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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 and special tests used in
diagnosing hepatic dysfunction.

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

1183

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

Branch of
hepatic artery
Hemorrhoidal
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
figo 36-3 Varices related to portal hypertension. Por- of the portal vein and hepatic artery are located on the
tai vein. its major tributaries. and the most impor- periphery of the lobule. and blood from both perfuses
tant collateral veins betvveen the portal and cavai the sinusoids. Peripherally located bile ducts drain the
systems . 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- osmotie pressure and thus the proper distribution of fluids
fers an amino group (NH2) to form nonessential amino aeÍds. between the vascular and interstitial compartments.
The tiver also Ís the only souree of some of the major plasma The tiver Ís the souree of several clotting faetors. It pro-
proteins. One of these major proteins Ís albumin, whÍeh Ís duees fibrinogen (faetor I), prothrombin (faetor Il), faetor V
neeessary for the maintenanee of a normal internal environ- (proaeeelerin), faetor VII (serum prothrombin eonversion ae-
ment and for fluÍd and eleetrolyte balance. Albumin, pro- eelerator), faetor IX (Christmas faetor), and faetor X (Stuart
dueed only in the tiver, Ís responsible for maintaining eolloid 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- [NH2J from amino acids). Bacteria in the GI tract are respon-
l
min and therefore requires adequate production and excre- sible for the ammonia formation in the gut. Peripheral blood
tion ofbile for its absorption. In addition to protein synthesis, ammonia leveIs are kept very low because the ammonia from
the liver catabolizes proteins as necessary for energy or glu- the gut is extracted from the enterohepatic circulation by the
cose production. liver and it, along with the ammonia produced in the liver, is
detoxified by conversion into urea, which is then excreted by
Fats the kidneys.
The liver is involved in multiple aspects of fat metabolismo Steroids and hormones (estrogen, progesterone, testoster-
Triglycerides in the diet are absorbed in chylomicrons. The chy- one, corticosterone, antidiuretic hormone, and aldosterone)
lomicrons are taken up by the liver, and the triglycerides are me- are inactivated by the liver. Liver diseases may depress this in-
tabolized to fatty acids. These fatty acids may be (1) oxidized and activation, resulting in pathologicallevels of these hormones.
utilized for energy by the liver and other body tissues; (2) me- The liver detoxifies many àrugs; barbiturates (except pheno-
tabolized to ketones; (3) converted to phospholipids; (4) used to barbital and barbital), amphetamines, and many sedatives are
combine with cholesterol, which is synthesized in the liver, metabolized by the liver. Detoxification decreases intestinal or
to form cholesterol esters; or (5) reesterified to triglycerides renal tubular reabsorption of potentially harmful substances
and combined with protein, cholesterol, and phospholipids to and facilitates intestinal or renal excretion. Pathological states
form lipoproteins. The liver also uses fatty acids released from of the liver may impair the effectiveness of detoxification.
adipose tissue storage sites for these same processes.
Storage of Minerais and Vitamins
Produetion of Bile Salts The liver stores reserves of various minerals and vitamins. This
Bile production is one of the major functions of the liver. Bile storage prevents abnormal internallevels from occurring, al-
is a complex compound composed of cholesterol, phospho- though the oral intake may be very irregular. Vitamins A, D,
lipids, bile salts, bile pigments (bilirubin), and very small and B12 are stored in sufficient quantities to prevent deficien-
amounts of proteins and electrolytes. Ninety-seven percent of cies for months. Vitamins E and K are also stored. lron in the
bile is water. Metabolites of drugs and other substances that form of ferritin is stored and can be used to resupply iron for
need to be excreted may also be found in bile. Bile salts hemoglobin formation as needed; copper is stored as well.
are necessary for the absorption of fats, cholesterol, and fat-
soluble vitamins, particularly vitamin K. Bile is released from Blood Reservoir
the liver and concentrated and stored in the gallbladder. The The liver, because of its tremendous vascular supply and sinu-
liver secretes approximately 700 ml of bile daily. The bile salts soidal system, can act as a reservoir for blood. When the ve-
released duiing each meal are reabsorbed into the enterohe- nous vascular volume becomes greater than can be handled by
patic circulation and recycled two or three times during a the right side of the heart, the excess blood can be stored in the
meal. Bile is reabsorbed along the total intestinal tract, but the liver. In the event of hemorrhage, the liver can release blood to
terminal ileum has a major role in its active reabsorption. If maintain systemic circulatory volume.
the terminal ileum is diseased or resected, reabsorption ofbile
does not occur and abnormal fat absorption results. PHYSIOLOGICAL CHANGES WITH AGING
As the body ages, the number and size of hepatic cells de-
Bilirubin Metabolísm crease, which results in an overall decrease in the size and
Bilirubin is a byproduct of the heme portion of red blood cells weight of the liver. Conversely, the formation of fibrous tissue
and is released when these cells are destroyed. The released within the liver increases, resulting in decreased protein syn-
bilirubin is not water soluble (unconjugated). Unconjugated thesis and possible changes in the production of enzymes that
bilirubin is carried in the blood bound to albumin and other assist in the metabolism of drugs, particularly anticonvul-
proteins. The liver extracts the unconjugated bilirubin from sants, psychotropic drugs, and oral anticoagulants. The nurse
the blood and combines it with glucoronide into a water- should be alert to the signs and symptoms of drug toxicity
soluble form (conjugated). The conjugated bilirubin is se- even when the drugs are administered in normal doses be-
creted into the bile and then enters the duodenum. In the GI cause the decreased metabolism in the liver can cause an ac-
tract, bilirubin is metabolized to urobilinogen. Urobilinogen cumulation of the drug. (See the Gerontological Assessment
is excreted in feces as stercobilin, giving feces its brown color, Box). Although age-related changes in the hepatic system have
or it is reabsorbed. Most of the reabsorbed urobilinogen is ex- not been fully studied, the common liver function tests usu-
tracted from the blood by the liver and recycled; some is ex- ally show normal results in elderly persons unless a patholog-
creted in the urine. ical condition exists.

Metabolie Detoxifieation
SUB.JECTIVE DATA
The liver has a prime role in metabolic detoxification or bio-
transformation of endogenous and exogenous substances. A thorough history is necessary to assess adequately the health
Ammonia (NH3) is a major toxic produet processed by the status of people with potential dysfunction of the hepatic sys-
liver. Ammonia is produced in the gut and the liver from the tem. These data assist in identifying immediate nursing needs
deamination of amino acids (the removal of the amino group and providing information necessary for helping patients to
Assessment of the Hepatic System chapter 36 1187

live with chronic problems of the hepatic system. Assessment


focuses on comfort status; nutritional status; fluid and elec- gero~to~29ic~~ s se s_s1XlLe.D!
trolyte status; elimination pattems; energy level; perception, ASSESSMENT
motion, and cognition; and potential exposure to toxins, as Monitor Effects of Medications
well as generalliving conditions and lifestyle. • Older patients seem to have more problems with both
the therapeutic effects of medications and drug to xic-
COMFORT STATUS ity. This may be due in part to the decrease in hepatic
Discomfort resulting from abdominal pain or pruritus (itch- circulation that accompanies aging as well as the de-
crease in the enzyme activity of the liver.
ing) may be one of the major problems of people with hepatic
• Standard doses of medication published in a formulary
dysfunction. The person may complain of continuous upper
may be too high for elderly patients. Most drug dos-
abdominal discomfort or a dull ache in the upper right quad- ages are calculated for healthy white adult men.
rant. The discomfort does not usually alter normal function- • Polypharmacy occurs when the elderly patient receives
ing, although it can cause ineffective breathing secondary to multi pie medications from multi pie prescribers.
the abdominal pain. The discomfort is most significant in that
Assess NutritionaI Status
it provides verification for the underlying pathological processo
• Because the liver has many functions that aim to main-
Comfort status may be altered because of the general body
tain energy stores and metabolism, the elderly patient
aching associated with acute viral infections of the hepatic sys- may show signs of fatigue if liver function has dimin-
tem. Most distressing to the patient is the pruritus usually as- ished enough to limit the available energy needed to
sociated with jaundice, which may cause significant discom- support activities of daily living.
fort. The elevated serum bilirubin that occurs with jaundice
COMMON DISORDERS IN ELDERS
causes capillary dilation in the skin, the source of the pruritus.
• Increased risk for drug toxicity
In addition, bilirubin is an irritating substance to the chemo-
• Polypharmacy
sensitive area of the skin. The history should include an assess- • Malnutrition
ment of factors that worsen itching and of measures that help
relieve it.

NUTRITIONAL STATUS giotensin, and aldosterone. These hormones increase sodium


People with hepatic dysfunction often experience alterations and water retention.
in nutritional status. Some hepatic problems result in Another factor causing fluid volume excess is the hypo-
anorexia, nausea, and vomiting. The patient should be ques- albuminemia that is associated with liver disease. The hypoal-
tioned about the occurrence of such episodes. Assessment buminemia decreases the osmotic pressure in the vasculature,
should include onset, precipitating factors, association with causing fluid to leave the vascular space and enter the intersti-
food or alcohol intake, and measures that provide relief. tial space, resulting in edema. Levels of electrolytes, particu-
Poor nutritional habits and malnutrition resulting from larly sodium, potassium, hydrogen, and bicarbonate, can be
lifestyle pattems or food intolerances may be present. A useful elevated or decreased.
method to assess the patient's nutritional status is to ask the To establish the patient's needs, the history collected
patient what he or she has eaten in the past 24 hours and as- should include information about:
certain whether this is the typical eating pattem. 1. Normal fluid and food intake and output
Alcohol use should also be assessed. Alcohol, which pro- 2. Abnormal fluid and electrolyte losses, such as vomiting, di-
vides calories but has no nutrient value, may hide weight loss arrhea, or bleeding
normally associated with malnutrition. In the case of chronic 3. Changes in weight, both losses and gains
alcohol use, muscle mass may have decreased while the over- 4. Occurrence of signs and symptoms of fluid or electrolyte
all weight remained stable. In addition, weight loss may be deficit, such as weakness, dizziness, syncope, and weight
masked by water retention. loss
People with chronic problems of the hepatic system of- 5. Occurrence of signs and symptoms of fluid or electrolyte
ten require treatment with special diets, such as low sodium, excess, such as edema in hands, feet, and legs; an increase
altered protein intake, and water restriction. The history in abdominal girth; and weight gain.
should include information about food intolerances and food
preferences. ELlMINATION PATTERNS
Intestinal and urinary elimination may be altered in people
FLUIO ANO ELECTROLYTE STATUS with liver problems. If there is an obstruction of bile flow, the
Hepatic dysfunction can be associated with volume deficit person may give a history of grayish-white or clay-colored
from nausea and vomiting or from acute bleeding with cir- stools and have dark amber, brown, or mahogany-colored
rhosis. Fluid volume excess typically occurs in people with he- urine. Blood in the urine or stools may be present. The nurse
patic dysfunction as a result of renal retention of sodium and can test for occult blood in the urine by using a reagent strip
water that is initiated by peripheral vasodilation. This expan- and test the stool by performing a Hematest or guaiac testo
sion of the vascular space effectively decreases the circulating A reported decrease in urine output or the occurrence of noc-
blood volume, which results in the release of renin, an- turia may result from sodium and water retention.
1188 unit vii ALTERATIONS IN METABOLlSM
,
ENERGY LEVEL nificant sources of contact with the hepatitis viruses). The
Because of altered nutrient intake, abnormal fluid and e!ec- environmental/social history also can he!p identify particular
trolyte status, and increased metabolic needs, people with he- persons, factors, or places associated with substance abuse, if
patic problems often report an activity intolerance to normal a problem exists. Data about persons, factors, or places asso-
daily activities or simply fatigue. Weakness may be reported, ciated with substance abuse are needed for long-term man-
and nursing care should be adjusted to provide for the pa- agement of drug and alcohol abuse (see Chapter 14).
tient's safety. As the underlying liver condition resolves, the fa-
tigue and weakness may resolve. However, the patient and OBJECTIVE DATA
family must understand that the energy leveI may take a long
time to return to normal. To assess the functioning of the hepatic system completely, a
thorough assessment of the total body is required. First, ex-
PERCEPTION, MOTION, ANO COGNITION amination of the overall appearance of the patient is neces-
Chronic health problems of the hepatic system can cause sary. Does the patient appear chronically or acute!y ill? Is the
changes in neurological functioning, particularly in re!ation individual attentive, restless, or lethargic? Does the person ap-
to the peripheral nervous system and higher cognitive func- pear nourished or malnourished? Is the skin jaundiced? Are
tions. The patient should be asked about alterations in sensa- the sclerae yellow? In a darker-skinned person, are the palms
tion in extremities, any noticeable changes in memory, of the hands or soles of the feet jaundiced? Are the oral mu-
episodes of forgetfulness or blackouts, and alterations in coor- cous membranes yellow? Are there any other signs of hepatic
dination or in the ability to do fine motor tasks. The onset of dysfunction, such as enlarged abdomen, palmar erythema,
any alterations, pattern of changes (continuous or intermit- change in secondary sexual characteristics, bruises, muscle
tent), and duration of any changes should be determined. wasting, or edema? Petechiae and spider angiomas, usually on
the nose, cheeks, or upper thorax, may be present.
EXPOSURE TO TOXINS After the general inspection, the assessment should focus on
Hepatic dysfunction can be caused by various agents, such as fluid status. Vital signs, including orthostatic changes, weight,
alcohol, drugs, industrial chemicals, and viruses. A history of temperature, skin turgor, mucous membrane moisture, pres-
exposure to any toxins must be elicited. A drug and alcohol ence of edema, and behavior changes should be assessed. To
history is necessary to determine whether the patient has been assess energy leve! and nutritional status, the patient's total
exposed to these two hepatotoxins. muscle mass and muscle strength should be examined.
The drug history should focus on prescription, over-the- While performing the assessment note the patient's mental
counter, and street drugs. For example, acetaminophen is a status, affect, and alertness. Note changes in facial expression,
drug often used by adolescents to commit suicide and can responsiveness, leve! of consciousness, and affect. Are there
cause severe liver damage in doses 10 times greater than the periods of confusion or disorientation? Is the affect appropri-
recommended dose. The liver damage is intensified by the ate for this situation? Because handwriting or the ability to
combination of acetaminophen and alcohol. The alcohol draw a box, triangle, or square deteriorates with decreasing
history should focus on normal amount of intake and time liver function, a sample of handwriting or a drawing of a geo-
since last intake. An occupational history he!ps to identify metric figure may be obtained from the patient.
potential toxins in the work environment such as methylene After a general impression of the total patient is obtained,
chloride solvents. An environmental/social history might the assessment should focus on the abdomen. The abdomen is
identify potential sources of viruses (see Box 36-2 for sig- 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-
. . Health History Necessary tening skin, protruding umbilicus, and bulging flanks. Palpate
to Identify Exposure or percuss the abdomen to ascertain the presence of a fluid
• to Hepatitis Viruses wave and shifting dullness, which are indicative of ascites. Pal-
~AAi'f't%'!G'jI9!~~~~~~T.!'~~w •..'~;
pation and percussion are also used to assess for hepatic ten-
Contact with persons with jaundice ~. derness, size, and consistency and the presence of hepatic
, Travei or visits to environments with poor sanitation j,

~ 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 ~ chronic hepatic dysfunction and should be percussed to de-
~ History of recent ear or body piercing or tattooing [ termine the size and location; defer palpation because of the
~ History of recent blood transfusions i' fragility of the enlarged spleen. Last, measure abdominal
~ Intravenous drug abuse (sharing of contaminated f' girth. Hemorrhoids caused by prolonged elevations in portal
~ needles) ~' system pressure may be present.
~. Occupational exposure (e.g., health service personnel :
~. with frequent blood contact, personnel in daycare cen- ~.
i" ters, personnel in centers of custodial care) DIAGNOSTIC TESTS
r History of hemodialysis
t~History of multi pie sex partners; male bisexual ar male ;;. Various tests he!p in assessing the status of the hepatic system.
F homosexual lifestyle Many of the tests require taking samples of blood; other tests
f~~~~~'.j.~~~=~~_~~i~ ,,~ are more extensive and may cause discomfort; still others may
Assessment of the Hepatic System chapte,. 36 1189

require fasting. The nurse is responsible for preparing the pa- move any jewelry, dentures and partial dentures if they contain
tient for the tests. The physical preparation of the patient will metal, or any other item that contains metal, such as hairpins
vary from institution to institution, and the nurse must know or limb prostheses. Patients should be assessed for claustro-
the routine preparation. In addition to the physical prepara- phobia before the procedure, because it may elicit this type of
tion, the nurse carries out appropriate teaching and monitor- response. Contraindications to MRl include a pacemaker and
ing of the patient before, during, and after the diagnostic tests. titanium or stainless steel prosthetic implants or prosthetic
heart valves.
LABORATORY TESTS
Multiple tests may be necessary to determine the extent and Radionuclide Imaging
seriousness of hepatic disease. To be of benefit many tests re- The liver may be outlined by radionuclide imaging techniques.
quire serial readings. The procedure, preparation, and inter- Selected radioisotopes are given intravenously. After the injec-
pretation of blood, stool, and urine studies used to eValuate tion of the radioisotope, the patient is placed in the supine po-
liver function are summarized in Table 36-1. sition, and a scintillation detector is passed over the abdomen in
the area of the liver. The radiation coming from the isotopes
RADIOLOGICAL TESTS immediately beneath the probe of the scanner is detected, am-
Radiographic tests are used to assist in identifying the cause of plified, and recorded. Scanning helps differentiate nonfunction-
hepatic dysfunction. Besides the examinations described in ing areas from normal tissue and to identify hepatic tumors,
the following section, abdominal films, barium swallow, bar- cysts, and abscesses. Usually a nonfunctioning area will appear
ium enema, and gastroscopy may be ordered (see Chapter 38). as an area of decreased activity. However, gallium-67 (67Ga) is
These tests help identify the presence of pathological GI con- preferentially taken up by hepatocellular carcinomas and ab-
ditions that may cause signs and syrnptoms similar to those scesses, and these areas will appear as areas of very heavy ra-
found in hepatic dysfunction. dioactivity. Adverse reactions to the radioisotopes used for ra-
dionuclide imaging are unusual, and the procedure is relatively
Ultrasonography safe. Discomfort is minimal. Only small amounts of radioactive
Ultrasonography of the liver is done to assess jaundice of material are given, and radiation precautions are not necessary.
unknown etiology, hepatomegaly, or suspected turnors. Addi- Only 67Ga scanning requires special preparation. 67Ga is ex-
tional information obtained from ultrasound includes liver creted by the GI tract. To avoid absorption of the radioisotope
size, shape, and location; cysts; abscesses; and filling or dilation by the G1 contents, laxatives and enemas are prescribed. The
defects. toilet should be flushed twice for bowel movements after the
The preparation of the patient for ultrasonography is rela- 67Gascanning to ensure the safety of the patient and others. UI-
tively simple. Usually the patient is not allowed to eat for 8 to trasonography, CT scanning, and MRl have replaced radionu-
12 hours before the procedure, because bowel gas in the G1 clide imaging in most instances of hepatic dysfunction.
tract will interfere with the testo Any residual barium needs to
be elirninated from the G1 tract before the testo The patient Angiography and Portal
must be well hydrated, beca use dehydration can decrease the Pressure Measurernents
ability of ultrasonography to distinguish between the liver and Catheterization of the hepatic artery, portal venous system (by
surrounding tissues. various routes), and hepatic vein allows the injection of a con-
trast medium and the visualization of the vascular supply of
Computed Tomography Scan the hepatic system. Angiography determines the patency of
Computed tomography (CT) scanning can also be used to as- the system and the presence of tumors, abscesses, coHateral
sess patients with potential hepatic problems. It is helpful in circulation, varices, and bleeding.
identifying problems similar to those described for ultra- Portal and hepatic vein pressure (wedged hepatic vein pres-
sonography. Contrast medium can be used with the CT scan sure) can be measured. These readings may be done in conjunc-
to intensify the appearance of vascular structures and hepatic tion with angiography or as a separate study. These measure-
parenchyrna. The patient should eat nothing for 8 to 12 hours ments help in determining the degree of portal hypertension.
before the test; if contrast medium is to be used, the patient The presence of allergy to contrast media must be ascer-
should be assessed for allergies to iodine or contrast media. tained before angiography is done. After both angiography
Adequate hydration is necessary when a contrast medium is and pressure readings, the insertion site is observed for bleed-
used. Barium studies should be done at least 4 days before the ing, and the patient's vital signs are checked every 15 minutes
CT scan or after the scan because the barium can interfere for 1 hour, every 30 minutes for 1 hour, every hour for
with test results. 4 hours, and then if the patient is stable, every 4 hours. Bedrest
is maintained for 24 to 48 hours after the testo
Magnetic Resonance Imaging
Magnetic resonance imaging (MRl) is used to detect liver tu- SPECIAL TESTS
mors. Because magnetic fields are used instead of radioactive Biopsy of the Liver
isotopes to produce the image, no special preparation of the A liver biopsy may be used to aid in establishing the cause of
patient is necessary. 1t is important to inform the patient that liver disease. In this procedure a specially designed needle is
this test is painless. The patient should be instructed to re- 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 .....
this time,'·3,5
_S"""'_-Ubfi~~"',~'-'f'IN:_amm:am_-'~~·~~ l
and a small piece of tissue is removed for study. This proce- test, and a sedative usually is given about 30 minutes before
dure is contraindicated in a patient who has an infection of the biopsy.
the right lower lobe of the lung, ascites, a blood dyscrasia, or a A liver biopsy is performed as follows, The patient lies supine;
problem with blood clotting, as well as in any patient unable the skin over the area selected (usually the eighth or ninth inter-
to cooperate by holding his or her breath, To avoid hemor- costal space) is cleansed and anesthetized with procaine hy-
rhage, vitamin K may be given parenterally for several days be- drochloride, A nick is made in the skin with a sharp scalpel blade.
fore and afier the biopsy is performed. A biopsy usually is not Then the patient is instructed to take several deep breaths and
done if the prothrombin time is below 40% of normaL The then to hold his or her breath while the needle is introduced
physician should explain the procedure to the patient, for ex- through the intercostal or subcostal tis sues into the liver, The
ample, the importance of being able to hold one's breath and special needle assembly is rotated to separate a fragment of
remain absolutely still when the needle is introduced, Move- tissue and then is withdrawn, The specimen is placed into an
ment of the chest may cause the needle to slip and to tear the appropriate container, which is labeled and sent to the pathol-
liver covering, Most hospitals require that the patient sign a ogy laboratory. A simple dressing is placed over the wound,
written permission form for the procedure to be done. Food The dangers of liver biopsy are accidental penetration of
and fluids may be withheld for several hours preceding the blood vessels, causing hemorrhage, or accidental penetration
Assessment of the Hepatic System chapter36 1193

of a biliary canniculi, causing a chemical peritolllns from Peritoneallavage can be done by either the closed or open
leakage of bile into the abdominal cavity. After the procedure method. In the closed method, a peritoneal dialysis catheter is !
the nurse should assess the patient for signs of hypovolemia inserted, and the peritoneal space is aspirated for gross blood. i
and shock. The patient's pulse and blood pressure should be If no gross blood is found, lavage is carried out with normal :1
monitored every 30 minutes for the first few hours after the saline. In the open method the peritoneum is exposed COffi-
procedure and then hourly for 24 hours. The patient's tem- pletely and then opened enough to allow entry of a dialysis
perature should be taken at least every 4 hours to determine a catheter. Again, gross blood is aspirated first, and if no blood
baseline and detect peritonitis. The physician may order pres- is found, lavage is carried out.
sure applied to the biopsy site to help stop any bleeding. An ef- Peritoneal lavage requires a complete explanation to the
fective way to apply pressure is to have the patient lie on the patient and significant others and informed consent. A naso-
right side with a small pillow or folded bath blanket placed gastric tube and Foley catheter are inserted before the proce-
under the costal margin for several hours after the biopsy. dure to prevent penetration of the intestines or bladder. In the
Bedrest is maintained for 24 hours after the testo closed method a local anesthetic is used, whereas in the open
method general anesthesia is necessary. Postprocedural care
Paracentesis involves monitoring for peritonitis and bleeding in patients
A paracentesis, or peritoneal tap, can be done to remove peri- who have closed peritoneal lavage. Patients who have open
toneal fluid (ascitic fluid) for cytological or other laboratory peritoneal lavage require general postanesthetic care (see
studies or to drain large volumes of ascitic fluidoWhen condi- Chapter 20).
tions such as respiratory distress, severe abdominal discom-
fort, or cardiac dysfunction are present because of the ascites, ENDOSCOPY
a paracentesis may be necessary. Repeated paracenteses are The hepatic system and gallbladder can be examined by several
not the treatment of choice for controlling cmonic, recurring types of endoscopic procedures. The endoscope can be in-
ascites because of complications. serted direetly through the peritoneum (peritoneoscopy),.thus
When paracentesis is performed, the skin is cleansed, and affording direet visualization of the abdominal organs and the
the abdominal wall is anesthetized. A long aspiration needle is taking of biopsy specirnens. Esophagoscopy and gastroscopy
inserted, and fluid is aspirated for diagnostic tests or drained can be used to diagnose esophageal varices or to perform in-
as necessary. In preparation for the procedure, the patient is jection sclerotherapy. An endoscopic retro grade cholan-
given a complete explanation and signs a consent form; the giopancreatography (ERCP) can be done to visualize and pro-
patient should void irnrnediately before the procedure to di- vide radiographic examination of the liver, gallbladder, and
minish the risk of puncturing the bladder. Sterile technique pancreas (see Chapter 38). Ali these procedures require that
must be maintained during the procedure. the patient be fasting at least 12 hours before the testoBefore
The complications of paracentesis include peritonitis, if ERCP the patient should be asked about allergies or sensitivi-
sterility is not maintained, and peritoneal bleeding resulting ties to x-ray dye.
from trauma to blood vessels.The patient's vital signs, includ- After the procedure, the nurse should assess the patient's
ing temperature, urine output, and skin temperature and ability to swallow. The patient's gag reflex may not return for
moisture, should be monitored for signs of peritonitis or 1 to 2 hours. After ERCP the patient should be monitored
bleeding. The patient's abdomen should be assessed for rigid- for signs of complications, which include perforation, sep-
ity and his or her sensorium for confusion. sis, and pancreatitis. Vital signs are usually taken every 30 min-
Removal of large amounts of fluid from the peritoneal utes and then hourly for 4 hours. N sedation is frequently used
space can result in hypovolemia and shock because additional during endoscopic procedures.
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 ANATOMY ANO PHYSIOLOGY
vital signs, mental status, urine output, skin temperature and • The liver is important for adequate energy production and
moisture, and status of mucous membranes. Protein and waste disposal.
potassium leveIs should also be monitored.
SUB.JECTIVE DATA
Peritoneal Lavage • Pathophysiological conditions of the liver result in discom-
fort, inadequate nutrition, fluid and electrolyte deficit or ex-
Peritoneal lavage may be used to assess damage to the liver
cess, bleeding, altered elimination, fatigue, and altered per-
from abdominal trauma in persons with altered states of con- ception, cognitive, and motor functioning.
sciousness who cannot give a satisfactory history. It may also
be used in patients with abdominal trauma when unexplained OB.JECTIVE DATA
hypotension is present, when unreliable physical examination • Pathophysiological conditions of the liver can result from
results are present, or when the patient requires general anes- exposure to various toxins, including drugs, alcohol, chem-
thesia for other injuries. 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 nosis, Am J Nurs 94( 1):43-48, 1994.
studies that are used to help identify the pathophysiologi- 3. Moseley RH: Approach to lhe patient with abnorma! liver chem-
cal state or other nursing needs. istries. In Kelley WN, editor: Textbook of internal medicine, ed 3, Phil-
• Radiologic, endoscopic, and other invasive tests are used to adelphia, 1997, Lippincott-Raven .
help in identifying the exact pathophysiological condition. 4. Renkes J: GI endoscopy: managing the full scope oí care, Nursing 93
23( 6):50-55, 1993.
References 5. Siconolfi LA: Clarifying the complexity oí liver function tests,
1. American Medica! Association: Prevention, diagnosis, and man- Nursing 95 25(5):39-44,1995.
agement of viraI hepatitis, Chicago, 1996, AMA: Division oí Hea!lh
Science.