JUDITH K.
SANDS
objectives After studying this chapter, the learner should be able to:
1 Describe the etiology, epidemiology, and pathophysiology
cer of the biliary tract.
2 Compare treatment alternatives for biliary tract disease.
3 Describe the nursing care needs of patients with disorders of the biliary system"
I 4 List the causes of acute and chronic pancreatitis.
5 Explain the pathophysiological basis for signs and symptoms
and pancreatic tumors.
6 Discuss management approaches for acute and chronic pancreatitis.
7 Develop nursing diagnoses, patient outcomes, and plans of interventions for patients who have
acute or chronic pancreatitis or cancer of the pancreas or who have had pancreatic surgery.
PROBLEMS OF THE GALLBLAOOER
The biliary system is affected by stones and obstruction, in-
flammation and infection, and cancer. Gallbladder disor-
ders are extremely common and affect millions of adults
every year.
CHOLELlTHIASIS/CHOLECYSTITISI
CHOLEOOCHOLITHIASIS
Etiology
Gallstones can occur anywhere in the biliary tree. The term
cholelithiasis refers to stone formation in the gallbladder and
represents the most common biliary disorder. Either acute or
chronic inflarnrnation, termed cholecystitis, can result, usually
precipitated by the presence of stones. When stones form in or
migrate to the common bile duct the condition is termed
choledocholithiasis. Figure 42-1 illustrates common sites for
gallstones.
Eighty percent of gallstones are composed of choles-
tereI. 19The remaining 20% are pigmented stones, which are
further classified as black or brown.'9 Although the precise
etiology of gallstones is unknown, the basic component of
supersaturation of the bile v,ith êholesterol is widely ac-
cepted. Because most healthy individuals experience super-
saturation of the bile at various times without developing
gallstones, it is clear that other factors are operational as
well. Risk factors for gallstones have been well identified
and include various clinical states associated with changes
in cholesterol formation and excretion (Research Box). The
risk factors for cholesterol gallstones are listed in the Risk
Factors Box on the next page. The development of pig-
mented stones is linked to disease states such as cirrhosis,
hemolytic disease, and chronic small bowel disease.19
of cholelithiasis, cholecystitis, and can-
of acute and chronic pancreatitis
Epidemiology
Cholelithiasis is a common health problem in the United
States. Stones affect about 10% of men and 15% of women
older than 55 years of age. An estimated 20 to 25 million adults
have gallstones, and 1 million new cases are diagnosed annu-
ally.'9 Many, if not most, patients are asymptomatic, and it is
theorized that a large number of cases remain undiagnosed.
Ten percent of persons with gallstones develop symptoms
within 5 years of diagnosis, and greater than 500,000 surgical
procedures are performed each year at an annual treatment
cost in excess of five billion dollars.16 These figures make
cholelithiasis and its associated disorders the most common
and costly digestive disease. Cholelithiasis is two times more
research'~i,
Relerence: Everhart JE: Contributions 01 obesity and weight loss to gall-
stone disease, Ann Intern Med 119(10):1029-1035,1993.
Obesity and the process of rapid weight loss are typically
identified as significant risk factors for the development
of gallstone disease. This study involved a data review of
studies related to the prevalence of gallstone disease
from 1966 to 1992. The data showed that obesity was a
strong risk factor for gallstones in women, particularly
during periods of rapid weight loss. Between 10% and
25% of obese persons will develop gallstones within a
few months of beginning a very low-calorie diet, with
perhaps one third of the total becoming symptomatic.
The risk is less strong in men and most strong in persons
with the highest body mass index and most rapid weight
1055. Treatment with ursodeoxycholic acid (ursodiol) dur-
ing weight 1055 effectively prevented the development of
stones. The effect of various diets on the incidence of
stone formation was not explored.
1373
1374 unit: viii Alterations in Digestion and Elimination

common in women, occurs most frequently in midclle-aged
and older persons, and affects American Indians, Mexican
Americans, and whites more frequently than African Ameri-
cans and Asians, although the incidence in Asians is increasing.
Pathophysiology
Bile is primarily composed of water plus conjugated bilirubin,
organic and inorganic ions, smali amounts of proteins, and
three lipids-bile salts, lecithin, and cholesterol. When the
balance of these three lipids remains intact, cholesterol is held
in solution. If the balance is upset, cholesterol can begin to
precipitate. Cholesterol gallstone formation is enhanced by
the production of a mucin glycoprotein, which traps choles-
terol particles. Supersaturation of the bile with cholesterol
also impairs gallbladder motility and contributes to stasis.
Cholesterol stones are hard, white or yellow-brown in color,
radiolucent, and can be quite large (up to 4 cm). The stones
most frequently occur in multipIes but can be solitary. The
process of stone formation is sIow. Stones are theorized
to grow steadily for 2 to 3 years and then stabilize in size.
Small bile duct
Eighty-five percent of ali stones are Iess than 2 cm in diameter.
Most are found in the galibIadder, but it is estimated that 15%
to 60% of persons oIder than age 60 who undergo surgery for
galistones also have stones in the common bile duct.8
Black pigmented stones form as the result of an increase in
unconjugated bilirubin and calcium with a corresponding de-
crease in bile salts. GalibIadder motility may also be impaired.
Brown stones develop in the intra- and extrahepatic ducts and
are usualiy preceded by bacterial invasion.
Although most persons with gallstones are asymptomatic,
choIecystitis can develop at any time, usualiy from a blockage
of the cystic duct by the stone or from edema and spasm ini-
tiated by the presence or passage of the stone. In acute chole-
cystitis the galibladder is enIarged and tense. A secondary bac-
terial infection can occur within several days and is the cause
of most of the serious consequences of the disease.
Classic clinicaI manifestations of symptomatic galistones in-
clude pain in the right upper quadrant (RUQ) of the abdomen,
which is described as severe and steady. The pain frequently ra-
diates to the right scapula or shoulder, has a sudden onset, and
persists for about 1 to 3 hours.8 It may awaken the patient at
night or be associated with the consumption of a large or high-
fat meal. Some patients experience nausea and vomiting and
may be febrile. Chills and fever are more likely with acute choIe-
cystitis. Patients are rareIy jaundiced. Bowel sounds may be ab-
sento Palpation of the RUQ causes a severe increase in pain and
temporary inspiratory arrest (Murphy's sign). The episode of
choIecystitis usualiy subsides in 1 to 4 days. Clinical manifesta-
tions of choIecystitis are summarized in Box 42-1.
The diagnosis of galistones is fairIy straightforward when
the classic symptoms are present. The diagnosis is more diffi-
cult when the symptoms are milder or reflect simply general
dyspepsia. It is estimated that up to 25% of patients with irri-
table bowel syndrome or peptic ulcer disease also have gali-
stones, and the exact etiology of the patient's symptoms needs
to be determined if possible.8 Researchers theorize that many
patients with "poor outcomes" after gallbladder surgery may
actualiy reflect situations where the gallbladder was not really
the source of the patient's dyspepsia.8•19

'.1.1
, If.M
. '""' -&
c;.~lnlCªh-n.'1J3Fl.1:;.f:.stªt.l "
..
ÇJl1S
i Cholecystitis
figo 42-1 Common sites of gallstones. Sudden onset pain in the RUO of the abdomen
Severe and steady in quality
Frequently radiates to the right scapula or shoulder
risk'act rs Persists for about 1 to 3 hours
May awaken the patient at night
Cholesterol Gallstones
May be associated with consumption of a large or
Obesity fatty meal
Middle age , Anorexia, nausea, and possibly vomiting
Pregnancy, multiparity, and the use of oral contra- Mild to moderate fever
ceptives Decreased or absent bowel sounds
Rapid weight loss (-5 pounds/wkl Acute abdominal enderness and a positive Murphy's
Hypercholesterolem ia, use of anticholesterol medications sign
Diseases of the ileum Elevated white blood cell count, slightly elevated serum
Gender (approximately twice as common in women) bilirubin and ai a 'ne phosphatase leveis
 =

- - 1..":erseveral acute at-

'C"er,:S ually the result of
e Gallbladder

Treatments
and Exocrine Pancreas chapter42 1375

Extracorporeal shock wave lithotripsy was pioneered in

::::e gal:.bla' .er wall that cause scarring,
ibly cerarion. Bacterial infection may
z.:so e resem. Parients with chronic disease often do not
see' help unril jaundice or other complications develop. Fig-
ure 42-2 shows the relationship between stone formation and
associated outcomes in uncomplicated gallbladder disease.
Collaborative Care Management
Diagnostic tests
Ultrasonography is the primary diagnostic tool for identi-
fying cholelithiasis. If the results of ultrasonography are in-
conclusive, oral cholecystography may be performed (Fig-
ure 42-3). Laboratory tests include white blood cell count,
serum bilirubin, alkaline phosphatases, and liver function.
Any additional diagnostic testing is performed to rule out
other causes of gastrointestinal (GI) discomfort.
I
Germany and adapted to the treatment of gallstones. Litho-
tripsy uses shock waves to disintegrate the stones. Extensive
selection criteria limit the use of this treatment to a small
II
number of patients with gallstones.19 Patients must also un-
dergo oral dissolution therapy after treatment to dissolve the
stone fragments. Recurrence is a problem, and the treatment,
including follow-up drug therapy, is tive times more expensive
than surgery. It is rarely a cost-effective option.8
Percutaneous drainage may be used as a primary treat-
ment for patients .with acute cholecystitis or to relieve in-
flammation and infection before surgery. The drainage tube
is placed percutaneously using sonographic guidance. An op-
erating scope may be introduced by dilating the tract to re-
move a stone. The procedure has good short-term results, but
since the gallbladder remains intact, recurrence rates run as
high as 50%.19

Medications Surgical management

Oral dissolution therapy with ursodeoxycholic acid Cholecystectomy was first performed in Berlin in 1882
(Actigall) may be prescribed for patients who are poor and evolved into a procedure with excellent effectiveness and
surgical risks or who refuse surgery. The drug gradually extremely low associated morbidity and mortality. lt is the
desaturates the bile, which allows space for the reuptake of
the cholesterol in the stones. The treatment is only effec-
tive when stones are less than 1.5 to 2 cm in diameter. A
full course of treatment takes from 1 to 3 years and is ex-
tremely expensive. Up to 50% of patients experience re-
currences within 5 years.19
Direct dissolution therapy with methyl-tert-butyl ether is
occasionally used in high-risk surgical patients. The drug is
instilled through a percutaneous catheter, which is monitored
fluoroscopically. Multiple drug instillations are required over
12 to 24 hours, which makes the treatment labor intensive for
the physician and extremely expensive.

Etiological factor~:' . .'.

(Age, gencler, multiparity,_obesjty, Iifestyle; pn~sence of other diseases)

CholedodTOlithiasis

I Asymptomatic.1

figo 42-2 The development of uncomplicated chole- figo 42-3 Oral cholecystogram. Radiolucencies
cystitis. (arrollVs) are caused by gallstones.
1376 unit viii Alterations in Digestion and Elimination
second most common surgical procedure performed in the
United States following cesarean section and serves as the
standard against which other gallstone treatments are mea-
sured.8 The main advantage of cholecystectomy is the fact that
it stops the disease. The recurrence rate is zero. The main dis-
advantage has always been that it is major abdominal surgery
with a11of the associated pain and disability. Hospital stays av-
eraged 3 to 7 days and recovery required 4 to 6 weeks.
Laparoscopic cholecystectomy was first performed in
France in 1987and in the United States in 1988,and by the early
1990s had revolutionized the care of patients with gallbladder
disease.16 Laparoscopic cholecystectomy offers several real ad-
vantages over traditional surgery. It is less invasive,which al-
lows a shorter healing and recuperation time; there is less scar-
ring; and, most important1y, the pain associated with the
proceáure ís sígnífjcantIy reduced. The hospital stay is less than
24 hours, and patients can return to normal activities in 2 to
3 days. It is conservative1y estimated that at least 80% of all
cholecystectomies are being performed laparoscopically today,
and the number continues to increase as surgical techniques
improve. Acute infection is the only remaining contraindica-
tion. When the laparoscopic cholecystectomy was first intro-
duced, the ability to explore the common bile duct was limited.
This limitation necessitated the use of open cholecystectomy
procedures with placement of a T-tube for drainage whenever
stones were present or suspected to be present in the common
bile duct. Surgical techniques have continued to improve, how-
ever, and laparoscopic approaches are now being successfully
combined with endoscopic exploration and sphincterotomyto
effective1ytreat patients with common bile duct stones.
Laparoscopic cholecystectomy is performed under general
anesthesia. The procedure consists of the creation of four
1/2-inch incisions made at the umbilicus, midJine in the epi-
gastric region, in the right upper quadrant at the midclavicu-
lar line, and at the anterior axillary line. Three to 4 L of car-
bon dioxide gas are introduced to insufflate the abdomen and
permit adequate visualization and the introduction of in-
struments. The operative field is magnified and projected on a
videoscreen, and a laser or cautery is used to dissect the gall-
bladder. The gallbladder is deflated and removed through the
umbilical incision. The CO2 is removed at the end of the pro-
cedure. lf problems develop during the procedure, it can be
rapidly converted to an open cholecystectomy.
The ski11of the surgeon is the primary determinant of out-
comes. The slight1yhigher rate ofbile duet injury associatedwith
the procedure is usual1yattributable to inexperience with the
technique. Laparoscopiccholecysteetomytakes about 90minutes
and is more expensivethan traditional open surgery.The short
hospital stayand tremendous patient satisfactionwith the proce-
dure, however, clearly outweigh the higher surgical costs. The
mild shoulder pain that patients may experiencefor up to 1week
is attributed to nerve irritation from distention and the CO2
gas,but the discomfort is easilymanaged with mild analgesics.
Diet
No diet is known to prevent the formation of gallstones.
Patients who are experiencing symptoms are encouraged to
follow a low-fat diet and eat sma11meals until definitive
therapy is completed. After treatment they can resume a nor-
mal diet.
Activity
There are no activity restrictions for persons with chole-
lithiasis, cholecystitis, or choledocholithiasis.
Referrals
Referrals would not general1ybe required for the manage-
ment of uncomplicated gallstones unless a serious comor-
bid condition necessitated the involvement of additional
professionals.
NURSING MANAGEMENT
OF THE PATIENT
UNDERGOING LAPAROSCOPIC
CHOLECYSTECTOMY
• PREOPERATIVE CARE
Patients will complete their preoperative preparation at
home before their arrival on the day of surgery. The nurse
will verify that the patient has had nothing by mouth
(NPO) and completed any required bowe1 preparation.
Preoperative teaching includes reviewing the scope and na-
ture of the surgi cal procedure and the care that will be
provided in the immediate postoperative period. The nurse
also ensures that the patient understands that the expected
pain is mild to moderate and can be successfu11ymanaged
with standard analgesics.
• POSTOPERATIVE CARE
The patient will be close1ymonitored in the immediate post-
operative period, and pain control will receive priority atten-
tion. A left side-lying Sims position can he1p to move the re-
tained gas pocket of CO2 away from the diaphragm and
decrease irritation. Deep breathing is encouraged. Foley
catheters and nasogastric tubes are common1y inserted during
the procedure and will be removed in the postanesthesia care
unit. As soon as the patient is sufficient1yalert, he or she will
be encouraged to sip clear fluids and get out of bed. Dressings
over the small incisions are monitored for bleeding. Healthy
patients with adequate home support may be discharged
when they are fu11yalert and have successfu11yvoided.
Patient/Family Education
Discharge instructions are straightforward. The patient is in-
structed to slowly resume normal activity over the next 2 to
3 days and consume a light diet. The patient is advised to
limit the intake of fatty and fried foods for the first few weeks
after surgery until tolerance is established. The incisions re-
quire minimal care, and the dressings can usually be removed
the next day. The patient is instructed to report the develop-
ment of redness, swellin ,or discharge from any incision, as
we11as the onset of feyer.pain, or tenderness in the abdomen.
Heavy lifting should e a ·oided.
 II
Management of Persons with Problems of the Gallbladder and Exocrine Pancreas chapter42 1377 ,i
A ClinicaI Pathway for the patient undergoing laparoscopic
cholecystectomy is shown below. The Guidelines for Care Box
more subtle symptoms and signs in the presence of cholecystitis.
Thus they can develop baeterernia before they seek help. Because
II
summarizes the care provided to a patient who undergoes tra- of the normal decrease in immune function with aging, they I,
ditional open cholecystectomy. are at greater risk for septic shock. Elderly patients have more
risks with surgery just because of their age.The laparoscopic
GERONTOLOGICAL CONSIDERATIONS cholecystectomy procedure is particularly effective in this age-
Gallbladder disease is seen more frequently with advancing age group as it decreases the period of immobility and recovery
but is treated in the same manner. Elderly persons may have substantially. Wound healing needs to be carefully monitored .

.',clinicai pa1:hway . Laparoscopíc Cholecystectomy Wíthout Complícatíons

DAY OF SURGERY
DAY OF ADMISSION DAY OF DISCHARGE
DAY 1 DAY 2

Diagnostic Tests Preoperative: CSC, UA

Postoperative: Hgb and Hct
edications PAR: IVs decreased to saline lock after nausea sub- Disc saline lock; PO analgesic
sides; IV analgesic, then PO
Treatments PAR: 1&0 q shift; VS q4hr x 4, then q8hr; assess Disc 1&0; VS q8hr; assess bowel sounds
bowel sounds q4hr; check drainage on bandages q8hr; remove bandages and reapply
q2hr bandages after shower if necessary
Diet NPO until nausea subsides, then c1ear liquids; ad- Regular diet, low fat
vance to full liquids, low fat
Activity Up in room with assistance about 6 to 10 hr after Up ad lib, OK to shower
surgery; T & OS q2hr
Consultations

08, Deepbreathing;Hct, hematocrit;Hgb, hemoglobin;PAR, postanesthesiarecovery;UA, urinalysis;VS,vital signs.

guidelines for care

The Person Undergoing Open Cholecystectomy
Preoperative
Teach patient the importance of frequent deep breathing
and use of incentive spirometer because the high inci-
sion and RUO pain predispose the patient to atelectasis
and right lower lobe pneumonia.
Explain the types of biliary drainage tubes that are
anticipated, if any.
Teach patient about the pain control plan to be used in the
postoperative period.
Postoperative
Place patient in low Fowler's position; assist to change po-
sition frequently.
Urge patient to deep breathe at regular intervals (every
1 to 2 hours) and to cough if secretions are present
until ambulating well. Assist patient to effectively
splint the incision. Encourage use of incentive spi-
rometer.
Give analgesics fairly liberally the first 2 to 3 days.
Use patient-controlled analgesia if possible. Meperidine
(Demerol) has been the drug of choice because it is be-
lieved to minimize spasms in the bile ducts, but mor-
phine is being used with increasing frequency.
Maintain a dry, intact dressing; usually a drain is inserted
near the stump of the cystic duct; some serous fluid
drainage is normal initially.
Encourage progressive ambulation when permitted.
Increase diet gradually to regular with fat content as toler-
ated (appetite and fat tolerance may be diminished if
there is externai biliary drainage).
Biliary Drainage
Connect any biliary drainage tubes to closed gravity drainage.
See Figure 42-4 and the Guidelines for Care Box on
p. 1378 for care of a T-tube.
Attach sufficient tubing 50 the patient can move without
restriction.
Explain to patient the importance of avoiding kinks,
clamping, or pulling of the tube.
Monitor the amount and color of drainage frequently;
measure and record drainage at least every shift.
Report any signs of peritonitis (abdominal pain, rigidity, or
fever) to the physician immediately.
Monitor color of urine and stools; stools will be grayish-
white if bile is flowing out a drainage tube, but the nor-
mal color should gradually reappear as externai drainage
diminishes and disappears.
1378 unit viii Alterations in Digestion and Elimination

SPECIAL ENVIRONMENTS FOR CARE
Criticai Care Management
Critical care management would not .be anticipated for any
phase of routine gallstone management. The surgical proce-
dures have an excellent safety record and are associated with a
less than 7% incidence of morbidity from any cause.
Home Care Management
Cholecystectomy is the foundation of care for gallstones, and
the procedure has become essentially same-day or overnight
surgery. Self-care management at home is therefore expected.
Most patients have no specific home care needs beyond rou-
tine monitoring of wound healing and the progressive return
to usual activities.17 For more complex procedures patients
may be discharged from the hospital with a T-tube in place.
Teaching concerning T-tube care is included in the Guidelines
for Care Box. Elderly patients may need some additional as-
'guide'ines for care
Managing a T-Tube
Purpose
A T-tube may be placed after surgical exploration of the
common bile duct to preserve patency of the common
duct and ensure drainage of bile until edema resolves
and bile is effectively draining into the duodenum. The
tube is usually connected to gravity drainage and can
be converted to a leg bag to limit its restrictiveness
and visibility. The patient may be discharged with the
T-tube in place (see Figure 42-4).
sistance at home when they undergo same-day surgery. These
needs are ideally identified and arranged before surgery.
COMPLlCATIONS
Transient mild diarrhea is the only adverse outcome that has
been consistently linked to cholecystectomy. The most com-
mon complication of nonsurgical management of gallstone
disease is recurrence, and it is clear that undiagnosed or in-
adequately treated gallbladder disease can result in serio
and even life-threatening complications, including over-
whelming sepsis and peritonitis. Chronic dyspepsia and sub-
clinical malabsorption are often included as possible compli-
cations of cholecystectomy, but there is no concrete evidence
that the reduction in the pool of bile salts and the loss of the
reservoir funetion of the gallbladder increase the incidence
of duodenal reflux or an alkaline shift in the gastric pH.16
Some researchers suggest that these so-called "complica-
tions" may actually reflect situations in which the patient's
original digestive symptoms were never related to the gall-
stones and therefore were not improved by their rem oval
(Research BOX).5
PRIMARY SCLEROSING CHOLANGITIS
Etiology/Epidemiology
Inflammation and scarring of the biliary tree occur most com-
monlyas a result of gallstones and bile duct infection. Parasites
are a common source of chronic duct infection in Asia and de-
veloping countries. When no cause for the bile duct injury can
be found, the process is called idiopathic or primary sclerosing
cholangitis (PSC).

General Care
Attach the tube to gravity drainage. Ensure that suffi-
cient tubing is in place to prevent pulling and restric-
tion of movement.
Check drainage every 2 hours on the first day ànd at
least once per shift on subsequent days.
Record output carefully. Initial drainage may be as
much as 500 to 1000 ml per day, but this amount
should steadily decrease as healing occurs.
Follow physician's order for initiating clamping of
the tube.
Monitor patient's response to c1amping and record in-
cidence of distress.
Unclamp the tube promptly if distress occurs.
Monitor the color of the stool. Stool is initially clay-
colored but regains pigmentation as bile again flows
into the duodenum.
Keep the skin clean and protected from bile drainage as
bile is extremely irritating to the skin.
Teach the patient to empty the bag and convert it to a
leg bag if discharge with the T-tube is planned.
Provide self-care teaching:
A daily shower is usually permitted.
A sterile dressing should be reapplied to the T-tube
entry site each day.
Zinc oxide may be used to protect the skin from irritation.
Redness, swelling, or drainage from the site and the figo 42-4 Section o' T- ube emerging from stab
development of fever should be promptly reported vvound may be placed over roll of gauze anchored
to the physician. to skin vvith adhesive spe to prevent its lumen from
being occluded b p'essure.
 anagement of Persons vvith Problems of the
The prevalence of PSC is unknown. Both genetic and im-
munological mechanisms are suspected in its development.
The disease may occur alone but is generally associated with
other disorders, most of which have a strong immunological
component. The closest link is with inflammatory bowel dis-
ease (IBD), particularly ulcerative colitis. Of patients with PSC
70% have IBD, although PSC only occurs in 2% to 4% of all
patients with IBDY The PSC may precede the diagnosis of
IBD or follow it from 1 to 20 years late r. The patients are usu-
ally male, and PSC is diagnosed in early or middle adulthood,
typically by the age of 45. PSC is the cause for about one third
of all patients needing liver transplantation.
Pathophysiology
Primary sclerosing cholangitis causes changes in and around
the large bile ducts from inflammation, obstruction, and intra-
and extrahepatic fibrosis. Strictures can usually be found in
multiple locations. These strictures are short and diffusely dis-
tributed and alternate with normal or dilated segments of the
ducts to create a beadlike appearance on x-ray. It is unusual for
the gallbladder or cystic duct to be involved. Liver biopsy shows
the combination of inflammation, fibrosis, proliferation, and
duetal obliteration that confirms the presence of the disease.
The disease proceeds in stages, and by stage 4, biliary cirrhosis
is present (Chapter 37), making the diagnosis complexo
Many patients are asymptomatic in early stages. Others are
seen with a combination of fatigue, fever, jaundice, abdominal
pain, and weight loss. Persistent severe pruritis can be a par-
ticularly difficult aspect of the disease. Patients may experi-
ence recurrent attacks of cholangitis.
Collaborative Care Management
The diagnosis of PSC is not easily established and is usually
made as part of a workup for cholecystitis or general nonulcer
dyspepsia. PSC causes elevated liver enzymes and serum
bilirubin levels, but the elevations in alkaline phosphatase are
research~~
Reference: Fenster LF,Lonborg R, Thirlby RC,Traverso LW: What
symptoms does cholecystectomy cure? Am J Surg 16(5):533-538, 1995.
This study attempted to evaluate the effectiveness of
cholecystectomy in relieving presenting GI problems.
Data were colleeted from 225 patients who underwent
laparoscopic cholecystectomy. Eighty-two percent had
documented gallstones before surgery, 91% experienced
biliary-related pain, and 77% had both. Eighty-two per-
cent also experienced related GI symptoms, e.g., bloat-
ing, gas, indigestion, and intolerance to fatty foods. The
study results showed that documented gallstone-related
pain was universally relieved by surgery, but pain was
only relieved in 52% of those without documented gall-
stones (acalculous cholecystitis). And, although nonpain
symptoms were extremely common in this population,
surgery only relieved the related symptoms in approxi-
mately 44% of the patients.
Gallbladder and Exocrine Pancreas chapf:er42 1379
considered to be a hallmark feature. Endoscopic retrograde
cholangiopancreatography (ERCP) (Chapter 38) is used to vi-
sualize the biliary tree. Liver biopsy helps rule out other causes
of the symptoms and assists in estimating the severity of the
liver damage.
The prognosis of PSC largely depends on its clinicai course,
which can be highly unpredictable. The aggressiveness of the
disease is influenced by the number and severity of infections
and the development of complications related to cirrhosis.
Death is usually the result of liver failure, bleeding, or sepsis,
but timely intervention with a liver transplant can significantly
alter the outcomes.23 Survival is typically about 10 years.
Drug therapy is aimed at reducing biliary tree infiarnma-
tion and preventing the scarring that leads to obstruction.
Steroids and other immunosuppressive agents have not been
effective, but the use of ursodeoxycholic acid has shown
promise even though its mechanism of action in PSC remains
unknown. Surgical procedures other than transplant have
been effective for diffuse disease. Endoscopic treatment to re-
move stones, relieve obstruction, dilate ducts, and place stent
tubes is ongoing but primarily in the form of clinicai trials.
Liver transplantation is the primary treatment option.
Patient/fami/y education
The uncertain nature of PSC is one of its most difticult
characteristics. Patients are instructed about the disease and
its possible outcomes and are prepared for the possibility of
the eventual need for liver transplant. Persistent jaundice may
negatively affect body image, and chronic severe pruritis can
be a daily nightmare. Some patients respond to cholestyr-
amine resin, which theoretically binds the itch-triggering
elements in the bile. The nurse also suggests that the patient
experiment with common interventions that may lessen itch-
ing. Possible strategies are summarized in the Guidelines
for Care Box. A low-fat diet is recommended to patients who
develop problems with diarrhea or steatorrhea, and the fat
guide'ines for care
Strategies to Control Pruritis
Avoid irritating clothing (wool or restrictive clothing).
Use tepid water for bathing rather than hot.
Experiment with nonirritating soaps and detergents.
Pat skin dry after bathing or showering; do not rub.
Apply emollient creams and lotions to dry skin
regularly.
Maintain a cool environment and ensure adequate
amounts of humidity in the air.
Avoid activities that increase body temperature or cause
sweating.
Experiment with treatments sueh as oatmeal baths.
Keep the fingernails short and eonsider use of cotton
gloves at night to minimize skin damage from
seratehing.
Use antipruritie medieations as ordered.
1380 unit viii Alterations in Digestion and Elimination
restriction usually prompt1y corrects the problem. Fat-soluble
vitamin replacement is often needed.
CARCINOMA OF THE BILlARY SYSTEM
Etiology/Epidemiology
Primary tumors of the gallbladder are extremely rare in clini-
cal practice, and their incidence may be declining beca use
of prompt surgical intervention for gallbladder disease. The
etiology is unknown. Gallbladder cancer occurs almost ex-
clusively in persons older than 60 years of age and is twice
as common in women.23 High-risk groups for gallbladder
disease in general have a slightly increased risk of gallblad-
der canceI.
Cancer can also develop in the bile ducts. This disease
process also typically affects patients between 50 and 70 years
of age. It demonstrates a striking link with the presence of in-
flammatory bowel disease.
Pathophysiology
Carcinoma can occur anywhere in the biliary system. It has
a very insidious onset and can metastasize by direct exten-
sion, through the lymphatics, and through the blood. Most
patients have no symptoms that are referable to the gall-
bladder. Others have symptoms similar to those seen with
cholelithiasis and cholecystitis because of obstruction and
inflammation.
Intermittent pain in the upper abdomen is the most com-
mon symptom. Anorexia, nausea, vomiting, weight loss,
and jaundice may also be present. The patient may have a pal-
pable abdominal mass. Signs and symptoms indica tive of
metastasis to the liver or pancreas may also be present.23 By
the time gallbladder cancer produces symptoms it is usually
incurable.
Collaborative Care Management
Surgery is the primary treatrnent for cancer of the gallblad-
der. If the disease is diagnosed incidentally, it may be confined
to the gallbladder and be curable with surgery. Cholecystec-
tomy with wedge resection of 3 to 5 cm of normal liver plus
lymph no de dissection is usually performed. Survival for
those with invasive disease is usually less than 2 years. Neither
radiotherapy nor chemotherapy has thus far improved patient
outcomes.
Treatment of bile duct cancer focuses on maintaining bile
flow. Surgery may be used to divert bile flow to the jejunum,
or stent tubes may be placed to attempt to maintain duct pa-
tency. When bile flow can be maintained, patients may live for
several years after diagnosis.
Pat:ient:/family educat:ion
Nursing intervention is focused on asslstmg the pa-
tient to self-manage the symptoms and possibly care for
bile drainage systems (see the Guidelines for Care Box on p.
1378). The remainder of care and teaching is generally sup-
portive as the patient and family face an uncertain haure and
poor prognosis. General care of the cancer patient is discussed
in Chapter 11.
PROBLEMS OF THE PANCREAS
ACUTE PANCREATITIS
Etiology
Acute pancreatitis occurs when obstruction of the outflow of
pancreatic secretions triggers acute inflammation in the gland.
The obstruction can progress to necrosis of the pancreatic ex-
ocrine and endocrine cells and can involve either the large or
small pancreatic ducts or both. The two major causes of acute
pancreatitis in the United States are gallbladder disease and al-
cohol abuse."·23 Together they account for about 80% of all
cases. Acute pancreatitis may be similar in presentation to
chronic pancreatitis, but it represents a different pathological
process.1I Other rare causes of pancreatitis include abdominal
or surgical trauma, obstruetion of the gland by neoplastic
growth, drug effects, a variety of infectious diseases, and other
chronic diseases of the GI tract.
Alcoho/-re/ated pancreatitis
The role of alcohol in the development of acute pancreati-
tis is well recognized clinically but remains poorly explained.
Alcohol is presumed to have a direct toxic effect on the pan-
creas in selected persons, probably through some genetic en-
zymatic abnormality. Extensive amounts of aIcohol over a
minimum period of several years are probably required to ini-
tiate the processo Alcohol also weakens cell membranes and
makes the acinar cells more vulnerable to injury. It is also
known to decrease the amount of trypsin inhibitor available,
which again increases the susceptibility of the pancreas to in-
jury. Alcohol is believed to initiate an asymptomatic pancre-
atitis in the organ before the first acute episode. Alcoholic
patients also typically develop chronic disease once an acute
episode has occurred, and the presence of chronic pancreati-
tis appears to make the pancreas even more vulnerable to the
damaging effects of alcohol.12·21.23Recurrent episodes of acute
pancreatitis are common.
Biliary pancreatitis
Transient obstruction of the ampulla ofVater by a gallstone
is considered to be a major cause ofbiliary pancreatitis. Stones
were found in the stool of more than 90% of patients with
gallstone pancreatitis in some studies. The obstruction does
not have to be prolonged to initiate acute inflammation. How
the obstruction activates the pancreatic enzymes is not under-
stood. The presence of tiny gallstones (microlithiasis or biliary
sludge) toa small to be identified by imaging studies, is be-
lieved to play a role. There is also considerable evidence that
structural abnormalities that lead to narrowing at the sphinc-
ter of Oddi can be considered a cause of biliary pancreatitis. It
is theorized that the various forms of obstruction can reverse
the normal pancreatic pressure gradient. This would permit
reflux of bile or duodenal contents into the pancreatic ducts
and possibly even cause small duct rupture.1I
Biliary pancreatitis begins acutely, but is likely to be mild in
course and followed by rapid recovery. It can, however, in se-
lected situations trigger rnassive pancreatic necrosis and lead
to death. It rarely leads to cnronic disease.
 Management of Persons with Problems of the Gallbladder
Epidemiology
The incidence of acute pancreatitis has increased in recent
years, but this increase may represent improved diagnostic ca-
pabilities rather than a true increase in cases. The current an-
nual incidence is estimated to be 0.1 to 0.5 cases per 1000pop-
ulation. Patients with biliary pancreatitis are likely to be 55 to
65 years of age and predominantly female, whereas patients
with alcohol-related pancreatitis are usually slightly younger
and predominantly male.
Acute pancreatitis may take a mild, severe, or fulminant
course. Pancreatitis has a fulminant course in approximately
5% to 15% of all patients, and 20% to 60% of these patients
will either die or face potentially lethal complications.6 The
overall mortality rate for pancreatitis remains at about 10%
despite improved diagnosis and more aggressive treatment.
Pathophysiology
The two major pathological varieties of acute pancreatitis are
the (1) acute interstitial form and (2) acute hemorrhagic
formoAlthough either form can be fatal, the interstitial form
is often a mi!der disease.
The defining characteristic of acute interstitial pancreatitis
is a diffusely swollen and inflamed pancreas, which retains its
normal anatomic features. There are minimal or no areas of
hemorrhage or necrosis in the gland. The interstitial spaces
become grossly swollen by extracellular edema, and the ducts
may contain purulent material. The acute hemorrhagic dis-
ease presents with a very different picture. The gland readily
shows acute inflammation, hemorrhage, and marked tissue
necrosis. Extensive fat necrosis is present in patients with ful-
minant disease, not just in the pancreas but throughout the
abdominal and thoracic cavities and subcutaneous tissues.23
. Ihterper-itoneol.
soponificotíon
oF calcium
figo 42-5 Summary of major pathological
and Exocrine Pancreas chapter42 1381
ecrosis of vessels can cause significant loss of blood, and ab-
scesses and infection form in areas of walled off necrotic tis-
sue. Systemic complications such as fat emboli, hypotension,
shock, and fluid overload are common.
Pancreatic juice normally contains only inactive forms of
the proteolytic enzymes. The pancreas secretes a trypsin in-
hibitor specifically to prevent activation within the gland, be-
cause once trypsinogen is activated to trypsin it can then acti-
vate the other enzymes as well. Activation of the pancreatic
enzymes before they reach the duodenum has long been rec-
ognized as a major component of the diseaseprocessoThe mys-
tery of acute pancreatitis is how that pathological sequence is
initiated. The etiológical roles of alcohol and bi!iary disease
have been discussed, but they fai! to fully explain the disease
process.22 Enzyme activation overwhelms all of the normal
protective mechanisms of the pancreas and initiates a massive
attack on the pancreatic tissues. Pancreatic autodigestion is ini-
tiated. Other systemic effects of the activated enzymes include:
• Activation of complement and kinin, producing increased
vascular permeability and vasodilation
• Increased stickiness of the inflammatory leukoeytes with
the formation of emboli, which plug the microvasculature
• Initiation of consumptive coagulopathy, leading to dissemi-
nated intravascular coagulation
• Increased permeability causing massive movement of fluids,
which leads to circulatory insufficiency
• Releaseof myocardial depressant factor, which further com-
promises cardiac function
• Activation of the renin-angiotension network, which impairs
renal function in conjunction with circulatory insufficiency
Figure 42-5 outlines the major pathological events that can
occur in acute pancreatitis .
events that occur in acute pancreatitis.
, 382 unit viii Alterations in Digestion and Elimination

The clinical manifestations of acute pancreatitis vary some-
what according to the severity of the attack. Acute pain in the
epigastric region is the hallmark feature of the disease. The pain
is usually steady in nature and may radiate to the back. It is typ-
ically worsened by lying supine, and patients may curve their
backs and draw their knees up toward the body in an attempt to
dirninish its intensity. The pain is variously attributed to stretch-
ing of the pancreatic capsule, obstruction of the biliary tree,
and/or chemical burning of the peritoneum by activated en-
zymes. In more severe forms of the disease the pain may be
agonizing.
Vomiting is a second common feature of acute pancreati-
tis. The severity of the vomiting varies and is typically wors-
ened by the ingestion of food or fluido Vomiting does not re-
lieve the pain and may become protracted. Physical findings
for patients with severe pancreatitis include abdominal ten-
derness and rigidity, progressive abdominal distention, and
decreased bowel activity. Fever is common, but it rarely ex-
ceeds 39° C. Fulminant disease may progress to hypovolemic
shock, ascites, acute tubular necrosis, and respiratory failure.
The clinical manifestations of mild and severe pancreatitis are
summarized in Box 42-2.
'.I.IIf··
. L""
l_, Iça,l~nJ,,-est-a1;!Qn
~.&: • pancreas; identify cysts, abscesses, and masses; and with con-
Acute Pancreatitis
PAIN
Steady and severe in nature, excruciating in fulminant
cases
Collaborative Care Management
Diagnostic tests
The diagnosis of acute pancreatitis is made initially from
the measurement of the serum amylase level, which rises
within a few hours of the onset of the disease. In mild disease
it may only remain elevated for a few days. There is no appar-
ent relationship between the severity of the disease and the
height of the enzyme levels.18 The levels of urinary amylase
may also be measured if the patient sustains adequate kidney
function. Serum lipase elevations are also diagnostic and per-
sist for up to 5 to 7 days.J8 Neither amylase nor lipase eleva-
tions are exclusive to pancreatic disease, which complicates di-
agnosis in questionable cases.
Other laboratory findings commonly seen with acute pan-
creatitis include leukocytosis, hyperglycemia, which may
reach leveIs as high as 500 to 900 mg/dl, and elevated liver
function tests. Hypocalcemia may develop from the sequester-
ing of calcium by fat necrosis in the abdomen, and this is usu-
ally a poor prognostic signo It may occur in conjunction with
low levels of both albumin and magnesium, especially in
chronic alcoholics.
Computed tomographic (CT) scanning has become the
gold standard for diagnosing acute pancreatitis, although it is
actually not needed except for patients with severe disease and
suspected complications. CT scans can estimate the size of the
trast medium can clearly diagnose hemorrhagic disease. Early
in the diagnostic process abdominal x-rays may be taken to
rule out ulcer perforation, and ultrasonography may be used
to rule out the presence of gallstones.

I
Located in the epigastric or umbilical region; may radi-
ate to the back Medications
Worsened by Iying supine; may be lessened by flexed There is no drug treatment for acute pancreatitis. Drug
knee, curved back positioning therapy to reduce pancreatic secretion with somatostatin,
histamine H2-receptor antagonists, anticholinergic agents,
~~r~~~~N~verity but is usually protracted li and glucagon has not been shown to have any therapeutic

~~:~~~~~:::::~~
Worsened by ingestion of food or fluid , effect. Pain management is the primary consideration, and
patients may require substantial amounts of opioids. Syn-
thetic narcotics such as meperidine (Demerol) have tradi-
tionally been used because they do not cause spasm in the

I
o'"". I.' sphincter of Oddi." Morphine, however, is now believed to
have minimal sphincter effects and is an extremely effective
ABDOMINAL FINDINGS • analgesic.
Fluid and electrolyte replacement is criticaI since the loss of
I
f
". Rigidity, tenderness, guarding
Distention
Decreased or absent peristalsis.
~I'~.':".

tl
intravascular fluid through membrane leakage averages 4 to
6 L and can easily exceed these levels in severe cases.3,23 Pre-
r: ADDITIONAL
ISymptoms
FEATURES OF FULMINANT
of hypovolemic shock
DISEASE r
!leI
vention of hypovolemic shock necessitates aggressive fluid
management. Urinary output should remain at or above 30 to
Oliguria: acute tubular necrosis ~ 50 ml/hr. Potassium losses can also be significant in both
• Ascites ~j vomitus and pancreatic fluids, and serum leveIs need to be
Jaundice i maintained. Hypocalcemia develops frequently and is care-
Respiratory failure ~; fully monitored. Replacement of calcium is initiated if the pa-
i Grey Turner's sign (bluish discoloration along the flanks)* f tient becomes symptomatic.23 Exogenous insulin may be
Cullen's sign (bluish discoloration around the umbilicus)* t needed in severe disease, but it is used cautiously because
*NOTE: These signs indicatethe accumulationof bloodinthese areas and these patients are very vulnerable to severe hypoglycemia
represent the presence of hemorrhagicpancreatitis. from decreased glycogen and glucagon reserves.
 Management of Persons with Problems of the Gallbladder and Exocrine Pancreas chap~er42 1383

Treatments
There are no known treatments for pancreatitis. Medical
therapy is direeted at general supportive care for most patients
with mild to moderate disease. The patient is generally given
NPO. Nasogastric suctioning has frequently been used, but is
probably not necessary unless the patient develops ileus or ex-
periences persistent vomiting.
More aggressive and invasive interventions are available for
patients who are at high risk for complications. The course of
acute pancreatitis is not readily apparent, and several clinical
prognostic rating scales have been developed to help clinicians
identify patients at greatest risk. The older system uses the cri-
teria of Ransom applied at admission and again within the
first 48 hours. The modified Glasgow criteria are easier to
apply clinically. These prognostic scoring systems are pre-
sented in Table 42-l.
Peritoneallavage has been used in patients with severe pan-
creatitis in the attempt to remove toxic substances. Clinical
trials have involved small numbers of patients, and results
have been somewhat inconsistent, but a trend toward a de-
crease in deaths related to pancreatic infection has been ob-
served. The removal of retained gallstones by ERCP reduces
overall morbidity in the select group of patients in whom an
obstructing stone can be identified.
Surgical management
Surgery is not a routine part of the management of acute
pancreatitis, but some procedures may be necessary to con-
trol related gallbladder problems, pseudocyst, or abscesso
Necrotic tissue may also be resected. Patients requiring
surgery typically have fulminant disease and are acutely ill.
The discussion of surgical intervention is included under
Complications on p. 1386.
Diet
The patient is given nothing by mouth until the abdominal
pain has subsided, and amylase levels return to normal. This
practice, in theory, rests the pancreas and limits or stops the
secretion of enzymes. Most patients do recover without com-
plications or sequelae.IO Oral tluids and feedings can usually
be resumed within 3 to 7 days and gradually advanced to a
normal diet once peristalsis is reestablished. There is no clini-
cal proof of the need for a low-fat diet or any other dietary re-
strictions during recovery except for abstinence from alcoho1.6
Total enteral or parenteral nutrition may be implemented
for patients who are unable to eat for extended periods of time
(Research Box). The early use of total parenteral nutrition
(TPN) does not appear to affect outcomes of patients with
mild pancreatitis, but its use significantly decreases morbidity
and mortality in severe and fulminant disease.11 Efforts are
made to keep plasma albumin levels above 3.5 gld and total
protein values above 6.5g/d, thereby maintaining a positive ni-
trogen balance. Ii
Activity
Bedrest is maintained during the acute phase of disease
management to decrease the body's overall metabolic de-
mands. Once the patient's condition has stabilized, activity can

research\~il
Relerence: McClave SA et ai: Comparison 01 the salety 01 early en-
Tvvo Representative Prognostic teral vs. parenteral nutrition in mild acute pancreatitis. J Parent Ent
Scoring Systems Used Nutr21(1l:14-20.1997.
in Acute Pancreatitis This study was designed to compare the safety, cos!, and
~..,-~~~ .~ ~ •• ~ .•....• :z=:"" ~~~
effectiveness of two methods of nutrition support for pa-
RANSOM GLASGOW
tients with mild acute pancreatitis. The study involved
WITHIN48HR 30 patients who were admitted with mild acute pancre-
ADMISSION OF ADMISSION atitis documented by the presence of pain and elevated
. Age >55 years Age >55 years serum amylase and lipase leveis. Patients were ran-
WBC >20,000 cell/mm3 WBC >15,000 domly assigned on admission to receive either total en-
LDH >350 IU/L Glucose >180 mg/dl teral nutrition (TEN) via a nasointestinal tube or total par-
AST >250 IU/L BUN >45 mg/dl enteral nutrition (TPN) by central or peripheral catheter.
Glucose >200 mg/dl Po, <60 mm Hg Nutrition support was initiated within 48 hours of admis-
't
Albumin <3.2 g/dl sion. No differences were noted between the groups on
INITIAL 48 HR !
Calcium <8 mg/dl admission in mean age, Ransom criteria, APACHE score.
Hematocrit decrease >10% LDH >600 IU/L or other prognostic screening tool.
BUN increase >5 mg/dl No deaths occurred in either group. No differences
Calcium <8 mg/dl were found in serial pain scores, the number of days be-
Po, <60 mm Hg fore normalization of blood values occurred, serum albu-
Base deficit >4 min leveis, or the incidence of nosocomial infection. The
Estimated fluid sequestra- cost of TPN, however, was more than four times greater
tion >6 L than the cost of TEN, and stress-induced glucose lev-
eis were significant in the TPN group. The study con-
Data Irom Ransom JAC et ai: Surg Gynecol Obstet 143:209. 1976 and cluded that isocaloric/isonitrogenous TEN via nasoin-
Neoptolemos VP et ai: Lancet2:979, 1988.
WBC, white blood cell count; LOH, lactic dehydrogenase; AS!, aspartate
testinal tube appears to be a cost-effective alternative to
aminotranslerase; BUN, blood urea nitrogen. intervention with TPN in this population.
NOTE: Presence 01 three or more lactors indicates poor prognosis.
1384 unit viii Alterations in Digestion and Elimination
be gradually increased based on the patient's tolerance. There
are no long-term restrictions.
Referrals
Patients with acute pancreatitis are severely ill and may
require the expertise of a variety of specialists during the
treatment and recovery periods. Fulminant illness may ne-
cessitate critical care monitoring and consultation. This is
particularly true for patients who develop respiratory com-
plications such as adult respiratory distress syndrome
(ARDS) or respiratory failure and require intubation and
mechanical ventilation. The nutrition support team will be
involved if TPN is initiated.
Any number of medical specialists may be consulted to
manage emergency complications. The surgeon is often
needed to drain abscesses, relieve obstruction, or debride
necrotic tissue. An enterostomal therapist may be consulted if
draining wounds are left open to heal by secondary intention.
In many patients alcohol abuse is the etiological stimulus
of acute pancreatitis, and continuation of alcohol use will in-
crease the risk of recurrent acute pancreatitis and chronic
pancreatitis in the future. The nurse needs to be knowledge-
able about resources available in the local community for sup-
porting individuals who want to become and remain absti-
nent from alcohol. The severe nature of acute pancreatitis may
serve as a stimulus for lifestyle change in some individuals. It
is important to use this opportunity to refer the person for al-
cohol treatment if possible.
NURSING MANAGEMENT
• ASSESSMENT
Subjective Data
Subjective data to be collected to assess the patient with acute
pancreatitis include:
Pain: steady and severe in nature and quality; located in the
epigastric or umbilical region, may radiate to back;
worsens when patient is supine
Nausea and vomiting, usually severe and protracted; wors-
ens by the ingestion of food or fluid; vomiting does not
relieve pain
History of gallbladder disease; long-term high alcohol intake
Objective Data
Objective data to be collected to assess the patient with acute
pancreatitis include:
General affect: patient looks distressed; sits with knees
pulled toward abdomen
Fever, generally <39 C
0
Abdominal rigidity, distention, guarding, and tenderness
Diminished or absent bowel sounds
Signs of dehydration: falling urine output, decreased skin
turgor, dry or sticky mucous membranes
Vital signs: evidence of hypovolemia; tachycardia, tachy-
pnea, normal to low blood pressure, restlessness, and
anxiety
Presence of Grey Turner's or Cullen's signs: bluish discol-
oration on flanks and/or around umbilicus
Jaundice
• NURSING DIAGNOSES
Nursing diagnoses are determined from analysis of patient
data. Nursing diagnoses for the person with acute pancreatitis
may include but are not limited to:
Diagnostic Title Possible Etiological Factors
Pain Inflammation of pancreas or
peritoneum
Fluid volume deficit Vomiting, fluid shifts in abdomen
Nutrition, aItered: less Nausea and vomiting; pain
than body requirements
Risk for impaired home Lack of knowledge about disease
maintenance process and therapeutic regimen
management
HeaIth maintenance, UnhealthY lifestyle patterns, in-
aItered cluding aIcoholism
• EXPECTED PATlENT OUTCOMES
Expected patient outcomes for the person with acute pancre-
atitis may include but are not limited to:
I. States that pain is controlled and does not appear to be in
pain (does not display distressed appearance, limited body
movement, or limited activity).
2. Will have adequate fluid volume as demonstrated by nor-
mal blood pressure, absence of orthostatic changes, normal
skin turgor, moist mucous membranes, and adequate urine
output.
3. Will gradually resume a normal oral diet without discom-
fort and regains lost weight .
4. Patient and significant others will be able to:
a. Describe the disease and the purpose of various inter-
ventions.
b. Explain the relationship between the etiological facto r
(e.g., alcoholism or biliary disease) and pancreatitis.
c. Explain plans for follow-up care.
5. Will assume safe and adequate health practices (e.g., con-
trols alcoholism if present as an etiological condition of
acute pancreatitis).
.INTERVENTIONS
Controlling Pain
Control of pain is a major priority, and either morphine or
meperidine (Demerol) may be used. Critically ill patients
may receive a continuous infusion of N narcotics supple-
mented by boluses as needed for breakthrough pain. Patient-
controlled analgesia should be used if feasible to allow for suc-
cessful pain management.14 The nurse will regularly and
frequently assess the patient's levei of pain and response to in-
terventions. The physician will be consulted for needed
changes in the regimen. An attitude occasionally encountered
in caring for patients with alcohol-induced pancreatitis is that
the patient is somehow "getting what he or she deserves," es-
pecially on repeat admission for recurrent disease. The nurse
must serve as the patient's advocate in the system, document-
 Management of Persons with Problems of the Gallbladder
ing the severity of the pain and ensuring that an effective plan
is in place to manage it.
Some patients find that the pain is decreased if they as-
sume a sitting position with the trunk flexed, or a side-Iying,
knee-chest position with their knees drawn up to the ab-
domen. Epidural analgesia can be used if pain is persistent
and not relieved by routine narcotic administration. Al-
though the research is currently inconclusive most patients
will be given nothing by mouth to "rest" the pancreas and de-
crease the autodigestive processoA nasogastric (NG) tube will
be inserted to keep the stomach decompressed if vomiting is
severe.
The nurse will also explore the use of a variety of non-
pharmacological pain relief strategies with the patient, includ-
ing distraction, imagery, massage, or back rub. The environ-
ment should also be kept quiet, comfortable, and conducive to
restoThese measures are used in addition to, and not in place
of, narcotic administration for pain control.
Maintaining Fluid and Electrolyte Balance
AB soon as the patient is admitted, the nurse should institute
monitoring related to fluid and electrolytestatus, cardiac output,
and renal status. It is a critical need. Monitoring includes intake
and output, vital signs, daily weights, abdominal girth, and all
routine laboratoryvalues with particular emphasis on potassium
and calcium levels.Physicalassessment will include assessing for
signsofhypokalernia and hypocalcernia (see Chapter 15).
An indwelling Foley catheter may be necessary, since de-
creased renal function can occur in association with hypoten-
sion and shock. Monitoring parameters and frequency of
monitoring will depend on the stability of the patient's condi-
tion. Fluids, electrolytes, colloids, or blood will be given as
necessary.
Aggressive fluid replacement will necessitate establishing
and maintaining large bore IV access. The nurse is responsible
for administering the fluids and for monitoring the patient's
response. The development of hypovolemic shock is of partic-
ular concern in the early days of the disease, and the nurse
watches carefully for the early signs that could indicate the de-
velopment of shock (see Chapter 17).The patient also is mon-
itored for hyperglycemia, and checks of blood glucose should
be performed four times a day. If severe hyperglycemia occurs,
it may be treated with insulin.
Promoting Adequate Nutrition
The patient will be given nothing by mouth and often has a
nasogastric tube in place. Good oral hygiene will be necessary
to decrease discomfort from NPO status and from the naso-
gastric tube. TPN may be used during the criticaI phase of the
illness for patients with severe disease. When the acute symp-
toms decrease (3 to 5 days), oral fluids and food are restarted.
The patient is given clear liquids and then slowly advanced to-
ward a regular diet. Tolerance for oral feedings is carefully as-
sessedas is the possibility of the return of pain. Frequent small
mealsare usually better tolerated in the early refeeding period.
The only diet restriction that needs to be followed after dis-
charge is the avoidance of alcohol.
and Exocrine Pancreas chapter42 1385
Patient/Family Education
Teaching the patient and significant others will be ongoing. At
the beginning of hospitalization, the patient and significant
others need basic information about the disease, the diagnos-
tic tests, and the treatment. Because of the pain and the dis-
tress acute pancreatitis causes and because of the severity of
the disease process, the patient and family may be experienc-
ing tremendous anxiety. Therefore explanations and instruc-
tions should be brief and as simple as possible and may need
to be repeated. Support and continuity of care also need to be
provided to help decrease anxiety. Education will be directed
toward preventing future attacks and maintaining a nutritious
diet. The patient must know that any recurrence of signs and
symptoms should be reported immediately. Follow-up care
must be explained in detail.
Health Promotion/Prevention
If unhealthy lifestyle patterns such as alcoholism are a cause of
acute pancreatitis, the nurse must work with the patient on
the problems. This care will not be instituted until the pa-
tient's condition is stabilized, but it must be introduced before
the patient leaves the hospital. See Chapter 14 for further in-
formation on coping with alcoholism.
If the patient's pancreatitis is related to biliary diseasé,it will
be important to stress the importance of treatrnent for gall-
stones.The episode of pancreatitis is frightening and could make
the patient reluctant to undergo any further medical or surgical
treatrnent. The nurse will reinforce the etiological role of biliary
disease in the development of pancreatitis and encourage the
patient to follow through on recommended treatrnent.
• EVALUATION
To evaluate the effectiveness of nursing interventions, com-
pare patient behaviors with those stated in the expected pa-
tient outcomes. Successful achievement of patient outcomes
for the patient with acute pancreatitis is indicated by:
la. States no pain.
b. Does not splint, grimace, and breathe shallowly.
2. Has hemodynamic measures within normal limits and
shows intake equal to output.
3a. Maintains NPO status as appropriate.
b. Consumes a well-balanced diet without nausea, vomiting,
or pain by discharge.
c. Returns to normal weight.
4a. Appropriately describes the disease, tests, and planned in-
terventions.
b. Appropriately describes the relationship between etiolog-
ical factors and the disease.
c. Appropriately describes and selects well-balanced diet.
5a. Correctly identifies planned follow-up treatrnent for bil-
iary disease.
b. Makes commitment to treatment for alcoholism.
GERONTOLOGICAL CONSIDERATIONS
Biliary disease becomes increasingly common as people age,
and biliary disease-related pancreatitis is most likely to occur
in the elderly patient. The severity of the disease is difficult to
1386 unit viii Alterations in Digestion and Elimination

predict, but elderly patients with acute pancreatitis may be-
come critically ill faster because of comorbid problems.
Elders are also more likely to develop complications related
to their disease-enforced immobility as well as to the pancre-
atitis. Respiratory complications are of particular concem,
and the elderly patient needs frequent respiratory assessment
and aggressive pulmonary hygiene during the acute stage of
the disease.
Infection is a common complication of pancreatitis (see
discussion under Complications), and elderly patients are less
able to withstand the stress imposed on the body by sepsis.
The same is true for the development of hypovolemia and
fluid shifts. These factors strain the cardiovascular system and
may overwhelm the elderly patient's ability to adapt and
respondo
SPECIAL ENVIRONMENTS FOR CARE
Criticai Care Management
Although most patients with pancreatitis recover without any
residual dysfunction, a minority experience life-threatening
disease. These patients will be managed in a criticaI care unit.
The nurse's major roles are collaborative with the physician
and involve ongoing monitoring of all systems and the pre-
vention or identification of complications.
Routine interventions will include hemodynamic mon-
itoring and aggressive fluid support. Critically ill patients
may also need cardiac support with drugs such as dopa-
mine. A pulmonary artery catheter may be inserted to assess
perfusion adequacy. Left ventricular dysfunction is a com-
mon problem.
The airway is compromised in several ways. Severe pain
limits diaphragmatic excursion, and both shock and sepsis
place extraordinary metabolic demands on the respiratory
system that can progress into full-blown ARDS in some pa-
tients. Prompt intubation and mechanical ventilation will be
crucial. Hypercoagulability increases the risk of pulmonary
embolism. Management includes supplemental oxygen, suc-
tioning as needed, and aggressive chest physiotherapy. Assess-
ment is conducted hourly. Respiratory failure accounts for a
disproportionate number of pancreatitis-related deaths.
In addition to the concems addressed above, the critically
ill patient with pancreatitis will receive TPN to support a pós-
itive nitrogen balance and may undergo peritoneal lavage
through a peritoneal catheter. Other interventions will be di-
rected at specific complications as they arise.
Home Care Management
Most patients with acute pancreatitis recover spontaneously
and can be discharged from the hospital within 1 to 2 weeks.
Patient needs for home care will be minimal if complications
did not develop. Normal activities are gradually resumed as
strength and activity tolerance increase.
make referrals to community programs for alcohol treatment
if the patient agrees. It is important to recognize, however, that
the decision to continue drinking is a matter of personal
choice. The nurse's role is to be certain that the patient has
all of the information that he or she needs to make an in-
formed decision about the future. A positive outcome cannot
be guaranteed.
COMPLlCATIONS
About 25% of patients who have acute pancreatitis will de-
velop complications, and most deaths associated with the dis-
ease occur in that group of patients. Complications may be
local or systemic. The systemic complications tend to occur
within the first week and have largely been discussed within
the context of the fulminant disease processo These include
complications such as hypovolemic shock, sepsis, renal failure,
and ARDS. The major complications of acute pancreatitis are
summarized in Box 42-3.
Pseudocysts
Pancreatic fluid or exudate forms in up to 50% of patients
with acute pancreatitis.6 Pseudocysts are rounded collections
of fluid enclosed in a fibrous capsule. This process occurs in
only 5% to 10% of all patients.6 Many pseudocysts resolve
spontaneously over time, and intervention is not always war-
ranted. However, pseudocysts can also become life threatening
if they obstruct neighboring structures, rupture or hemor-
., Major Complicatians
•• af Acute Pancreatitis
~~~.s~~._:a;;:" .._~:,;;~=:l;t=.f'",.......,;.
CARDIOVASCULAR
Hypotension/shock from hypovolemia or hypo-
albuminemia
HEMATOLOGICAL
Leukocytosis from generalized inflammation or sec-
ondary infections, anemia from blood loss, dissemi-
nated intravascular coagulation (OIC) from unknown
causes
RESPlRATORY
Atelectasis, pneumonia, pleural effusion, adult respira-
tory distress syndrome (AROS)
GASTROINTESTINAL
GI bleeding
PANCREATIC
Pancreatic pseudocysts, pancreatic necrosis or phleg-
mon, pancreatic abscesses, pancreatic ascites
RENAL

Patients with alcoholism present a unique challenge as Oliguria and acute tubular necrosis
even the pain and anxiety of acute pancreatitis may not be suf- METABOLIC
ficient motivation for them to abstain from alcohol. The nurse Hyperglycemia, hypocalcemia, hyperlipidemia
will discuss the importance of abstinence with the patient and
 Management of Persons with Problems of the Gallbladder
rhage, or become infected. A "wait and see" policy is generally
followed, and the cysts are monitored regularly. Inflammatory
exudate from the pancreas may form into an inflamed mass,
which is called a phlegmon. Intervention is again not indicated
unless bleeding or infection develops. As with pseudocysts
the pWegmon may be drained, surgically debrided, or resected
as needed.
Pancrea~icInfec~ion
As treatment for systemic complications has improved, pan-
creatic infection has become the most frequent cause of seri-
ous morbidity and mortality associated with acute pancreati-
tis. Infection typically appears 8 to 20 days after the onset of
pancreatitis and has a 100% mortality rate if untreated.2 In-
fection usually develops in the are as of necrosis created by
fulminant disease. The initial diagnosis of infection can be
complicated by the fact that acute pancreatitis itself manifests
with the common symptoms of inflammation and infection.
Infection-related fever, however, typically exceeds 39° C, and
the patient's clinical condition deteriorates.
CT scanning allows for the accurate identification of areas
af necrosis, which can then be aspirated by CT-guided needle
aspiration. Gram stain and culture can then identify the spe-
cific organisms responsible for the infection. Broad-spectrum
antibiotics are initiated immediately, but definitive therapy re-
quires percutaneous drainage or surgical debridement. At-
tempts to prevent the development of infection with the rou-
tine use of antibiotics have not proven to be effective,
although irnipenem (Primaxin) is able to effectively penetrate
the capsule of the pancreas and shows promise.
Percutaneous drainage is used most effectively with in-
fected pseudocysts because there is minimal particulate mat-
ter present that can clog the tubes. The traditional surgical ap-
proach had been to excise as much necrotic material as
possible and then place multiple large-bore sump drains in
the operative areas to remove infected material.2 Continuous
saline infusion and suction were needed to maintain tube pa-
tency. Many surgeons now recommend an open method in
which the resected are as are packed, and the dressings are
changed under anesthesia every 2 to 3 days until granulation
is well underway. The abdomen is left open and eventually
doses over an absorbable mesh barrier. A feeding tube is
placed once granulation is underway. The development of fis-
tulae can complicate the healing processo
Chronic Pancreatitís
Patients with alcohol-induced acute pancreatitis are believed
to already have asymptomatic chronic disease when they ex-
perience their first acute episode. If the patient continues to
drink, the likelihood of recurrence is extremely high. Chronic
pancreatitis is discussed below.
CHRONIC PANCREATITIS
Etiology/Epídemiology
Chronic pancreatitis is present when recurrent bouts of in-
flammation lead to progressive injury and scarring of pan-
and Exocrine Pancreas chapter42 1387
creatic tissue with gradual fibrous replacement of the normal
tissue.21·23The progressive degeneration of the gland makes
chronic pancreatitis a separate disorder from recurrent acute
pancreatitis in which pancreatic function essentially returns
to normal when the inflammation subsides.'·23 Chronic pan-
creatitis occurs almost exclusively in alcaholics and is more
common in men. Other potential causes of chronic pancre-
atitis include neoplasms, structural problems, and, rarely,
inflammatory problems such as inflammatory bowel dis-
ease and primary sclerosing cholangitis. Biliary tract disease
remains the primary causative facto r in acute recurrent
pancreatitis.
Pathophysiology
The basic pathological change of chronic pancreatitis is de-
struction of the exocrine parenchyma and replacement with
fibrous tissue. This process is associated with varying de-
grees of duct dilatation. Scarring and fibrotic changes may
occur throughout the pancreas or be limited to selected
areas. Calcium salts may be deposited in both the ducts and
the parenchyma, usually in areas of fat necrosis. Ductal ob-
struction occurs secondarily. The factors that influence the
solubility of calcium in the calcium-rich pancreatic secre-
tions are not well identified. As the process becomes increas-
ingly severe the islets of Langerhans are also involved and
destroyed.
The role of alcohol in both acute and chronic pancreati-
tis remains obscure. Alcohol appears to act as a direct toxin,
but since only a minority of heavy drinkers develop prob-
lems, some genetic defect must also exist that allows alcohol
to have such detrirnental effects. The pathological nature of
the alcohol-induced injury is believed to be similar to that
occurring in acute pancreatitis. In addition there is evidence
of small protein plugs in the acinar ductules. Secretions are
more viscous and tend to form calcium-containing stones.
Trypsinogen and other proteases are activated by poorly un-
derstood mechanisms.
The patient with chronic pancreatitis may initially have
signs and symptoms identical to those described for the pa-
tient with acute pancreatitis, with pain being the major man-
ifestation. The pain occurs in the right or left upper quadrant,
in the back, or throughout the total abdomen. It is severe and
constant and is not relieved by food ingestion or antacids.
Nausea, vomiting, and abdominal distention may be present,
but they are usually secondary to the pain.
In the alcoholic patient it is very difficult to decide where
acute pancreatitis leaves off and chronic disease begins. Theo-
retically the dense fibrosis can entrap and alter the pancreatic
nerves, affecting both sensory and motor functions.1 It is pos-
sible that much of the pain is eventually related to this nerve
entrapment, although the pain is not different in nature or
severity from that which accompanies acute pancreatitis.' It is
frequently worsened by eating and needs narcotic administra-
tion for control.
Pancreatic insufficiency begins once 80% of the pancreatic
tissue is destroyed. Symptoms include diarrhea, which is
1388 unit viii Alterations in Digestion and Elimination
often steatorrhea, and marked weight loss. Diabetes is com-
mon and mayprecede other clinicai symptoms. Unique meta-
bolic derangements in glucose metabolism create a strong vul-
nerability to hypoglycemia and a smaller need for insulin.
Oral hypoglycemic agents are not effective. Malabsorption
leads to clinicai deficiency in vitamins E and B12 and other
fat-soluble vitamins, but patients rarely develop overt symp-
toms of deficiency.
A history of acute pancreatitis is the best diagnostic con-
nection to chronic disease. Amylase and lipase levels will ris e
during recurrent attacks, and both fasting and postprandial
hyperglycemia are usually present. Stool examination can
quantify the severity of the steatorrhea and malabsorption.
CT scanning is the basis of diagnosis and can demonstrate fi-
brosis, atrophy, duct dilatation, and calculi.
Collaborative Care Management
Effective management of abdominal pain is the greatest chal-
lenge with chronic pancreatitis. Patients who continue to
drink alcohol will continue to have pain, and even abstinence
is eventually no guarantee of relief. Patients can usually adapt
to the malabsorption and steatorrhea, but the persistent pain
may lead to drug dependence and motivate the patient to un-
dergo risky surgical procedures, which are frequently accom-
panied by poor outcomes and multiple complications.
Flare-ups of chronic pancreatitis are managed just like
acute disease. Bowel rest is maintained, and attention is paid
to managing the acute pain. Ongoing care involves the use of
a low-fat diet and supplemental pancreatic enzymes. These
extraets will increase the patient's body weight and improve
absorption, inereasing the patient's general sense of well-
being. The recommended diet is high in protein and carbohy-
drates and may provide as much as 3000 to 6000 calories/day.
The use of medium-chain triglycerides to improve the pa-
tient's 'nutritional state is being evaluated in several research
trials. Fat-soluble vitamin replacement may also be indicated,
and the management of diabetes often requires the use of
insulin.
Chronic pancreatitis affects the small ducts of the pancreas
and is not amenable to surgical correction. Surgical interven-
tion is frequently used to attempt to relieve the chronie ab-
dominal pain, but there are no proven surgical solutions. Ex-
tensive pancreatic resection or pancreatectomy may be
performed in patients who are unable to refrain from drink-
ing alcoho!. Sympathectomy is occasionally performed to re-
lease the entrapped nerves.
The nurse serves as the patient's advocate in the search
for eomfort. Concerns about drug dependenee must not be
allowed to prevent the patient from receiving adequate and
necessary analgesia. Health care providers can easily be-
come exasperated with patients who are unable or unwill-
ing to stop drinking and can begin to consider the pain of
chronic pancreatitis as appropriate retribution for the pa-
tient's addiction. This attitude can seriously eompromise
the patient's care.
In some instances the patient has had negative experiences
with pain management during previous hospitalizations for
exacerbations and thus believes that analgesics are not being
given because the health team does not care about him or her.
The involvement of a pain management team is desirable if
such services are available. See Chapter 12 for further discus-
sion of pain management.
Patient/falTJi/y education
The role of alcohol in the etiology and progression of
chronic pancreatitis is unequivocal, and yet many alcoholics
find themselves unable or unwilling to abstain from alcohol
use. The nurse consults with a substance abuse specialist to
develop a consistent and appropriate approach for the pa-
tient's care and ensures that the patient has ali the data neces-
sary to make informed decisions about his or her present and
future. Information coneerning community resources for al-
cohol treatment should be current and accurate and offered to
the patient. The involvement of the family is encouraged if the
dynamics are supportive.
Family members and health care workers need to be helped
to understand and accept that ultimately it is the patient's
right to make fundamental decisions about his or her own
care, even when these decisions do not appear to be in the pa-
tient's own best interests.
The patient also needs to learn how to modify the diet
and use pancreatic enzyme replacement effectively to control
diarrhea and maintain a stable weight. Timing of the med-
ications is critica!. The nurse teaches the patient to take the
eapsules 1 to 2 hours before, during, or after meals. Powders
can be mixed directly with food. Patients are informed that
these products frequently produce a bad taste and may alter
the taste of foods. The patient is instructed to monitor the
body's response to the supplements and consistently track
weight changes. The anorexia and poor eating habits com-
monly associated with long-term alcohol use makes adher-
ence to a high-protein, high-calorie diet difficult. The use of
vitamin supplements is encouraged if recommended by the
physician.
Patients who continue to drink alcohol will always be
just one step away from their next flare-up or complication.
The nurse provides the patient with written material that
outlines the symptoms of complications and encourages the
patient to adhere to the plan for continued follow up. A
Nursing Care Plan for the patient with chronic pancreatitis
is found on p. 1389.
CANCER OF THE PANCREAS
Etiology/Epidemiology
Cancer of the panereas may arise from any of the elements of
the pancreas, although most involve the ductal epithelium and
are adenocarcinomas. Both benign and malignant tumors can
also arise from the islet cells but these are rare.1S Tumors of the
islet cells usually retain some endocrine functions and tend to
have a better prognosis than adenoeareinomas.
Pancreatic cancer usually occurs in persons older than
50 years of age, but it can develop at any point in the lifespan.
It is much more common in men. The etiology is unknown,
but an association has been noted with cigarette smoking and
 • • • Person with Chronic Pancreatitis
I
I
DATA Mr. 1. is a 52-year-old self-employed accountant with a ing much less. The pain starts so quickly when I drink that [ j
12-year history of acknowledged alcoholism. He experienced his have really been steadily decreasing my intake. I don't under-
first attack of acute pancreatitis 4 years ago and chronic pancre- stand why this should happen now. What's the use? The doctor
I
atitis has since been diagnosed. He is admitted now with another said the pain would stop if I stopped drinking so much and look II
flare-up of the disease. at me now. Maybe I should just drink myself to death and get it
Mr. 1. has made several efforts to stop drinking and has even over with."
undergone inpatient alcohol treatment. His longest period of so- Other data on admission include:
briety has been about 6 months. Some life stressor has always pre- • Blood pressure is 94/60, pulse is 92, and respirations are 22 and
cipitated his descent into alcohol dependency. His wife accompa- shallow. Temperature is 99.8° F.
nies him to the hospital but is quick to say"I don't think that I can • Bloodwork shows the following abnormalities: hemoglobin of
take much more of this. He's killing himself and nothing I say or 10.2 g, red blood cell count of 2.9 million, K+ of 3.0 mg/dl,
do is changing that. I don't think I can stay around any longer serum calcium of 8.2 mg/dl, and glucose of 162 mg/dl.
watching him die. It hurts toa much." [nitial care orders include:
Mr. T.'s admission assessment shows a thin, poorly nourished • IV of 1000 ml of 5% dextrose in li, N saline with 20 mEq of KCI
man who appears older than his stated age. He reports the pres- at 125 rnlIhr
ence of: • NPO
• Acute abdominal pain that is generally localized in the mid- • Monitor intake and output, daily weight, and abdominal girth
epigastric region and radiates to the back. He rates the pain as once daily
an 8 on a 10-point scale in severity. • Demeroll00 mg IM q 3 hr PRN for pain
• Steady and protracted vomiting that began late yesterday af- • Insert NG tube and attach to low intermittent suction if vomit-
ternoon. He has had nothing to eat or drink for more than ing persists past 4 PM
12 hours. • Accucheck 4 times daily per protocol, cal! house officer if glu-
Large, 50ft, and foul-smelling stools that have been increasing cose> 160
in frequency and severity over the last few weeks. He has lost • Monitor c10selyfor hypovolemic shock, e1ectrolyte imbalance,
12 pounds. delirium tremens (DTs)
• A history of decreased alcohol use over the last 3 months. Mr. T • Call substance abuse resource counselor for DT protocol initia-
says "I know no one will believe me but I've really been drink- tion if needed

NURSING DIAGNOSIS Acute pain related to distention of pancreatic capsule and activation of pancreatic enzymes

States pain is effectively controlled
with pharmacological and nonphar-
macological methods.
1. Assess pain leveis frequently, espe-
cially before and after administra-
tion of analgesics.
a. Document pain leveis on flow
sheet.
2. Administer meperidine q3h as
needed.
a. Encourage patient to use anal-
gesics on a regular rather than
PRN basis.
b. Validate your acceptance ofthe
reality ofthe patient's pain and
its severity.
c. Evaluate effectiveness of the
narcotic order. Collaborate with
physician to make adjustments
in dose or drug as needed.
3. Collaborate with Mr. T to determine
the nonpharmacological methods
that help to reduce his pain.
a. Position him in a mid to high
Fowler's position with his knees
flexed.
b. Explore his experience with
strategies such as distraction,
massage, relaxation, and guided
imagery.
1. Frequent assessment is essential to
validate the nature and severity of
the patient's pain experience.
a. Recording on a flow sheet allows
for a pattem of pain to be estab-
lished and the effectiveness of
pain control to be evaluated.
2. Synthetic narcotics are effective
analgesics and do not cause spasm
in the sphincter of Oddi.
a. A regular time schedule of drug
use allows for a steady blood
levei to be established.
b. Patients with chronic pancreatitis
are frequently labeled "drug
seekers" by staff.
c. Acute pain can be immobilizing.
Morphine may be substituted
for meperidine.
3. Nonpharmacological methods
allow the patient a degree of con-
trol of the pain experience.
a. This position is theorized to re-
duce tension on the abdomen.
b. Ali of these can be effective
methods of pain control, but the
patient must have an open mind
and be willing to experiment
with new strategies.

Continued
- 1390 unit viii Alterations in Digestion and Elimination

Person with Chronic Pancreatitis-cont'd

NURSING DIAGNOSIS Risk for f1uid volume deficit related to vomiting, NPO status, hyperglycemia, and
increased capillary permeability

Maintains balance of fluids and elec-
trolytes; intake and output are bal-
anced; weight is stable.
1. Assess fluid and electrolyte status
each shift.
a. Maintain accurate intake and
output.
b. Weigh daily.
c. Assess skin turgor and status of
mucous membranes each shift.
d. Monitor cardiovascular response
to fluid replacement.
e. Measure abdominal girth daily or
as ordered.
2. Monitor blood glucose 4 times daily.
a. Administer sliding-scale insulin
per protocol.
3. Monitor for hypokalemia and
hypocalcemia:
muscle weakness, cramping
numbness and tingling in finger-
tips or around mouth; positive
Chvostek's and Trousseau's sign
1. Patient is at risk for hypovolemic
shock and dehydration. May lose
4 to 14 L of fluid into the abdomen.
Fluid replacement is based on esti-
mates of losses. A urine output of
30 to 50 ml/hr is essential to pre-
vent the onset of acute tubular
necrosis.
Fluid and gas accumulation in GI
tract can result in significant ab-
dominal distention.
2. Destruction of the beta cells and
islets of Langerhans produces se-
vere hyperglycemia. Because of
the risk of labile hypoglycemia, in-
sulin is not given unless glucose
levei continues to rise.
3. Large amounts of potassium are
lost through vomiting and in the
pancreatic secretions; calcium is
believed to bind with free fats and
can drop to leveis that increase
neural excitability.

NURSING DIAGNOSIS Altered nutrition: less than body requirements related to vomiting, NPO status, and
malabsorption caused by loss of function of pancreatic enzymes

Receives sufficient nutrients by mouth
or TPN to maintain stable body
weight, keeps albumin leveis above
3.8 g/dl, and produces normal stools.
1. Maintain NPO status and bed rest
until patient's condition stabilizes.
2. Assess current nutritional and elimi-
nation status.
3. Monitor daily weight and serum
protein and albumin leveis.
4. initiate TPN if NPO status needs to
be protracted.
5. Reinitiate oral feedings once ab-
dominai pain is controlled and amy-
lase/lipase leveis stabilize.
6. Offer small, frequent feedings to the
patient's tolerance; assess patient
response.
a. Restrict fat in diet if steatorrhea
persists.
7. Evaluate composition and volume of
stools. Adjust dose of pancreatic en-
zymes to achieve normal elimination.
1. NPO status is theorized to reduce
the secretion of pancreatic en-
zymes. Bed rest decreases the
body's metabolic rate.
2. Patients with chronic pancreatitis
are often malnourished before the
attack from alcoholism and malab-
sorption.
3. These parameters provide the best
ongoing data about nutritional
status.
4. If pain is not controlled promptly the
rapid catabolism of the disease must
be counteracted by TPN to prevent
life-threatening complications.
5. Once pain and enzyme leveis are
stable there is no contraindication
to oral feeding, and the severity
of malabsorption needs to be es-
tablished.
6. This feeding pattem minimizes
distention and malabsorption
symptoms.
a. Malabsorption primarily affects
digestion of fats.
7. Malabsorption manifests itself as
large-volume, greasy, foul-smelling
stools. Adequate enzyme replace-
ment will restore the stool to near
normal.

Continueo
 Management of Persons with Problems of the Gallbladder and Exocrine Pancreas chapter42 1391

,íJ; Person wíth Chroníc Pancreatítís-cont'd

NURSING DIAGNOSIS Risk for ineffective management of therapeutic regimen related to inability to abstain
from alcohol and inadequate knowledge of management of malabsorption and hyperglycemia
•• 01 •

Verbalizes understandíng of disease
process, role of alcohol, and pharma-
cological management of symptoms.
Makes commitment to abstain from
alcohol.
1. Assess patient's current under-
standing of the disease process and
the role of alcohol in its recurrence.
2. Assess patient's interest and com-
mitment to abstain from alcohol.
a. Assess knowledge of community
resources for treatment and sup-
porto Refer as appropriate.
3. Assess for symptoms of DTs during
first 48 to 72 hours. Consult with
substance abuse specialist if
needed.
4. Teach patient correct use of pancre-
atic enzymes:
• Take with each meal and snack.
Monitor weight and stool consis-
tency to judge need for dosage ad-
justment.
5. Teach patient about the nature and
planned management of diabetes.
a. Teach symptoms to report:
Hyperglycemia: frequent urina-
tion, thirst, lethargy, abdominal
cramping
• Hypoglycemia: anxiety, tachy-
cardia, diaphoresis
6. Encourage patient to make commit-
ment to changing his lifestyle and
gaining control of his disease and
his life.
1. This establishes a baseline for
planning and intervention.
2. Patient has stated his attempts to
decrease alcohol use. Wife has
stated the end of her tolerance for
his continued use 01 alcohol.
3. Patient may not be truthful about
current levei of use. Withdrawal
carries a high mortality in acutely
ill patients and necessitates spe-
cialty asisstance ..
4. Malabsorption is permanent, and
patient will develop serious nutri-
ent deficiencies if enzymes are not
adequately replaced. Dosage ad-
justments can be safely made by a
well-informed patient.
5. Insulin may be needed to control
the diabetes of chronic pancreati-
tis, but hypoglycemia must be pre-
vented. Patient will remain hyper-
glycemic but must know how to
recognize ketoacidosis.
6. Patients with chronic pancreatitis
often have given up hope on them-
selves and their ability to inlluence
the future.

research ~
Reference:PriceTF,PayneRL,OberletinerMG: Familialpancreatic
cancer in SouthLouisiana,Cancer Nurs 19(4):275-282, 1996.
This study explored a possible familial predisposition to pan-
creatic cancer among a Cajun heritage population in the Aca-
diana region of Louisiana. The study was descriptive in nature
and used a questionnaire to explore cancer incidence and risk
lactors. Thirty-eight patients or family surrogates were en-
rolled from among the 140 possible cancer patients docu-
mented during the year of study. Sampling was difficult as pa-
tients rapidly beca me extremely ill or died. Of the sample
sixty-five percent reported Cajun ancestry. They reported a to-
tal of 366 first-degree reiatives of whom 44 had also developed
pancreatic cancer. This represented an incidence rate lar
above national norms where pancreatic cancer accounts for
only 2% of ali new cancer diagnoses. The sample incidence
rate was comparable to that of lung cancer. African Ameri-
cans had the highest incidence (32 per 100,000 versus 17 per
100,000 nationwide). The incidence rate was also signifi-
cantly increased for whites (18 per 100,000 versus 10 per
100,000 nationwide). Heavy prolonged cigarette smoking
was shown to be a clear risk facto r, which has been true in
ali samples. Although flawed by sampling difficulties, the
study does appear to confirm the presence of a significant
familial risk for pancreatic cancer in this unique population.

the presence of long-standing diabetes, especia1ly in women.
Incidences of familial c1ustering of cases point to a hereditary
component (Research Box). A link with chronic pancreatitis
has been suggested but remains unproven.
Pathophysiology
Pancreatic cancers usually deve10p in the head of the gland
and vary dramatically in size at the time of diagnosis. The
tumor is usually deeply encased in normal tissue and is poor1y
demarcated. The common duct is often obstructed and dis-
tended by the presence of the tumor. Metastasis has almost
always occurred before the tumor produces its first symp-
toms beca use there is no capsule surrounding the pancreas
to prevent the growth and spread of the tumor. Direct ex-
tension of the lesion may cause its spread to the posterior
wall of the stomach, the duodenal wall, the colon, and the
1392 unit viii Alterations in Digestion and Elimination
eommon bile dueto Vital blood vessels in the are a are also fre-
quently involved.
Pain is the earliest and most eommon symptom of panere-
atie eaneeI. The pain is usually deseribed as epigastric in loca-
tion and steady and severe in character. It occurs or is wors-
ened by lying down and bears no relationship to meals. The
pain is relentlessly progressive in nature. Weight loss fre-
quently accompanies the pain and can be dramatic. Anorexia
is also common. ]aundice and pruritis will typically develop
when bile duet obstruetion oecurs. Diarrhea and/or steator-
rhea develop fairly late in the disease. Diabetes may aIso
develop.
Collaborative Care Management
The diagnosis of pancreatic eancer is often first ma de based on
the pattem of symptoms and then is confirmed through
CT scanning. Guided needJe biopsy may be performed at
the same time. A histological diagnosis is important in plan-
ning eare.9
Cancer of the panereas is usually fatal within 6 months re-
gardJess of treatment. Less than 2% of patients survive 2 years.
The treatment is generally surgical, aIthough surgery has not
been proven to improve survival. Obstruction is a common
problem with large tumors involving the pancreatie head, and
surgi cal bypass is frequently attempted. Procedures include
gastrojejunostomy to bypass the duodenurn and choledocho-
jejunostomy to relieve biliary obstruction. Endoseopic place-
ment of stent tubes to support biliary drainage is increasingly
considered as an altemative to surgery. Stents may be placed
internally or inserted for externaI drainage.
Surgeons who are attempting curative procedures may use
the more aggressive Whipple proeedure or total pancreatec-
tomy (Figure 42-6). Neither radiotherapy nor ehemotherapy
Cystic duct
Gollblodder Stomoch
Jejunum / ordered.
figo 42-6 Pancreatoduodenectomy (Whipple's proce-
dure) vvith anastomosis.
aIone has had any positive effeets on the course of the diseaSI
but combination protocols used in research trials appear t
extend life e>""Pectancyto nearly 1 year.
Patient/farnily education
Pain management is an ongoing chaIlenge with panereati
cancer and is often the primary determinant of quality of lift
The nurse serves as the patient's advoeate in the health car
system to establish an effective pain management protoec
and continuously adapt it to changes in the patient's condi
tion. The nurse provides careful teaching about the use of nar
cotic anaIgesics and the inevitable development of toleranc
and physicaI dependence (see Chapter 12). Instruetion is alsl
provided about expeeted side effeets and their managemen1
Other general measures are those provided to any patient witl
ÍDvasive eaneer (see Chapter 11). Nursing care of the patien
undergoing pancreatie surgery is summarized in the Guide
lines for Care Box.
guide'ines ~or carE
The Person Undergoing Pancreatic Surgery
Preoperative Care
Provi de thorough teaching about planned surgical pro-
cedure and expected postoperative care.
Monitor prothrombin time and other clotting studies;
vitamin K and other c10tting factors may be ad-
ministered.
Assess nutritional status. Administer TPN if ordered.
Postoperative Care
Monitor vital parameters every hour. Criticai care place-
ment is usualiy necessary.
Check vital signs, intake and output, and hemody-
namic parameters.
Perform blood gas, oxygen saturation. and routine
blood studies.
Se alert to signs of bleeding or shock.
Maintain urine output at 30 to 50 ml/hr.
Initiate pulmonary hygiene every hour with deep
breathing, coughing as needed, and use of incentive
spirometry.
Establish effective pain management regimen. Monitor
every hour.
Monitor dressings and drainage tubes. Keep skin clear
of drainage.
Maintain nutritional support with TPN.
Initiate oral feedings with clear Iiquids. Advance as
tolerated.
Monitor blood glucose and administer insulin as or-
dered.
Monitor patient's weight and the development of
steatorrhea.
Administer pancreatic enzyme replacement as
Assess for signs of dumping syndrome (see
Chapter 40).
Provide support for patient and family and initiate dis-
charge planning.
 Management of Persons vvith Problems of the
• supplements. Pain management is extremely difficult if the
1 Mrs. Blue has a T-tube present after an abdominal
cholecystectomy. What may normally occur after the
remova I of her T-tube? What complication should the
nurse be alert for? Why? How should he or she
respond?
2 In what ways would your assessment findings for a
person with chronic pancreatitis differ from those for
a person with acute pancreatitis?
3 Mr. Ryan 77, is being treated for acute pancreatitis re-
lated to biliary obstruction. What aspect of this type
of pancreatitis differs from acute alcohol-induced
pancreatitis?
CHOlE L1THIASIS/CHOlECYSTITIS/
CHOlEDOCHOllTHIASIS
11 Cholelithiasis and cholecysitis are common health prob-
lems. Risk factors include obesity, female gender, multipar-
ity, use of birth control pills, and middle age.
• Biliary tract surgery by laparoscopic cholecystectomy is the
treatment of choice for gallbladder disease.
If acute cholecystitis occurs, pain, nausea, and vomiting,
and fluid and electrolyte problems may be of concern.
• Patient problems requiring nursing attention after open
cholecystectomy include ineffective breathing pattern,
pain, and management of the T-tube.
PRIMARY SClEROSING CHOLANGITIS
• Primary sclerosing cholangitis is usually idiopathic in etiol-
ogy but frequently occurs in conjunction with IBD. There is
no treatment, and most patients eventually require liver
transplant.
CARCINOMA OF THE BILlARY SYSTEM
• Carcinoma of the biliary system is insidious and can be
asymptomatic until late in the disease.
PANCREATIC DISORDERS
• Pancreatitis may be acute or chronic.
• Acute pancreatitis can result in criticai fluid and electrolyte
problems, metabolic disturbances, and pain.
• Most cases resolve spontaneously, but the mortality from
hemorrhagic forms is high.
• Care in acute pancreatitis focuses on pain management,
fluid resuscitation to prevent shock, resting the pancreas by
NPO status, and collaborative monitoring for complications.
• Chronic pancreatitis is progressive and usually results from
alcoholism. It is not reversible.
• Chronic pancreatitis results in pain, malabsorption and
steatorrhea and possibly diabetes mellitus.
• Abstinence from alcohol use is the primary treatment ob-
jective in patients with chronic pancreatitis.
Gallbladder and Exocrine Pancreas chapter42 1393
• Malabsorption is treated with the use of pancreatic enzyme
patient continues to drink alcohol.
• Cancer of the pancreas is insidious and has a very poor
prognosis. In rare instances a pancreatoduodenectomy
may be performed.
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