic system.
Many of the tests require taking samples of blood; other tests
are more extensive and may cause discomfort; still others may
 Assessment
require fasting. The nurse is responsible for preparing the pa-
tient for the tests. The physical preparation of the patient will
vary from institution to institution, and the nurse must know
the routine preparation. In addition to the physical prepara-
tion, the nurse carries out appropriate teaching and monitor-
ing of the patient before, during, and after the diagnostic tests.
LABORATORY TESTS
Multiple tests may be necessary to determine the extent and
seriousness of hepatic disease. To be of benefit many tests re-
quire serial readings. The procedure, preparation, and inter-
pretation of blood, stool, and urine studies used to eValuate
liver function are summarized in Table 36-1.
RADIOLOGICAL TESTS
Radiographic tests are used to assist in identifying the cause of
hepatic dysfunction. Besides the examinations described in
the following section, abdominal films, barium swallow, bar-
ium enema, and gastroscopy may be ordered (see Chapter 38).
These tests help identify the presence of pathological GI con-
ditions that may cause signs and syrnptoms similar to those
found in hepatic dysfunction.
Ultrasonography
Ultrasonography of the liver is done to assess jaundice of
unknown etiology, hepatomegaly, or suspected turnors. Addi-
tional information obtained from ultrasound includes liver
size, shape, and location; cysts; abscesses; and filling or dilation
defects.
The preparation of the patient for ultrasonography is rela-
tively simple. Usually the patient is not allowed to eat for 8 to
12 hours before the procedure, because bowel gas in the G1
tract will interfere with the testo Any residual barium needs to
be elirninated from the G1 tract before the testo The patient
must be well hydrated, beca use dehydration can decrease the
ability of ultrasonography to distinguish between the liver and
surrounding tissues.
Computed Tomography Scan
Computed tomography (CT) scanning can also be used to as-
sess patients with potential hepatic problems. It is helpful in
identifying problems similar to those described for ultra-
sonography. Contrast medium can be used with the CT scan
to intensify the appearance of vascular structures and hepatic
parenchyrna. The patient should eat nothing for 8 to 12 hours
before the test; if contrast medium is to be used, the patient
should be assessed for allergies to iodine or contrast media.
Adequate hydration is necessary when a contrast medium is
used. Barium studies should be done at least 4 days before the
CT scan or after the scan because the barium can interfere
with test results.
Magnetic Resonance Imaging
Magnetic resonance imaging (MRl) is used to detect liver tu-
mors. Because magnetic fields are used instead of radioactive
isotopes to produce the image, no special preparation of the
patient is necessary. 1t is important to inform the patient that
this test is painless. The patient should be instructed to re-
of the Hepatic System chapte,. 36 1189
move any jewelry, dentures and partial dentures if they contain
metal, or any other item that contains metal, such as hairpins
or limb prostheses. Patients should be assessed for claustro-
phobia before the procedure, because it may elicit this type of
response. Contraindications to MRl include a pacemaker and
titanium or stainless steel prosthetic implants or prosthetic
heart valves.
Radionuclide Imaging
The liver may be outlined by radionuclide imaging techniques.
Selected radioisotopes are given intravenously. After the injec-
tion of the radioisotope, the patient is placed in the supine po-
sition, and a scintillation detector is passed over the abdomen in
the area of the liver. The radiation coming from the isotopes
immediately beneath the probe of the scanner is detected, am-
plified, and recorded. Scanning helps differentiate nonfunction-
ing areas from normal tissue and to identify hepatic tumors,
cysts, and abscesses. Usually a nonfunctioning area will appear
as an area of decreased activity. However, gallium-67 (67Ga) is
preferentially taken up by hepatocellular carcinomas and ab-
scesses, and these areas will appear as areas of very heavy ra-
dioactivity. Adverse reactions to the radioisotopes used for ra-
dionuclide imaging are unusual, and the procedure is relatively
safe. Discomfort is minimal. Only small amounts of radioactive
material are given, and radiation precautions are not necessary.
Only 67Ga scanning requires special preparation. 67Ga is ex-
creted by the GI tract. To avoid absorption of the radioisotope
by the G1 contents, laxatives and enemas are prescribed. The
toilet should be flushed twice for bowel movements after the
67Gascanning to ensure the safety of the patient and others. UI-
trasonography, CT scanning, and MRl have replaced radionu-
clide imaging in most instances of hepatic dysfunction.
Angiography and Portal
Pressure Measurernents
Catheterization of the hepatic artery, portal venous system (by
various routes), and hepatic vein allows the injection of a con-
trast medium and the visualization of the vascular supply of
the hepatic system. Angiography determines the patency of
the system and the presence of tumors, abscesses, coHateral
circulation, varices, and bleeding.
Portal and hepatic vein pressure (wedged hepatic vein pres-
sure) can be measured. These readings may be done in conjunc-
tion with angiography or as a separate study. These measure-
ments help in determining the degree of portal hypertension.
The presence of allergy to contrast media must be ascer-
tained before angiography is done. After both angiography
and pressure readings, the insertion site is observed for bleed-
ing, and the patient's vital signs are checked every 15 minutes
for 1 hour, every 30 minutes for 1 hour, every hour for
4 hours, and then if the patient is stable, every 4 hours. Bedrest
is maintained for 24 to 48 hours after the testo
SPECIAL TESTS
Biopsy of the Liver
A liver biopsy may be used to aid in establishing the cause of
liver disease. In this procedure a specially designed needle is
inserted through the chest or abdominal wall into the liver,
1190 unit vii ALTERATIONS IN METABOLlSM

=.-.._--:::-~ ....
:..'"'::.
r_-e.:et:se,~..•~ •.._ ~~.:~ S:::.~••.•.
FUNCTION AND TEST PROCEDURE AND PREPARATION INTERPRETATION

Fat metabolism
Serum total cholesterol Venipuncture; fasting may be required Normal levei is 140-220 mg/dl of blood; approxi-
and cholesterol esters mately 70% is cholesterol este r; in hepatocellular
disease, amount of total serum cholesterol and
cholesterol ester may be decreased; in obstructive
biliary tract disease, total serum cholesterol is in-
creased, but amount of esterified cholesterol is de-
creased; normal cholesterol leveis rise with age.
Serum phospholipids Venipuncture; no special preparation Normal levei is 150-250 mg/dl; serum phospho- i
lipids tend to be low in severe hepatocellular dis- i
ease and high in obstructive biliary tract disease. r
Protein metabolism
Total serum protein Venipuncture; no special preparation Normal levei is 6-8 g/dl; measures ali serum pro-
tein; may be normal in hepatocellular disease be-
cause increased serum globulin will replace de-
creased serum albumin; increased serum
globulin is seen in chronic inflammatory disease,
neoplastic diseases, and biliary obstruction.
Albumin Venipuncture; no special preparation Normal levei is 3.4-5.0 g/dl; albumin made only in
liver; in hepatocellular disease there may be a de-
crease in serum albumin leveI. i
Protein electrophoresis Venipuncture; no special prep- Normal fractions in relation to total serum protein !
aration; protein fraction of blood (100%) are albumin, 52-68%; a-globulins, 12-17%; ~
will migrate in characteristic direc- ,l3-globulins, 7-15%; and immune serum globulins !
tions in electrical field; after separa- (y-globulins), 9-19%; in severe hepatocellular
tion of fractions, specimen stained, damage, amount of albumin may be decreased;
and densitometer used to measure inflammatory processes of the liver may produce
amounts of various serum protein increased amounts of a,-globulins, neoplastic dis-
ease is associated with increased leveis of a2"
globulins, and some patients with obstructive bil-
iary tract disease may have high leveis of
,l3-globulins.
Immunoglobulins Venipuncture; no special preparation Five classes of antibodies: IgA, IgG, IgM, IgF, and i
IgO; IgA and IgG are often increased in the pres-
ence of cirrhosis; IgG is elevated in the presence of i
chronic active hepatitis; biliary cirrhosis and hepa- ti
titis A cause an increase in the IgM component.
Blood urea nitrogen Venipuncture; no special preparation Normal is 10-20 mg/dl; in severe hepatocellular
(BUN) disease if portal venous flow is obstructed, levei
may decrease; varies with dietary protein intake
and fluid volume.
Serum prothrombin time Venipuncture; no special preparation; Normal PT is 12-15 sec; it is compared with a con-
(PT) reflects activity of extrinsic and trol levei; the normal PT is calculated based on
common coagulation pathways, in- the institution's control and therefore may differ
cluding prothrombin, fibrinogen, between institutions; may be expressed as Inter-
and factors V, VII, IX, and X national Normalized Ratio (INR); PT reflects activ-
ity of extrinsic and common coagulation path-
ways, including prothrombin, fibrinogen, and
factors V, VII, IX, and X; PT may be increased in
hepatocellular disease because of the inability of
liver to produce clotting factors or in obstructive
hepatic or biliary tract disease beca use of the
malabsorption of vitamin K; persistence of abnor- ~
mal PT after parenteral administration of vitamin
K indicates hepatocellular damage.
Serum partia I thrombo- Venipuncture; no special preparation; Normal PTI is 68-82 sec with standard technique,
plastin time (PTI) and reflects activity of intrinsic and com- APTI is 32-46 sec; as with the PT,the normal value
activated partial throm- mon coagulation pathways may differ between institutions depending on the
boplastin time (APTI) control used; PTI reflects activity of intrinsic and
common coagulation pathways; PTI and APTI will
be increased in hepatocellular disease because of
the inability of liver to produce clotting factors.

Continued
 Assessment of the Hepatic System chapter 36 1191

dasv,' Laboratory Tests of Liver Function-cont'd

~~.~'S' ~-;;;:ç~'* _
FUNCTION ANO TEST PROCEOURE ANO PREPARATION INTERPRETATION

Blood ammonia leveis Venipuncture; may require fasting Normal levei is less than 75 fLg/dl; may be ele-
vated in severe hepatocellular disease beca use of
obstruction of portal blood flow and rarely be-
cause of decreased urea synthesis.
Bilirubin metabolism
Total bilirubin Venipuncture, no special preparation Total serum bilirubin measures both conjugated
Conjugated (direct) and unconjugated bilirubin; normal total serum
Unconjugated (indirect) bilirubin values range from 0.1-1 mg/dl; conju-
gated bilirubin acts directly with diazo reagents;
unconjugated bilirubin requires addition of
methyl alcohol; thus the terms direct and indirect;
conjugated bilirubin increases in the presence of
hepatocellular or obstructive biliary tract disease;
unconjugated bilirubin is elevated in the pres-
ence of increased hemolysis of red blood cells or
hepatocellular disease.
Urine bilirubin Spot urine specimen; no special Normally no bilirubin is excreted in urine; urine
preparation with abnormal bilirubin is mahogany colored and
has a yellow foam when shaken (foam test); un-
conjugated bilirubin even in excess is not excreted
in urine beca use it is not water soluble; conjugated
serum bilirubin leveis greater than 0.4 mg/dl will
lead to conjugated bilirubin being excreted in
urine because it is water soluble and indicates he-
patocellular or obstructive biliary tract disease;
bilirubinuria may be present before jaundice.
Urine urobilinogen 24-hr urine collection or 2-hr after- Normally 0.2-1.2 units found in specimen; fresh
noon collection urine urobilinogen is colorless; decreased
amounts of urine urobilinogen found in obstruc-
tive biliary tract disease; increased amounts
found in hepatocellular disease; alterations in in-
testinal flora by broad-spectrum antibiotics may
change testo
Fecal urobilinogen . Stool specimen; no special preparation Normally 90-280 mg/day; presence of fecal uro-
bilinogen (stercobilin) gives stool brown color;
absence of stercobilin causes stools to become
clay (grayish white) to white colored; increased
amounts of stercobilin found with increased he-
molysis of red blood cells; absence of fecal ster-
cobilin indicates obstructive biliary tract disease.
Serum enzymes
Asparate aminotrans- Venipuncture; no special preparation Normal values vary depending on measurement
ferase (AST), formerly used; these enzymes are present in hepatic cells;
called serum glutamic- with necrosis of hepatic cells, enzymes are re-
oxaloacetic transami- leased and elevated serum leveis will be found;
nase (SGOT) GGT is found in high leveis in liver cells as well
Alanine aminotransferase as kidneys; ALT is primarily present in liver cells;
(ALT), formerly called AST is also present in high leveis in skeletal and
serum glutamic pyruvic heart muscle; LDH is also present in heart cells,
transaminase (SGPT) kidney cells, skeletal muscle cells, and erythro-
Lactic dehydrogenase cytes, but in each tissue the LDH enzyme has a
(LDH) characteristic composition: thus the tissue source
y-Glutamyl transpepti- of elevated serum LDH leveis can be determined
dase (GGT) (y-glutamyl- by isoenzyme tests; with the other three enzyme
transferase) tests, necrosis of other organs must be ruled out;
GGT is elevated early in Iiver disease, and eleva-
tion persists as long as cellular damage contin-
ues; GGT is routinely elevated in alcohol-induced
liver disease, and increased leveis are often seen
before other abnormal test results occur.
: :it:::' H ti ;g; ti: -@
Continued
1192 unit vii ALTERATIONS IN METABOLlSM

kffi5HiJiSI Laboratory Tests of Liver Function-cont'd

r-~~iCà#?::.lf,;?4~~r~a\'iiO;j~{i;~~~ ~l!!lI!l __ lI!i!l!! 1llm'l".

~. FUNCTION AND TEST PROCEDURE AND PREPARATION INTERPRETATION

~, Alkaline phosphatase Venipuncture; no special preparation Normal values vary depending on measurement
t, used; this enzyme originates in liver, bone, intes-
f,
i
"',,' tine, and placenta; alkaline phosphatase is
slightly to moderately elevated in hepatocellular

I
disease but extremely elevated in obstructive bil-
iary tract and bone disease, t
Antigens and antibodies of Venipuncture; no special preparation Normally, no hepatitis antigens are found in the fi,
viral hepatitis serum or other body fluids; hepatitis A virus ~
(HAV) can be found in the stool during the last r
part of the incubation period and early prodromal
phase; IgM-class anti-HAVappears in the acute
and early eonvalescent period and is used to di- I'
agnose hepatitis A; IgG-class anti-HAV becomes ~
detectable during the convalescent period and r.
confers immunity; hepatitis B has many assoei- ~
ated serum particles; complete hepatitis B virus I·...
(HBV) is also called Dane particle;
a core antigen (HBcAg) ean be found in the liver,
an antibody (anti-HBc) ean be found in the blood,
and the presenee of anti-HBc indicates past infec-
tion with HBV at some undefined time; a surface
antigen (HBsAg) and severa I subtypes and anti-
body (anti-HBs) are also measurable; HBsAg is
one of the antigens measured to diagnose hepati-
tis B, and its presence indieates infectivity; pres-
ence of anti-HBs indicates past infection and im- ,
munity to HBV, presenee of passive antibodies 8
from HBIG, or immune response from HBV vac-
cine; hepatitis Be antigen (HBeAg) indicates high
infectivity and its antibody (anti-HBe) chronic in-
fectivity; enzyme-Iinked immunosorbent assay
(ELISA) has detected antibodies to hepatitis C
(anti-HCV) in people who have been exposed to
hepatitis C; however, the antibodies do not ap-
pear in most people until at least 5 months after
exposure to the virus; an enterically transmitted
virus that was previously related to hepatitis
non-A non-B has been identified and labeled hep- I
atitis E (HEV); anti-HEV has been deteeted using ,
ELISA but .iS not available in the United States at t

W':; ~t
and a small piece of tissue is removed for study. This proce-
dure is contraindicated in a patient who has an infection of
the right lower lobe of the lung, ascites, a blood dyscrasia, or a
problem with blood clotting, as well as in any patient unable
to cooperate by holding his or her breath, To avoid hemor-
rhage, vitamin K may be given parenterally for several days be-
fore and afier the biopsy is performed. A biopsy usually is not
done if the prothrombin time is below 40% of normaL The
physician should explain the procedure to the patient, for ex-
ample, the importance of being able to hold one's breath and
remain absolutely still when the needle is introduced, Move-
ment of the chest may cause the needle to slip and to tear the
liver covering, Most hospitals require that the patient sign a
written permission form for the procedure to be done. Food
and fluids may be withheld for several hours preceding the
.....
this time,'·3,5
_S"""'_-Ubfi~~"',~'-'f'IN:_amm:am_-'~~·~~ l
test, and a sedative usually is given about 30 minutes before
the biopsy.
A liver biopsy is performed as follows, The patient lies supine;
the skin over the area selected (usually the eighth or ninth inter-
costal space) is cleansed and anesthetized with procaine hy-
drochloride, A nick is made in the skin with a sharp scalpel blade.
Then the patient is instructed to take several deep breaths and
then to hold his or her breath while the needle is introduced
through the intercostal or subcostal tis sues into the liver, The
special needle assembly is rotated to separate a fragment of
tissue and then is withdrawn, The specimen is placed into an
appropriate container, which is labeled and sent to the pathol-
ogy laboratory. A simple dressing is placed over the wound,
The dangers of liver biopsy are accidental penetration of
blood vessels, causing hemorrhage, or accidental penetration
 Assessment
of a biliary canniculi, causing a chemical peritolllns from
leakage of bile into the abdominal cavity. After the procedure
the nurse should assess the patient for signs of hypovolemia
and shock. The patient's pulse and blood pressure should be
monitored every 30 minutes for the first few hours after the
procedure and then hourly for 24 hours. The patient's tem-
perature should be taken at least every 4 hours to determine a
baseline and detect peritonitis. The physician may order pres-
sure applied to the biopsy site to help stop any bleeding. An ef-
fective way to apply pressure is to have the patient lie on the
right side with a small pillow or folded bath blanket placed
under the costal margin for several hours after the biopsy.
Bedrest is maintained for 24 hours after the testo
Paracentesis
A paracentesis, or peritoneal tap, can be done to remove peri-
toneal fluid (ascitic fluid) for cytological or other laboratory
studies or to drain large volumes of ascitic fluidoWhen condi-
tions such as respiratory distress, severe abdominal discom-
fort, or cardiac dysfunction are present because of the ascites,
a paracentesis may be necessary. Repeated paracenteses are
not the treatment of choice for controlling cmonic, recurring
ascites because of complications.
When paracentesis is performed, the skin is cleansed, and
the abdominal wall is anesthetized. A long aspiration needle is
inserted, and fluid is aspirated for diagnostic tests or drained
as necessary. In preparation for the procedure, the patient is
given a complete explanation and signs a consent form; the
patient should void irnrnediately before the procedure to di-
minish the risk of puncturing the bladder. Sterile technique
must be maintained during the procedure.
The complications of paracentesis include peritonitis, if
sterility is not maintained, and peritoneal bleeding resulting
from trauma to blood vessels.The patient's vital signs, includ-
ing temperature, urine output, and skin temperature and
moisture, should be monitored for signs of peritonitis or
bleeding. The patient's abdomen should be assessed for rigid-
ity and his or her sensorium for confusion.
Removal of large amounts of fluid from the peritoneal
space can result in hypovolemia and shock because additional
fluid can shift from the intravascular compartment into the
peritoneal cavity; this risk is minimal in the patient with cir-
rhosis and edema. Protein and potassium are commonly lost
during paracentesis. The patient should be monitored for hy-
povolemia after the procedure. Data to be assessed include
vital signs, mental status, urine output, skin temperature and
moisture, and status of mucous membranes. Protein and
potassium leveIs should also be monitored.
Peritoneal Lavage
Peritoneal lavage may be used to assess damage to the liver
from abdominal trauma in persons with altered states of con-
sciousness who cannot give a satisfactory history. It may also
be used in patients with abdominal trauma when unexplained
hypotension is present, when unreliable physical examination
results are present, or when the patient requires general anes-
thesia for other injuries.
of the Hepatic System chapter36 1193
Peritoneallavage can be done by either the closed or open
method. In the closed method, a peritoneal dialysis catheter is !
inserted, and the peritoneal space is aspirated for gross blood. i
If no gross blood is found, lavage is carried out with normal :1
saline. In the open method the peritoneum is exposed COffi-
pletely and then opened enough to allow entry of a dialysis
catheter. Again, gross blood is aspirated first, and if no blood
is found, lavage is carried out.
Peritoneal lavage requires a complete explanation to the
patient and significant others and informed consent. A naso-
gastric tube and Foley catheter are inserted before the proce-
dure to prevent penetration of the intestines or bladder. In the
closed method a local anesthetic is used, whereas in the open
method general anesthesia is necessary. Postprocedural care
involves monitoring for peritonitis and bleeding in patients
who have closed peritoneal lavage. Patients who have open
peritoneal lavage require general postanesthetic care (see
Chapter 20).
ENDOSCOPY
The hepatic system and gallbladder can be examined by several
types of endoscopic procedures. The endoscope can be in-
serted direetly through the peritoneum (peritoneoscopy),.thus
affording direet visualization of the abdominal organs and the
taking of biopsy specirnens. Esophagoscopy and gastroscopy
can be used to diagnose esophageal varices or to perform in-
jection sclerotherapy. An endoscopic retro grade cholan-
giopancreatography (ERCP) can be done to visualize and pro-
vide radiographic examination of the liver, gallbladder, and
pancreas (see Chapter 38). Ali these procedures require that
the patient be fasting at least 12 hours before the testoBefore
ERCP the patient should be asked about allergies or sensitivi-
ties to x-ray dye.
After the procedure, the nurse should assess the patient's
ability to swallow. The patient's gag reflex may not return for
1 to 2 hours. After ERCP the patient should be monitored
for signs of complications, which include perforation, sep-
sis, and pancreatitis. Vital signs are usually taken every 30 min-
utes and then hourly for 4 hours. N sedation is frequently used
during endoscopic procedures.
ANATOMY ANO PHYSIOLOGY
• The liver is important for adequate energy production and
waste disposal.
SUB.JECTIVE DATA
• Pathophysiological conditions of the liver result in discom-
fort, inadequate nutrition, fluid and electrolyte deficit or ex-
cess, bleeding, altered elimination, fatigue, and altered per-
ception, cognitive, and motor functioning.
OB.JECTIVE DATA
• Pathophysiological conditions of the liver can result from
exposure to various toxins, including drugs, alcohol, chem-
icals, and viruses.
1194 unit vii ALTERATIONS IN METABOLlSM

DIAGNOSTIC TESTS 2. McMillan-Jackson M, Rymer TE: Vira! hepatitis: anatomy oí a diag-

• Liver dysfunction results in multiple abnormalities in blood
studies that are used to help identify the pathophysiologi-
cal state or other nursing needs.
• Radiologic, endoscopic, and other invasive tests are used to
help in identifying the exact pathophysiological condition.
References
1. American Medica! Association: Prevention, diagnosis, and man-
agement of viraI hepatitis, Chicago, 1996, AMA: Division oí Hea!lh
Science.
nosis, Am J Nurs 94( 1):43-48, 1994.
3. Moseley RH: Approach to lhe patient with abnorma! liver chem-
istries. In Kelley WN, editor: Textbook of internal medicine, ed 3, Phil-
adelphia, 1997, Lippincott-Raven .
4. Renkes J: GI endoscopy: managing the full scope oí care, Nursing 93
23( 6):50-55, 1993.
5. Siconolfi LA: Clarifying the complexity oí liver function tests,
Nursing 95 25(5):39-44,1995.