management pancreas and gallbladder

JUDITH K. SANDS

objectives After studying this chapter, the learner should be able to:1 Describe the etiology, epidemiology, and pathophysiology of cholelithiasis, cholecystitis, and can-

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 of acute and chronic pancreatitis

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 haveacute 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 adultsevery year.

CHOLELlTHIASIS/CHOLECYSTITISICHOLEOOCHOLITHIASISEtiologyGallstones can occur anywhere in the biliary tree. The termcholelithiasis refers to stone formation in the gallbladder andrepresents the most common biliary disorder. Either acute orchronic inflarnrnation, termed cholecystitis, can result, usuallyprecipitated by the presence of stones. When stones form in ormigrate to the common bile duct the condition is termedcholedocholithiasis. Figure 42-1 illustrates common sites forgallstones.

Eighty percent of gallstones are composed of choles-tereI. 19The remaining 20% are pigmented stones, which arefurther classified as black or brown.'9 Although the preciseetiology of gallstones is unknown, the basic component ofsupersaturation of the bile v,ith êholesterol is widely ac-cepted. Because most healthy individuals experience super-saturation of the bile at various times without developinggallstones, it is clear that other factors are operational aswell. Risk factors for gallstones have been well identifiedand include various clinical states associated with changesin cholesterol formation and excretion (Research Box). Therisk factors for cholesterol gallstones are listed in the RiskFactors 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

EpidemiologyCholelithiasis is a common health problem in the UnitedStates. Stones affect about 10% of men and 15% of womenolder than 55 years of age. An estimated 20 to 25 million adultshave gallstones, and 1million new cases are diagnosed annu-ally.'9 Many, if not most, patients are asymptomatic, and it istheorized that a large number of cases remain undiagnosed.Ten percent of persons with gallstones develop symptomswithin 5 years of diagnosis, and greater than 500,000 surgicalprocedures are performed each year at an annual treatmentcost in excess of five billion dollars.16 These figures makecholelithiasis and its associated disorders the most commonand 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 typicallyidentified as significant risk factors for the developmentof gallstone disease. This study involved a data review ofstudies related to the prevalence of gallstone diseasefrom 1966 to 1992. The data showed that obesity was astrong risk factor for gallstones in women, particularlyduring periods of rapid weight loss. Between 10% and25% of obese persons will develop gallstones within afew months of beginning a very low-calorie diet, withperhaps one third of the total becoming symptomatic.The risk is less strong in men and most strong in personswith the highest body mass index and most rapid weight1055. Treatment with ursodeoxycholic acid (ursodiol) dur-ing weight 1055 effectively prevented the development ofstones. The effect of various diets on the incidence ofstone formation was not explored.

1373

1374 unit: viii Alterations in Digestion and Elimination

common in women, occurs most frequently in midclle-agedand older persons, and affects American Indians, MexicanAmericans, and whites more frequently than African Ameri-cans and Asians, although the incidence in Asians is increasing.

PathophysiologyBile is primarily composed of water plus conjugated bilirubin,organic and inorganic ions, smali amounts of proteins, andthree lipids-bile salts, lecithin, and cholesterol. When thebalance of these three lipids remains intact, cholesterol is heldin solution. If the balance is upset, cholesterol can begin toprecipitate. Cholesterol gallstone formation is enhanced bythe production of a mucin glycoprotein, which traps choles-terol particles. Supersaturation of the bile with cholesterolalso 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 stonesmost frequently occur in multipIes but can be solitary. Theprocess of stone formation is sIow. Stones are theorizedto grow steadily for 2 to 3 years and then stabilize in size.

Small bile duct

figo 42-1 Common sites of gallstones.

risk'act rsCholesterol Gallstones

ObesityMiddle agePregnancy, multiparity, and the use of oral contra-ceptives

Rapid weight loss (-5 pounds/wklHypercholesterolem ia, use of anticholesterol medicationsDiseases of the ileumGender (approximately twice as common in women)

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 forgalistones also have stones in the common bile duct.8

Black pigmented stones form as the result of an increase inunconjugated 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 andare usualiy preceded by bacterial invasion.

Although most persons with gallstones are asymptomatic,choIecystitis can develop at any time, usualiy from a blockageof 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 causeof 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, andpersists for about 1 to 3 hours.8 It may awaken the patient atnight or be associated with the consumption of a large or high-fat meal. Some patients experience nausea and vomiting andmay 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 andtemporary inspiratory arrest (Murphy's sign). The episode ofchoIecystitis 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 whenthe classic symptoms are present. The diagnosis is more diffi-cult when the symptoms are milder or reflect simply generaldyspepsia. 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 needsto be determined if possible.8 Researchers theorize that manypatients with "poor outcomes" after gallbladder surgery mayactualiy reflect situations where the gallbladder was not reallythe source of the patient's dyspepsia.8•19

'.1.1If.M '""' -& ", . c;.~lnlCªh-n.'1J3Fl.1:;.f:.stªt.l ..ÇJl1Si Cholecystitis

Sudden onset pain in the RUO of the abdomenSevere and steady in qualityFrequently radiates to the right scapula or shoulderPersists for about 1 to 3 hoursMay awaken the patient at nightMay be associated with consumption of a large orfatty meal

, Anorexia, nausea, and possibly vomitingMild to moderate feverDecreased or absent bowel soundsAcute abdominal enderness and a positive Murphy'ssign

Elevated white blood cell count, slightly elevated serumbilirubin and ai a 'ne phosphatase leveis

e Gallbladder and Exocrine Pancreas chapter42 1375 III

TreatmentsExtracorporeal shock wave lithotripsy was pioneered in

Germany and adapted to the treatment of gallstones. Litho-tripsy uses shock waves to disintegrate the stones. Extensiveselection criteria limit the use of this treatment to a smallnumber of patients with gallstones.19 Patients must also un-dergo oral dissolution therapy after treatment to dissolve thestone fragments. Recurrence is a problem, and the treatment,including follow-up drug therapy, is tive times more expensivethan 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 tubeis 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, butsince the gallbladder remains intact, recurrence rates run ashigh as 50%.19

=

Collaborative Care Management

Diagnostic testsUltrasonography 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 outother causes of gastrointestinal (GI) discomfort.

- - 1..":erseveral acute at-'C"er,:S ually the result of

::::e gal:.bla' .er wall that cause scarring,ibly cerarion. Bacterial infection may

z.:so e resem. Parients with chronic disease often do notsee' help unril jaundice or other complications develop. Fig-ure 42-2 shows the relationship between stone formation andassociated outcomes in uncomplicated gallbladder disease.

MedicationsOral dissolution therapy with ursodeoxycholic acid

(Actigall) may be prescribed for patients who are poorsurgical risks or who refuse surgery. The drug graduallydesaturates the bile, which allows space for the reuptake ofthe cholesterol in the stones. The treatment is only effec-tive when stones are less than 1.5 to 2 cm in diameter. Afull 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 isoccasionally used in high-risk surgical patients. The drug isinstilled through a percutaneous catheter, which is monitoredfluoroscopically. Multiple drug instillations are required over12 to 24 hours, which makes the treatment labor intensive forthe physician and extremely expensive.

Etiological factor~:' . .'.(Age, gencler, multiparity,_obesjty, Iifestyle; pn~sence of other diseases)

CholedodTOlithiasis

I Asymptomatic.1

Surgical managementCholecystectomy was first performed in Berlin in 1882

and evolved into a procedure with excellent effectivenessandextremely low associated morbidity and mortality. lt is the

figo 42-2 The development of uncomplicated chole-cystitis.

figo 42-3 Oral cholecystogram. Radiolucencies(arrollVs) are caused by gallstones.

1376 unit viii Alterations in Digestion and Elimination

second most common surgical procedure performed in theUnited States following cesarean section and serves as thestandard against which other gallstone treatments are mea-sured.8 The main advantage of cholecystectomy is the fact thatit stops the disease. The recurrence rate is zero. The main dis-advantage has alwaysbeen that it is major abdominal surgerywith 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 inFrance in 1987and in the United States in 1988,and by the early1990shad revolutionized the care of patients with gallbladderdisease.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 than24 hours, and patients can return to normal activities in 2 to3 days. It is conservative1yestimated that at least 80% of allcholecystectomies are being performed laparoscopically today,and the number continues to increase as surgical techniquesimprove. 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 cholecystectomyprocedures with placement of a T-tube for drainage wheneverstones were present or suspected to be present in the commonbile duct. Surgical techniques have continued to improve, how-ever, and laparoscopic approaches are now being successfullycombined with endoscopic exploration and sphincterotomytoeffective1ytreat patients with common bile duct stones.

Laparoscopic cholecystectomy is performed under generalanesthesia. The procedure consists of the creation of four1/2-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 andpermit adequate visualization and the introduction of in-struments. The operative field is magnified and projected on avideoscreen, and a laser or cautery is used to dissect the gall-bladder. The gallbladder is deflated and removed through theumbilical incision. The CO2 is removed at the end of the pro-cedure. lf problems develop during the procedure, it can berapidly converted to an open cholecystectomy.

The ski11of the surgeon is the primary determinant of out-comes.The slight1yhigher rate ofbile duet injury associatedwiththe procedure is usual1yattributable to inexperience with thetechnique. Laparoscopiccholecysteetomytakesabout 90minutesand is more expensivethan traditional open surgery.The shorthospital stayand tremendous patient satisfactionwith the proce-dure, however, clearly outweigh the higher surgical costs. Themild shoulder pain that patients may experiencefor up to 1weekis attributed to nerve irritation from distention and the CO

2

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 definitivetherapy is completed. After treatment they can resume a nor-mal diet.

ActivityThere are no activity restrictions for persons with chole-

lithiasis, cholecystitis, or choledocholithiasis.

ReferralsReferrals would not general1ybe required for the manage-

ment of uncomplicated gallstones unless a serious comor-bid condition necessitated the involvement of additionalprofessionals.

NURSING MANAGEMENTOF THE PATIENT

UNDERGOING LAPAROSCOPICCHOLECYSTECTOMY

• PREOPERATIVE CAREPatients will complete their preoperative preparation athome before their arrival on the day of surgery. The nursewill 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 beprovided in the immediate postoperative period. The nursealso ensures that the patient understands that the expectedpain is mild to moderate and can be successfu11ymanagedwith standard analgesics.

• POSTOPERATIVE CAREThe 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 anddecrease irritation. Deep breathing is encouraged. Foleycatheters and nasogastric tubes are common1y inserted duringthe procedure and will be removed in the postanesthesia careunit. As soon as the patient is sufficient1yalert, he or she willbe encouraged to sip clear fluids and get out of bed. Dressingsover the small incisions are monitored for bleeding. Healthypatients with adequate home support may be dischargedwhen 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 to3 days and consume a light diet. The patient is advised tolimit the intake of fatty and fried foods for the first few weeksafter surgery until tolerance is established. The incisions re-quire minimal care, and the dressings can usually be removedthe next day. The patient is instructed to report the develop-ment of redness, swellin ,or discharge from any incision, aswe11as the onset of feyer.pain, or tenderness in the abdomen.Heavy lifting should e a ·oided.

Management of Persons with Problems of the Gallbladder and Exocrine Pancreas chapter42 1377

A ClinicaI Pathway for the patient undergoing laparoscopiccholecystectomy is shown below. The Guidelines for Care Boxsummarizes the care provided to a patient who undergoes tra-ditional open cholecystectomy.

GERONTOLOGICAL CONSIDERATIONSGallbladder disease is seen more frequently with advancing agebut is treated in the same manner. Elderly persons may have

more subtle symptoms and signs in the presence of cholecystitis.Thus they can develop baeterernia before they seek help. Becauseof the normal decrease in immune function with aging, theyare at greater risk for septic shock. Elderly patients have morerisks with surgery just because of their age.The laparoscopiccholecystectomy procedure is particularly effective in this age-group as it decreases the period of immobility and recoverysubstantially. Wound healing needs to be carefully monitored .

II

,iIII,

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

DAY OF SURGERYDAY OF ADMISSIONDAY 1

DAY OF DISCHARGEDAY 2

Diagnostic Tests

edications

Treatments

Diet

Activity

Preoperative: CSC, UAPostoperative: Hgb and Hct

PAR: IVs decreased to saline lock after nausea sub-sides; IV analgesic, then PO

PAR: 1&0 q shift; VS q4hr x 4, then q8hr; assessbowel sounds q4hr; check drainage on bandagesq2hr

NPO until nausea subsides, then c1ear liquids; ad-vance to full liquids, low fat

Up in room with assistance about 6 to 10 hr aftersurgery; T & OS q2hr

Disc saline lock; PO analgesic

Disc 1&0; VS q8hr; assess bowel soundsq8hr; remove bandages and reapplybandages after shower if necessary

Regular diet, low fat

Up ad lib, OK to shower

Consultations

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

guidelines for care

Biliary DrainageConnect any biliary drainage tubes to closed gravity drainage.See Figure 42-4 and the Guidelines for Care Box onp. 1378 for care of a T-tube.Attach sufficient tubing 50 the patient can move withoutrestriction.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, orfever) 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 drainagediminishes and disappears.

The Person Undergoing Open CholecystectomyMaintain a dry, intact dressing; usually a drain is insertednear the stump of the cystic duct; some serous fluiddrainage 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 ifthere is externai biliary drainage).

PostoperativePlace 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 presentuntil ambulating well. Assist patient to effectivelysplint 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.

PreoperativeTeach patient the importance of frequent deep breathingand use of incentive spirometer because the high inci-sion and RUO pain predispose the patient to atelectasisand right lower lobe pneumonia.Explain the types of biliary drainage tubes that areanticipated, if any.Teach patient about the pain control plan to be used in thepostoperative period.


SPECIAL ENVIRONMENTS FOR CARECriticai Care Management

Critical care management would not .be anticipated for anyphase of routine gallstone management. The surgical proce-dures have an excellent safety record and are associated with aless than 7% incidence of morbidity from any cause.

Home Care Management

Cholecystectomy is the foundation of care for gallstones, andthe procedure has become essentially same-day or overnightsurgery. 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 returnto usual activities.17 For more complex procedures patientsmay be discharged from the hospital with a T-tube in place.Teaching concerning T-tube care is included in the Guidelinesfor Care Box. Elderly patients may need some additional as-

'guide'ines for careManaging a T-Tube

Purpose

A T-tube may be placed after surgical exploration of thecommon bile duct to preserve patency of the commonduct and ensure drainage of bile until edema resolvesand bile is effectively draining into the duodenum. Thetube is usually connected to gravity drainage and canbe converted to a leg bag to limit its restrictivenessand visibility. The patient may be discharged with theT-tube in place (see Figure 42-4).

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 atleast once per shift on subsequent days.

Record output carefully. Initial drainage may be asmuch as 500 to 1000 ml per day, but this amountshould steadily decrease as healing occurs.

Follow physician's order for initiating clamping ofthe 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 flowsinto the duodenum.

Keep the skin clean and protected from bile drainage asbile is extremely irritating to the skin.

Teach the patient to empty the bag and convert it to aleg 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-tubeentry site each day.

Zinc oxide may be used to protect the skin from irritation.Redness, swelling, or drainage from the site and thedevelopment of fever should be promptly reportedto the physician.

sistance at home when they undergo same-day surgery. Theseneeds are ideally identified and arranged before surgery.

COMPLlCATIONSTransient mild diarrhea is the only adverse outcome that hasbeen consistently linked to cholecystectomy. The most com-mon complication of nonsurgical management of gallstonedisease is recurrence, and it is clear that undiagnosed or in-adequately treated gallbladder disease can result in serioand 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 evidencethat the reduction in the pool of bile salts and the loss of thereservoir funetion of the gallbladder increase the incidenceof duodenal reflux or an alkaline shift in the gastric pH.16Some researchers suggest that these so-called "complica-tions" may actually reflect situations in which the patient'soriginal digestive symptoms were never related to the gall-stones and therefore were not improved by their rem oval(Research BOX).5

PRIMARY SCLEROSING CHOLANGITISEtiology/EpidemiologyInflammation and scarring of the biliary tree occur most com-monlyas a result of gallstones and bile duct infection. Parasitesare a common source of chronic duct infection in Asia and de-veloping countries. When no cause for the bile duct injury canbe found, the process is called idiopathic or primary sclerosingcholangitis (PSC).

figo 42-4 Section o' T- ube emerging from stabvvound may be placed over roll of gauze anchoredto skin vvith adhesive spe to prevent its lumen frombeing occluded b p'essure.

anagement of Persons vvith Problems of the Gallbladder and Exocrine Pancreas chapf:er42 1379

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 withother disorders, most of which have a strong immunologicalcomponent. The closest link is with inflammatory bowel dis-ease (IBD), particularly ulcerative colitis. Of patients with PSC70% have IBD, although PSC only occurs in 2% to 4% of allpatients with IBDY The PSC may precede the diagnosis ofIBD 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 thirdof all patients needing liver transplantation.

Pathophysiology

Primary sclerosing cholangitis causes changes in and aroundthe large bile ducts from inflammation, obstruction, and intra-and extrahepatic fibrosis. Strictures can usually be found inmultiple locations. These strictures are short and diffusely dis-tributed and alternate with normal or dilated segments of theducts to create a beadlike appearance on x-ray. It is unusual forthe gallbladder or cystic duct to be involved. Liver biopsy showsthe combination of inflammation, fibrosis, proliferation, andduetal obliteration that confirms the presence of the disease.The disease proceeds in stages, and by stage 4, biliary cirrhosisis present (Chapter 37), making the diagnosis complexo

Many patients are asymptomatic in early stages. Others areseen with a combination of fatigue, fever, jaundice, abdominalpain, and weight loss. Persistent severe pruritis can be a par-ticularly difficult aspect of the disease. Patients may experi-ence recurrent attacks of cholangitis.


The diagnosis of PSC is not easily established and is usuallymade as part of a workup for cholecystitis or general nonulcerdyspepsia. PSC causes elevated liver enzymes and serumbilirubin levels, but the elevations in alkaline phosphatase are

research~~Reference: Fenster LF,Lonborg R,Thirlby RC,Traverso LW: Whatsymptoms does cholecystectomy cure? Am J Surg 16(5):533-538,1995.

This study attempted to evaluate the effectiveness ofcholecystectomy in relieving presenting GI problems.Data were colleeted from 225 patients who underwentlaparoscopic cholecystectomy. Eighty-two percent haddocumented gallstones before surgery, 91% experiencedbiliary-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. Thestudy results showed that documented gallstone-relatedpain was universally relieved by surgery, but pain wasonly relieved in 52% of those without documented gall-stones (acalculous cholecystitis). And, although nonpainsymptoms were extremely common in this population,surgery only relieved the related symptoms in approxi-mately 44% of the patients.

considered to be a hallmark feature. Endoscopic retrogradecholangiopancreatography (ERCP) (Chapter 38) is used to vi-sualize the biliary tree. Liver biopsy helps rule out other causesof the symptoms and assists in estimating the severity of theliver damage.

The prognosis of PSC largely depends on its clinicai course,which can be highly unpredictable. The aggressiveness of thedisease is influenced by the number and severity of infectionsand 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 significantlyalter 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 beeneffective, but the use of ursodeoxycholic acid has shownpromise even though its mechanism of action in PSC remainsunknown. Surgical procedures other than transplant havebeen effective for diffuse disease. Endoscopic treatment to re-move stones, relieve obstruction, dilate ducts, and place stenttubes 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 difticultcharacteristics. Patients are instructed about the disease andits possible outcomes and are prepared for the possibility ofthe eventual need for liver transplant. Persistent jaundice maynegatively affect body image, and chronic severe pruritis canbe a daily nightmare. Some patients respond to cholestyr-amine resin, which theoretically binds the itch-triggeringelements in the bile. The nurse also suggests that the patientexperiment with common interventions that may lessen itch-ing. Possible strategies are summarized in the Guidelinesfor Care Box. A low-fat diet is recommended to patients whodevelop problems with diarrhea or steatorrhea, and the fat

guide'ines for careStrategies 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 skinregularly.

Maintain a cool environment and ensure adequateamounts of humidity in the air.

Avoid activities that increase body temperature or causesweating.

Experiment with treatments sueh as oatmeal baths.Keep the fingernails short and eonsider use of cottongloves at night to minimize skin damage fromseratehing.

Use antipruritie medieations as ordered.


restriction usually prompt1y corrects the problem. Fat-solublevitamin replacement is often needed.

CARCINOMA OF THE BILlARY SYSTEMEtiology/EpidemiologyPrimary tumors of the gallbladder are extremely rare in clini-cal practice, and their incidence may be declining beca useof prompt surgical intervention for gallbladder disease. Theetiology is unknown. Gallbladder cancer occurs almost ex-clusively in persons older than 60 years of age and is twiceas common in women.23 High-risk groups for gallbladderdisease in general have a slightly increased risk of gallblad-der canceI.

Cancer can also develop in the bile ducts. This diseaseprocess also typically affects patients between 50 and 70 yearsof age. It demonstrates a striking link with the presence of in-flammatory bowel disease.

PathophysiologyCarcinoma can occur anywhere in the biliary system. It hasa very insidious onset and can metastasize by direct exten-sion, through the lymphatics, and through the blood. Mostpatients have no symptoms that are referable to the gall-bladder. Others have symptoms similar to those seen withcholelithiasis and cholecystitis because of obstruction andinflammation.

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 ofmetastasis to the liver or pancreas may also be present.23 Bythe time gallbladder cancer produces symptoms it is usuallyincurable.

Collaborative Care ManagementSurgery is the primary treatrnent for cancer of the gallblad-der. If the disease is diagnosed incidentally, it may be confinedto the gallbladder and be curable with surgery. Cholecystec-tomy with wedge resection of 3 to 5 cm of normal liver pluslymph no de dissection is usually performed. Survival forthose with invasive disease is usually less than 2 years. Neitherradiotherapy nor chemotherapy has thus far improved patientoutcomes.

Treatment of bile duct cancer focuses on maintaining bileflow. 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 forseveral 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 forbile 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 andpoor prognosis. General care of the cancer patient is discussedin Chapter 11.

PROBLEMS OF THE PANCREAS

ACUTE PANCREATITISEtiologyAcute pancreatitis occurs when obstruction of the outflow ofpancreatic 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 orsmall pancreatic ducts or both. The two major causes of acutepancreatitis in the United States are gallbladder disease and al-cohol abuse."·23 Together they account for about 80% of allcases. Acute pancreatitis may be similar in presentation tochronic pancreatitis, but it represents a different pathologicalprocess.1I Other rare causes of pancreatitis include abdominalor surgical trauma, obstruetion of the gland by neoplasticgrowth, drug effects, a variety of infectious diseases, and otherchronic diseases of the GI tract.

Alcoho/-re/ated pancreatitisThe 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 aminimum period of several years are probably required to ini-tiate the processo Alcohol also weakens cell membranes andmakes the acinar cells more vulnerable to injury. It is alsoknown 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. Alcoholicpatients also typically develop chronic disease once an acuteepisode has occurred, and the presence of chronic pancreati-tis appears to make the pancreas even more vulnerable to thedamaging effects of alcohol.12·21.23Recurrent episodes of acutepancreatitis are common.

Biliary pancreatitis

Transient obstruction of the ampulla ofVater by a gallstoneis considered to be a major cause ofbiliary pancreatitis. Stoneswere found in the stool of more than 90% of patients withgallstone pancreatitis in some studies. The obstruction doesnot have to be prolonged to initiate acute inflammation. Howthe obstruction activates the pancreatic enzymes is not under-stood. The presence of tiny gallstones (microlithiasis or biliarysludge) toa small to be identified by imaging studies, is be-lieved to play a role. There is also considerable evidence thatstructural abnormalities that lead to narrowing at the sphinc-ter of Oddi can be considered a cause of biliary pancreatitis. Itis theorized that the various forms of obstruction can reversethe normal pancreatic pressure gradient. This would permitreflux of bile or duodenal contents into the pancreatic ductsand possibly even cause small duct rupture.1I

Biliary pancreatitis begins acutely, but is likely to be mild incourse and followed by rapid recovery. It can, however, in se-lected situations trigger rnassive pancreatic necrosis and leadto death. It rarely leads to cnronic disease.


EpidemiologyThe incidence of acute pancreatitis has increased in recentyears, 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 to65 years of age and predominantly female, whereas patientswith alcohol-related pancreatitis are usually slightly youngerand predominantly male.

Acute pancreatitis may take a mild, severe, or fulminantcourse. Pancreatitis has a fulminant course in approximately5% to 15% of all patients, and 20% to 60% of these patientswill either die or face potentially lethal complications.6 Theoverall mortality rate for pancreatitis remains at about 10%despite improved diagnosis and more aggressive treatment.

PathophysiologyThe two major pathological varieties of acute pancreatitis arethe (1) acute interstitial form and (2) acute hemorrhagicformoAlthough either form can be fatal, the interstitial formis often a mi!der disease.

The defining characteristic of acute interstitial pancreatitisis a diffusely swollen and inflamed pancreas, which retains itsnormal anatomic features. There are minimal or no areas ofhemorrhage or necrosis in the gland. The interstitial spacesbecome grossly swollen by extracellular edema, and the ductsmay contain purulent material. The acute hemorrhagic dis-ease presents with a very different picture. The gland readilyshows acute inflammation, hemorrhage, and marked tissuenecrosis. Extensive fat necrosis is present in patients with ful-minant disease, not just in the pancreas but throughout theabdominal and thoracic cavities and subcutaneous tissues.23

ecrosis of vesselscan 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 ofthe 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 pancreaticenzymes 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 isinitiated. The etiológical roles of alcohol and bi!iary diseasehave been discussed, but they fai! to fully explain the diseaseprocess.22 Enzyme activation overwhelms all of the normalprotective mechanisms of the pancreas and initiates a massiveattack 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 massivemovement 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 insufficiencyFigure 42-5 outlines the major pathological events that canoccur in acute pancreatitis .

. Ihterper-itoneol.soponificotíon

oF calcium

figo 42-5 Summary of major pathological events that occur in acute pancreatitis.

, 382 unit viii Alterations in Digestion and Elimination

*NOTE:These signs indicatethe accumulationofbloodinthese areas andrepresent the presence of hemorrhagicpancreatitis.

'.I.IIf·· L"" l ~.&: •. l_, Iça, ~nJ,,-est-a1;!QnAcute PancreatitisPAINSteady and severe in nature, excruciating in fulminantcases

Located in the epigastric or umbilical region; may radi-ate to the back

Worsened by Iying supine; may be lessened by flexedknee, curved back positioning

Medications

There is no drug treatment for acute pancreatitis. Drugtherapy to reduce pancreatic secretion with somatostatin,histamine H2-receptor antagonists, anticholinergic agents,and glucagon has not been shown to have any therapeuticeffect. Pain management is the primary consideration, andpatients 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 thesphincter of Oddi." Morphine, however, is now believed tohave minimal sphincter effects and is an extremely effectiveanalgesic.

Fluid and electrolyte replacement is criticaI since the loss ofintravascular fluid through membrane leakage averages 4 to6 L and can easily exceed these levels in severe cases.3,23 Pre-vention of hypovolemic shock necessitates aggressive fluidmanagement. Urinary output should remain at or above 30 to50 ml/hr. Potassium losses can also be significant in bothvomitus and pancreatic fluids, and serum leveIs need to bemaintained. Hypocalcemia develops frequently and is care-fully monitored. Replacement of calcium is initiated if the pa-tient becomes symptomatic.23 Exogenous insulin may beneeded in severe disease, but it is used cautiously becausethese patients are very vulnerable to severe hypoglycemiafrom decreased glycogen and glucagon reserves.

Collaborative Care ManagementDiagnostic testsThe diagnosis of acute pancreatitis is made initially from

the measurement of the serum amylase level, which riseswithin a few hours of the onset of the disease. In mild diseaseit may only remain elevated for a few days. There is no appar-ent relationship between the severity of the disease and theheight of the enzyme levels.18 The levels of urinary amylasemay also be measured if the patient sustains adequate kidneyfunction. 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 mayreach leveIs as high as 500 to 900 mg/dl, and elevated liverfunction 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 withlow levels of both albumin and magnesium, especially inchronic alcoholics.

Computed tomographic (CT) scanning has become thegold standard for diagnosing acute pancreatitis, although it isactually not needed except for patients with severe disease andsuspected complications. CT scans can estimate the size of thepancreas; identify cysts, abscesses, and masses; and with con-trast medium can clearly diagnose hemorrhagic disease. Earlyin the diagnostic process abdominal x-rays may be taken torule out ulcer perforation, and ultrasonography may be usedto rule out the presence of gallstones.

The clinical manifestations of acute pancreatitis vary some-what according to the severity of the attack. Acute pain in theepigastric region is the hallmark feature of the disease. The painis usually steady in nature and may radiate to the back. It is typ-ically worsened by lying supine, and patients may curve theirbacks and draw their knees up toward the body in an attempt todirninish 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 beagonizing.

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 findingsfor patients with severe pancreatitis include abdominal ten-derness and rigidity, progressive abdominal distention, anddecreased bowel activity. Fever is common, but it rarely ex-ceeds 39° C. Fulminant disease may progress to hypovolemicshock, ascites, acute tubular necrosis, and respiratory failure.The clinical manifestations of mild and severe pancreatitis aresummarized in Box 42-2.

I~~r~~~~N~verity but is usually protracted liWorsened by ingestion of food or fluid ,

I~~:~~~~~:::::~~o'"". I.'

ABDOMINAL FINDINGS •

".Rigidity, tenderness, guarding ~I'~.':".IDistentionf Decreased or absent peristalsis. tl

r: ADDITIONAL FEATURES OF FULMINANT DISEASE rISymptoms of hypovolemic shock !leI

Oliguria: acute tubular necrosis ~• Ascites ~j

Jaundice iRespiratory failure ~;

i Grey Turner's sign (bluish discoloration along the flanks)* fCullen's sign (bluish discoloration around the umbilicus)* t

Management of Persons with Problems of the Gallbladder and Exocrine Pancreas chap~er42 1383

Surgical management

Surgery is not a routine part of the management of acutepancreatitis, but some procedures may be necessary to con-trol related gallbladder problems, pseudocyst, or abscessoNecrotic tissue may also be resected. Patients requiring

Treatments

There are no known treatments for pancreatitis. Medicaltherapy is direeted at general supportive care for most patientswith mild to moderate disease. The patient is generally givenNPO. Nasogastric suctioning has frequently been used, but isprobably not necessary unless the patient develops ileus or ex-periences persistent vomiting.

More aggressive and invasive interventions are available forpatients who are at high risk for complications. The course ofacute pancreatitis is not readily apparent, and several clinicalprognostic rating scales have been developed to help cliniciansidentify patients at greatest risk. The older system uses the cri-teria of Ransom applied at admission and again within thefirst 48 hours. The modified Glasgow criteria are easier toapply 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. Clinicaltrials have involved small numbers of patients, and resultshave 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 reducesoverall morbidity in the select group of patients in whom anobstructing stone can be identified.

research\~ilRelerence: McClave SA et ai: Comparison 01 the salety 01 early en-teral vs. parenteral nutrition in mild acute pancreatitis. J Parent EntNutr21(1l:14-20.1997.

This study was designed to compare the safety, cos!, andeffectiveness of two methods of nutrition support for pa-tients with mild acute pancreatitis. The study involved30 patients who were admitted with mild acute pancre-atitis documented by the presence of pain and elevatedserum amylase and lipase leveis. Patients were ran-domly assigned on admission to receive either total en-teral nutrition (TEN) via a nasointestinal tube or total par-enteral nutrition (TPN) by central or peripheral catheter.Nutrition support was initiated within 48 hours of admis-sion. No differences were noted between the groups onadmission in mean age, Ransom criteria, APACHE score.or other prognostic screening tool.

No deaths occurred in either group. No differenceswere found in serial pain scores, the number of days be-fore normalization of blood values occurred, serum albu-min leveis, or the incidence of nosocomial infection. Thecost of TPN, however, was more than four times greaterthan the cost of TEN, and stress-induced glucose lev-eis were significant in the TPN group. The study con-cluded that isocaloric/isonitrogenous TEN via nasoin-testinal tube appears to be a cost-effective alternative tointervention with TPN in this population.

Activity

Bedrest is maintained during the acute phase of diseasemanagement to decrease the body's overall metabolic de-mands. Once the patient's condition has stabilized, activity can

Diet

The patient is given nothing by mouth until the abdominalpain has subsided, and amylase levels return to normal. Thispractice, in theory, rests the pancreas and limits or stops thesecretion of enzymes. Most patients do recover without com-plications or sequelae.IO Oral tluids and feedings can usuallybe resumed within 3 to 7 days and gradually advanced to anormal 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 implementedfor 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 withmild pancreatitis, but its use significantly decreases morbidityand mortality in severe and fulminant disease.11 Efforts aremade to keep plasma albumin levels above 3.5 gld and totalprotein values above 6.5g/d, thereby maintaining a positive ni-trogen balance. Ii

surgery typically have fulminant disease and are acutely ill.The discussion of surgical intervention is included underComplications on p. 1386.

't!

WITHIN48HROF ADMISSIONAge >55 yearsWBC >15,000Glucose >180 mg/dlBUN >45 mg/dlPo, <60 mm HgAlbumin <3.2 g/dlCalcium <8 mg/dlLDH >600 IU/L

INITIAL 48 HRHematocrit decrease >10%BUN increase >5 mg/dlCalcium <8 mg/dlPo, <60 mm HgBase deficit >4Estimated fluid sequestra-tion >6 L

ADMISSION. Age >55 years

WBC >20,000 cell/mm3

LDH >350 IU/LAST >250 IU/LGlucose >200 mg/dl

Data Irom Ransom JAC et ai: Surg Gynecol Obstet 143:209. 1976 andNeoptolemos VP et ai: Lancet2:979, 1988.WBC, white blood cell count; LOH, lactic dehydrogenase; AS!, aspartateaminotranslerase; BUN, blood urea nitrogen.NOTE: Presence 01 three or more lactors indicates poor prognosis.

Tvvo Representative PrognosticScoring Systems Usedin Acute Pancreatitis

~..,-~~~ .~ ~ •• ~ .•....• :z=:"" ~~~

RANSOM GLASGOW


be gradually increased based on the patient's tolerance. Thereare no long-term restrictions.

Presence of Grey Turner's or Cullen's signs: bluish discol-oration on flanks and/or around umbilicus

Jaundice

• NURSING DIAGNOSESNursing diagnoses are determined from analysis of patientdata. Nursing diagnoses for the person with acute pancreatitismay include but are not limited to:

.INTERVENTIONSControlling Pain

Control of pain is a major priority, and either morphine ormeperidine (Demerol) may be used. Critically ill patientsmay 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 andfrequently assess the patient's levei of pain and response to in-terventions. The physician will be consulted for neededchanges in the regimen. An attitude occasionally encounteredin caring for patients with alcohol-induced pancreatitis is thatthe patient is somehow "getting what he or she deserves," es-pecially on repeat admission for recurrent disease. The nursemust serve as the patient's advocate in the system, document-

• EXPECTED PATlENT OUTCOMESExpected 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 bodymovement, or limited activity).

2. Will have adequate fluid volume as demonstrated by nor-mal blood pressure, absence of orthostatic changes, normalskin turgor, moist mucous membranes, and adequate urineoutput.

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 ofacute pancreatitis).

ReferralsPatients with acute pancreatitis are severely ill and may

require the expertise of a variety of specialists during thetreatment and recovery periods. Fulminant illness may ne-cessitate critical care monitoring and consultation. This isparticularly true for patients who develop respiratory com-plications such as adult respiratory distress syndrome(ARDS) or respiratory failure and require intubation andmechanical ventilation. The nutrition support team will beinvolved if TPN is initiated.

Any number of medical specialists may be consulted tomanage emergency complications. The surgeon is oftenneeded to drain abscesses, relieve obstruction, or debridenecrotic tissue. An enterostomal therapist may be consulted ifdraining wounds are left open to heal by secondary intention.

In many patients alcohol abuse is the etiological stimulusof acute pancreatitis, and continuation of alcohol use will in-crease the risk of recurrent acute pancreatitis and chronicpancreatitis 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 mayserve as a stimulus for lifestyle change in some individuals. Itis important to use this opportunity to refer the person for al-cohol treatment if possible.

NURSING MANAGEMENT

• ASSESSMENTSubjective Data

Subjective data to be collected to assess the patient with acutepancreatitis include:

Pain: steady and severe in nature and quality; located in theepigastric 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 notrelieve pain

History of gallbladder disease; long-term high alcohol intake

Objective Data

Objective data to be collected to assess the patient with acutepancreatitis include:

General affect: patient looks distressed; sits with kneespulled toward abdomen

Fever, generally <390 CAbdominal rigidity, distention, guarding, and tendernessDiminished or absent bowel soundsSigns of dehydration: falling urine output, decreased skin

turgor, dry or sticky mucous membranesVital signs: evidence of hypovolemia; tachycardia, tachy-

pnea, normal to low blood pressure, restlessness, andanxiety

Diagnostic TitlePain

Fluid volume deficitNutrition, aItered: lessthan body requirements

Risk for impaired homemaintenancemanagement

HeaIth maintenance,aItered

Possible Etiological FactorsInflammation of pancreas orperitoneum

Vomiting, fluid shifts in abdomenNausea and vomiting; pain

Lack of knowledge about diseaseprocess and therapeutic regimen

UnhealthY lifestyle patterns, in-cluding aIcoholism


ing the severity of the pain and ensuring that an effective planis 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 persistentand not relieved by routine narcotic administration. Al-though the research is currently inconclusive most patientswill be given nothing by mouth to "rest" the pancreas and de-crease the autodigestive processoA nasogastric (NG) tube willbe inserted to keep the stomach decompressed if vomiting issevere.

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 torestoThese measures are used in addition to, and not in placeof, narcotic administration for pain control.

Maintaining Fluid and Electrolyte BalanceAB soon as the patient is admitted, the nurse should institutemonitoring related to fluid and electrolytestatus, cardiac output,and renal status. It is a critical need. Monitoring includes intakeand output, vital signs, daily weights, abdominal girth, and allroutine laboratoryvalues with particular emphasis on potassiumand calcium levels.Physicalassessmentwill include assessingforsignsofhypokalernia and hypocalcernia (seeChapter 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 ofmonitoring will depend on the stability of the patient's condi-tion. Fluids, electrolytes, colloids, or blood will be given asnecessary.

Aggressive fluid replacement will necessitate establishingand maintaining large bore IV access.The nurse is responsiblefor administering the fluids and for monitoring the patient'sresponse. The development of hypovolemic shock is of partic-ular concern in the early days of the disease, and the nursewatches 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 shouldbe performed four times a day. If severe hyperglycemia occurs,it may be treated with insulin.

Promoting Adequate NutritionThe patient will be given nothing by mouth and often has anasogastric tube in place. Good oral hygiene will be necessaryto decrease discomfort from NPO status and from the naso-gastric tube. TPN may be used during the criticaI phase of theillness 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 slowlyadvanced to-ward a regular diet. Tolerance for oral feedings is carefully as-sessedas is the possibility of the return of pain. Frequent smallmealsare 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.

Patient/Family EducationTeaching the patient and significant others will be ongoing. Atthe beginning of hospitalization, the patient and significantothers 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 ofthe 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 needto be repeated. Support and continuity of care also need to beprovided to help decrease anxiety. Education will be directedtoward preventing future attacks and maintaining a nutritiousdiet. The patient must know that any recurrence of signs andsymptoms should be reported immediately. Follow-up caremust be explained in detail.

Health Promotion/PreventionIf unhealthy lifestylepatterns such as alcoholism are a cause ofacute pancreatitis, the nurse must work with the patient onthe problems. This care will not be instituted until the pa-tient's condition is stabilized, but it must be introduced beforethe 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 willbe important to stress the importance of treatrnent for gall-stones.The episode of pancreatitis is frightening and could makethe patient reluctant to undergo any further medical or surgicaltreatrnent. The nurse will reinforce the etiological role of biliarydisease in the development of pancreatitis and encourage thepatient to followthrough on recommended treatrnent.

• EVALUATIONTo evaluate the effectiveness of nursing interventions, com-pare patient behaviors with those stated in the expected pa-tient outcomes. Successful achievement of patient outcomesfor 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 andshows 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 CONSIDERATIONSBiliary disease becomes increasingly common as people age,and biliary disease-related pancreatitis is most likely to occurin the elderly patient. The severity of the disease is difficult to


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 relatedto their disease-enforced immobility as well as to the pancre-atitis. Respiratory complications are of particular concem,and the elderly patient needs frequent respiratory assessmentand aggressive pulmonary hygiene during the acute stage ofthe disease.

Infection is a common complication of pancreatitis (seediscussion under Complications), and elderly patients are lessable to withstand the stress imposed on the body by sepsis.The same is true for the development of hypovolemia andfluid shifts. These factors strain the cardiovascular system andmay overwhelm the elderly patient's ability to adapt andrespondo

SPECIAL ENVIRONMENTS FOR CARECriticai Care Management

Although most patients with pancreatitis recover without anyresidual dysfunction, a minority experience life-threateningdisease. These patients will be managed in a criticaI care unit.The nurse's major roles are collaborative with the physicianand 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 patientsmay also need cardiac support with drugs such as dopa-mine. A pulmonary artery catheter may be inserted to assessperfusion adequacy. Left ventricular dysfunction is a com-mon problem.

The airway is compromised in several ways. Severe painlimits diaphragmatic excursion, and both shock and sepsisplace extraordinary metabolic demands on the respiratorysystem that can progress into full-blown ARDS in some pa-tients. Prompt intubation and mechanical ventilation will becrucial. Hypercoagulability increases the risk of pulmonaryembolism. Management includes supplemental oxygen, suc-tioning as needed, and aggressive chest physiotherapy. Assess-ment is conducted hourly. Respiratory failure accounts for adisproportionate number of pancreatitis-related deaths.

In addition to the concems addressed above, the criticallyill patient with pancreatitis will receive TPN to support a pós-itive nitrogen balance and may undergo peritoneal lavagethrough a peritoneal catheter. Other interventions will be di-rected at specific complications as they arise.

Home Care Management

Most patients with acute pancreatitis recover spontaneouslyand can be discharged from the hospital within 1 to 2 weeks.Patient needs for home care will be minimal if complicationsdid not develop. Normal activities are gradually resumed asstrength and activity tolerance increase.

Patients with alcoholism present a unique challenge aseven the pain and anxiety of acute pancreatitis may not be suf-ficient motivation for them to abstain from alcohol. The nursewill discuss the importance of abstinence with the patient and

make referrals to community programs for alcohol treatmentif the patient agrees. It is important to recognize, however, thatthe decision to continue drinking is a matter of personalchoice. The nurse's role is to be certain that the patient hasall of the information that he or she needs to make an in-formed decision about the future. A positive outcome cannotbe guaranteed.

COMPLlCATIONSAbout 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 belocal or systemic. The systemic complications tend to occurwithin the first week and have largely been discussed withinthe context of the fulminant disease processo These includecomplications such as hypovolemic shock, sepsis, renal failure,and ARDS. The major complications of acute pancreatitis aresummarized in Box 42-3.

Pseudocysts

Pancreatic fluid or exudate forms in up to 50% of patientswith acute pancreatitis.6 Pseudocysts are rounded collectionsof fluid enclosed in a fibrous capsule. This process occurs inonly 5% to 10% of all patients.6 Many pseudocysts resolvespontaneously over time, and intervention is not always war-ranted. However, pseudocysts can also become life threateningif they obstruct neighboring structures, rupture or hemor-

••., Major Complicatians

af Acute Pancreatitis~~~.s~~._:a;;:" .._~:,;;~=:l;t=.f'",.......,;.

CARDIOVASCULARHypotension/shock from hypovolemia or hypo-albuminemia

HEMATOLOGICALLeukocytosis from generalized inflammation or sec-ondary infections, anemia from blood loss, dissemi-nated intravascular coagulation (OIC) from unknowncauses

RESPlRATORYAtelectasis, pneumonia, pleural effusion, adult respira-tory distress syndrome (AROS)

GASTROINTESTINALGI bleeding

PANCREATICPancreatic pseudocysts, pancreatic necrosis or phleg-mon, pancreatic abscesses, pancreatic ascites

RENALOliguria and acute tubular necrosis

METABOLICHyperglycemia, hypocalcemia, hyperlipidemia


rhage, or become infected. A "wait and see" policy is generallyfollowed, and the cysts are monitored regularly. Inflammatoryexudate from the pancreas may form into an inflamed mass,which is called a phlegmon. Intervention is again not indicatedunless bleeding or infection develops. As with pseudocyststhe pWegmon may be drained, surgically debrided, or resectedas 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 ofpancreatitis and has a 100% mortality rate if untreated.2 In-fection usually develops in the are as of necrosis created byfulminant disease. The initial diagnosis of infection can becomplicated by the fact that acute pancreatitis itself manifestswith the common symptoms of inflammation and infection.Infection-related fever, however, typically exceeds 39° C, andthe patient's clinical condition deteriorates.

CT scanning allows for the accurate identification of areasaf necrosis, which can then be aspirated by CT-guided needleaspiration. Gram stain and culture can then identify the spe-cific organisms responsible for the infection. Broad-spectrumantibiotics 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 penetratethe 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 aspossible and then place multiple large-bore sump drains inthe operative areas to remove infected material.2 Continuoussaline infusion and suction were needed to maintain tube pa-tency. Many surgeons now recommend an open method inwhich the resected are as are packed, and the dressings arechanged under anesthesia every 2 to 3 days until granulationis well underway. The abdomen is left open and eventuallydoses over an absorbable mesh barrier. A feeding tube isplaced once granulation is underway. The development of fis-tulae can complicate the healing processo

Chronic PancreatitísPatients with alcohol-induced acute pancreatitis are believedto already have asymptomatic chronic disease when they ex-perience their first acute episode. If the patient continues todrink, the likelihood of recurrence is extremely high. Chronicpancreatitis is discussed below.

CHRONIC PANCREATITISEtiology/EpídemiologyChronic pancreatitis is present when recurrent bouts of in-flammation lead to progressive injury and scarring of pan-

creatic tissue with gradual fibrous replacement of the normaltissue.21·23The progressive degeneration of the gland makeschronic pancreatitis a separate disorder from recurrent acutepancreatitis in which pancreatic function essentially returnsto normal when the inflammation subsides.'·23 Chronic pan-creatitis occurs almost exclusively in alcaholics and is morecommon 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 diseaseremains the primary causative facto r in acute recurrentpancreatitis.

PathophysiologyThe basic pathological change of chronic pancreatitis is de-struction of the exocrine parenchyma and replacement withfibrous tissue. This process is associated with varying de-grees of duct dilatation. Scarring and fibrotic changes mayoccur throughout the pancreas or be limited to selectedareas. Calcium salts may be deposited in both the ducts andthe parenchyma, usually in areas of fat necrosis. Ductal ob-struction occurs secondarily. The factors that influence thesolubility 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 anddestroyed.

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 alcoholto have such detrirnental effects. The pathological nature ofthe alcohol-induced injury is believed to be similar to thatoccurring in acute pancreatitis. In addition there is evidenceof small protein plugs in the acinar ductules. Secretions aremore 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 havesigns 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 andconstant 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 whereacute pancreatitis leaves off and chronic disease begins. Theo-retically the dense fibrosis can entrap and alter the pancreaticnerves, affecting both sensory and motor functions.1 It is pos-sible that much of the pain is eventually related to this nerveentrapment, although the pain is not different in nature orseverity from that which accompanies acute pancreatitis.' It isfrequently worsened by eating and needs narcotic administra-tion for control.

Pancreatic insufficiency begins once 80% of the pancreatictissue is destroyed. Symptoms include diarrhea, which is


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. Malabsorptionleads to clinicai deficiency in vitamins E and B12 and otherfat-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 eduring recurrent attacks, and both fasting and postprandialhyperglycemia are usually present. Stool examination canquantify 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 ManagementEffective management of abdominal pain is the greatest chal-lenge with chronic pancreatitis. Patients who continue todrink alcohol will continue to have pain, and even abstinenceis eventually no guarantee of relief. Patients can usually adaptto the malabsorption and steatorrhea, but the persistent painmay 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 likeacute disease. Bowel rest is maintained, and attention is paidto managing the acute pain. Ongoing care involves the use ofa low-fat diet and supplemental pancreatic enzymes. Theseextraets will increase the patient's body weight and improveabsorption, 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 researchtrials. Fat-soluble vitamin replacement may also be indicated,and the management of diabetes often requires the use ofinsulin.

Chronic pancreatitis affects the small ducts of the pancreasand 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 beperformed 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 searchfor eomfort. Concerns about drug dependenee must not beallowed to prevent the patient from receiving adequate andnecessary 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 ofchronic pancreatitis as appropriate retribution for the pa-tient's addiction. This attitude can seriously eompromisethe patient's care.

In some instances the patient has had negative experienceswith pain management during previous hospitalizations for

exacerbations and thus believes that analgesics are not beinggiven because the health team does not care about him or her.The involvement of a pain management team is desirable ifsuch 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 ofchronic pancreatitis is unequivocal, and yet many alcoholicsfind themselves unable or unwilling to abstain from alcoholuse. The nurse consults with a substance abuse specialist todevelop 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 andfuture. Information coneerning community resources for al-cohol treatment should be current and accurate and offered tothe patient. The involvement of the family is encouraged if thedynamics are supportive.

Family members and health care workers need to be helpedto understand and accept that ultimately it is the patient'sright to make fundamental decisions about his or her owncare, 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 dietand use pancreatic enzyme replacement effectively to controldiarrhea and maintain a stable weight. Timing of the med-ications is critica!. The nurse teaches the patient to take theeapsules 1 to 2 hours before, during, or after meals. Powderscan be mixed directly with food. Patients are informed thatthese products frequently produce a bad taste and may alterthe taste of foods. The patient is instructed to monitor thebody's response to the supplements and consistently trackweight 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 ofvitamin supplements is encouraged if recommended by thephysician.

Patients who continue to drink alcohol will always bejust one step away from their next flare-up or complication.The nurse provides the patient with written material thatoutlines the symptoms of complications and encourages thepatient to adhere to the plan for continued follow up. ANursing Care Plan for the patient with chronic pancreatitisis found on p. 1389.

CANCER OF THE PANCREASEtiology/EpidemiologyCancer of the panereas may arise from any of the elements ofthe pancreas, although most involve the ductal epithelium andare adenocarcinomas. Both benign and malignant tumors canalso arise from the islet cells but these are rare.1S Tumors of theislet cells usually retain some endocrine functions and tend tohave a better prognosis than adenoeareinomas.

Pancreatic cancer usually occurs in persons older than50 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

DATA Mr. 1. is a 52-year-old self-employed accountant with a12-year history of acknowledged alcoholism. He experienced hisfirst attack of acute pancreatitis 4 years ago and chronic pancre-atitis has since been diagnosed. He is admitted now with anotherflare-up of the disease.

Mr. 1. has made several efforts to stop drinking and has evenundergone inpatient alcohol treatment. His longest period of so-briety has been about 6 months. Some life stressor has always pre-cipitated his descent into alcohol dependency. His wife accompa-nies him to the hospital but is quick to say"I don't think that I cantake much more of this. He's killing himself and nothing I say ordo is changing that. I don't think I can stay around any longerwatching him die. It hurts toa much."

Mr. T.'s admission assessment shows a thin, poorly nourishedman who appears older than his stated age. He reports the pres-ence of:• Acute abdominal pain that is generally localized in the mid-

epigastric region and radiates to the back. He rates the pain asan 8 on a 10-point scale in severity.

• Steady and protracted vomiting that began late yesterday af-ternoon. He has had nothing to eat or drink for more than12 hours.Large, 50ft, and foul-smelling stools that have been increasingin frequency and severity over the last few weeks. He has lost12 pounds.

• A history of decreased alcohol use over the last 3 months. Mr. Tsays "I know no one will believe me but I've really been drink-

• • • Person with Chronic Pancreatitis

ing much less. The pain starts so quickly when I drink that [have really been steadily decreasing my intake. I don't under-stand why this should happen now. What's the use? The doctorsaid the pain would stop if I stopped drinking so much and lookat me now. Maybe I should just drink myself to death and get itover with."Other data on admission include:

• Blood pressure is 94/60, pulse is 92, and respirations are 22 andshallow. Temperature is 99.8° F.

• Bloodwork shows the following abnormalities: hemoglobin of10.2 g, red blood cell count of 2.9 million, K+ of 3.0 mg/dl,serum calcium of 8.2 mg/dl, and glucose of 162 mg/dl.[nitial care orders include:

• IV of 1000ml of 5% dextrose in li, N saline with 20 mEq of KCIat 125 rnlIhr

• NPO• Monitor intake and output, daily weight, and abdominal girth

once daily• Demeroll00 mg IM q 3 hr PRN for pain• Insert NG tube and attach to low intermittent suction if vomit-

ing persists past 4 PM

• Accucheck 4 times daily per protocol, cal! house officer if glu-cose> 160

• Monitor c10selyfor hypovolemic shock, e1ectrolyte imbalance,delirium tremens (DTs)

• Call substance abuse resource counselor for DT protocol initia-tion if needed

IIjIII

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

States pain is effectively controlledwith 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 asneeded.

a. Encourage patient to use anal-gesics on a regular rather thanPRN basis.

b. Validate your acceptance ofthereality ofthe patient's pain andits severity.

c. Evaluate effectiveness of thenarcotic order. Collaborate withphysician to make adjustmentsin dose or drug as needed.

3. Collaborate with Mr. T to determinethe nonpharmacological methodsthat help to reduce his pain.a. Position him in a mid to high

Fowler's position with his kneesflexed.

b. Explore his experience withstrategies such as distraction,massage, relaxation, and guidedimagery.

1. Frequent assessment is essential tovalidate the nature and severity ofthe patient's pain experience.a. Recording on a flow sheet allows

for a pattem of pain to be estab-lished and the effectiveness ofpain control to be evaluated.

2. Synthetic narcotics are effectiveanalgesics and do not cause spasmin the sphincter of Oddi.a. A regular time schedule of drug

use allows for a steady bloodlevei to be established.

b. Patients with chronic pancreatitisare frequently labeled "drugseekers" by staff.

c. Acute pain can be immobilizing.Morphine may be substitutedfor meperidine.

3. Nonpharmacological methodsallow 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 effectivemethods of pain control, but thepatient must have an open mindand be willing to experimentwith new strategies.

Continued

-1390 unit viii Alterations in Digestion and Elimination

Person with Chronic Pancreatitis-cont'dNURSING DIAGNOSIS Risk for f1uid volume deficit related to vomiting, NPO status, hyperglycemia, andincreased capillary permeability

Maintains balance of fluids and elec-trolytes; intake and output are bal-anced; weight is stable.

1. Assess fluid and electrolyte statuseach 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 insulinper protocol.

3. Monitor for hypokalemia andhypocalcemia:

muscle weakness, crampingnumbness and tingling in finger-tips or around mouth; positiveChvostek's and Trousseau's sign

1. Patient is at risk for hypovolemicshock and dehydration. May lose4 to 14 L of fluid into the abdomen.Fluid replacement is based on esti-mates of losses. A urine output of30 to 50 ml/hr is essential to pre-vent the onset of acute tubularnecrosis.Fluid and gas accumulation in GItract can result in significant ab-dominal distention.

2. Destruction of the beta cells andislets of Langerhans produces se-vere hyperglycemia. Because ofthe risk of labile hypoglycemia, in-sulin is not given unless glucoselevei continues to rise.

3. Large amounts of potassium arelost through vomiting and in thepancreatic secretions; calcium isbelieved to bind with free fats andcan drop to leveis that increaseneural excitability.

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

Receives sufficient nutrients by mouth 1. Maintain NPO status and bed rest 1.or TPN to maintain stable body until patient's condition stabilizes.weight, keeps albumin leveis above3.8 g/dl, and produces normal stools.

2. Assess current nutritional and elimi- 2.nation status.

3. Monitor daily weight and serum 3.protein and albumin leveis.

4. initiate TPN if NPO status needs to 4.be protracted.

5. Reinitiate oral feedings once ab- 5.dominai pain is controlled and amy-lase/lipase leveis stabilize.

6. Offer small, frequent feedings to thepatient's tolerance; assess patientresponse.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.

NPO status is theorized to reducethe secretion of pancreatic en-zymes. Bed rest decreases thebody's metabolic rate.Patients with chronic pancreatitisare often malnourished before theattack from alcoholism and malab-sorption.These parameters provide the bestongoing data about nutritionalstatus.If pain is not controlled promptly therapid catabolism of the disease mustbe counteracted by TPN to preventlife-threatening complications.Once pain and enzyme leveis arestable there is no contraindicationto oral feeding, and the severityof malabsorption needs to be es-tablished.

6. This feeding pattem minimizesdistention and malabsorptionsymptoms.a. Malabsorption primarily affects

digestion of fats.7. Malabsorption manifests itself as

large-volume, greasy, foul-smellingstools. Adequate enzyme replace-ment will restore the stool to nearnormal.

Continueo


,íJ; Person wíth Chroníc Pancreatítís-cont'd

NURSING DIAGNOSIS Risk for ineffective management of therapeutic regimen related to inability to abstainfrom alcohol and inadequate knowledge of management of malabsorption and hyperglycemia

•• 01 •

Verbalizes understandíng of diseaseprocess, role of alcohol, and pharma-cological management of symptoms.

Makes commitment to abstain fromalcohol.

1. Assess patient's current under-standing of the disease process andthe 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 duringfirst 48 to 72 hours. Consult withsubstance abuse specialist ifneeded.

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 andplanned management of diabetes.a. Teach symptoms to report:

Hyperglycemia: frequent urina-tion, thirst, lethargy, abdominalcramping

• Hypoglycemia: anxiety, tachy-cardia, diaphoresis

6. Encourage patient to make commit-ment to changing his lifestyle andgaining control of his disease andhis life.

1. This establishes a baseline forplanning and intervention.

2. Patient has stated his attempts todecrease alcohol use. Wife hasstated the end of her tolerance forhis continued use 01 alcohol.

3. Patient may not be truthful aboutcurrent levei of use. Withdrawalcarries a high mortality in acutelyill patients and necessitates spe-cialty asisstance ..

4. Malabsorption is permanent, andpatient will develop serious nutri-ent deficiencies if enzymes are notadequately replaced. Dosage ad-justments can be safely made by awell-informed patient.

5. Insulin may be needed to controlthe diabetes of chronic pancreati-tis, but hypoglycemia must be pre-vented. Patient will remain hyper-glycemic but must know how torecognize ketoacidosis.

6. Patients with chronic pancreatitisoften have given up hope on them-selves and their ability to inlluencethe future.

research ~Reference:PriceTF,PayneRL,OberletinerMG: Familialpancreaticcancer 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 natureand used a questionnaire to explore cancer incidence and risklactors. 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 samplesixty-five percent reported Cajun ancestry. They reported a to-tal of 366 first-degree reiatives of whom 44 had also developed

the presence of long-standing diabetes, especia1ly in women.Incidences of familial c1ustering of cases point to a hereditarycomponent (Research Box). A link with chronic pancreatitishas been suggested but remains unproven.

Pathophysiology

Pancreatic cancers usually deve10p in the head of the glandand vary dramatically in size at the time of diagnosis. The

pancreatic cancer. This represented an incidence rate larabove national norms where pancreatic cancer accounts foronly 2% of ali new cancer diagnoses. The sample incidencerate was comparable to that of lung cancer. African Ameri-cans had the highest incidence (32 per 100,000 versus 17 per100,000 nationwide). The incidence rate was also signifi-cantly increased for whites (18 per 100,000 versus 10 per100,000 nationwide). Heavy prolonged cigarette smokingwas shown to be a clear risk facto r, which has been true inali samples. Although flawed by sampling difficulties, thestudy does appear to confirm the presence of a significantfamilial risk for pancreatic cancer in this unique population.

tumor is usually deeply encased in normal tissue and is poor1ydemarcated. The common duct is often obstructed and dis-tended by the presence of the tumor. Metastasis has almostalways occurred before the tumor produces its first symp-toms beca use there is no capsule surrounding the pancreasto prevent the growth and spread of the tumor. Direct ex-tension of the lesion may cause its spread to the posteriorwall of the stomach, the duodenal wall, the colon, and the


figo 42-6 Pancreatoduodenectomy (Whipple's proce-dure) vvith anastomosis.

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. Thepain is relentlessly progressive in nature. Weight loss fre-quently accompanies the pain and can be dramatic. Anorexiais also common. ]aundice and pruritis will typically developwhen bile duet obstruetion oecurs. Diarrhea and/or steator-rhea develop fairly late in the disease. Diabetes may aIsodevelop.


The diagnosis of pancreatic eancer is often first ma de based onthe pattem of symptoms and then is confirmed throughCT scanning. Guided needJe biopsy may be performed atthe 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 notbeen proven to improve survival. Obstruction is a commonproblem with large tumors involving the pancreatie head, andsurgi cal bypass is frequently attempted. Procedures includegastrojejunostomy to bypass the duodenurn and choledocho-jejunostomy to relieve biliary obstruction. Endoseopic place-ment of stent tubes to support biliary drainage is increasinglyconsidered as an altemative to surgery. Stents may be placedinternally or inserted for externaI drainage.

Surgeons who are attempting curative procedures may usethe more aggressive Whipple proeedure or total pancreatec-tomy (Figure 42-6). Neither radiotherapy nor ehemotherapy

guide'ines ~or carEThe 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 routineblood studies.

Se alert to signs of bleeding or shock.Maintain urine output at 30 to 50 ml/hr.

Initiate pulmonary hygiene every hour with deepbreathing, coughing as needed, and use of incentivespirometry.

Establish effective pain management regimen. Monitorevery hour.

Monitor dressings and drainage tubes. Keep skin clearof drainage.

Maintain nutritional support with TPN.Initiate oral feedings with clear Iiquids. Advance astolerated.

Monitor blood glucose and administer insulin as or-dered.

Monitor patient's weight and the development ofsteatorrhea.Administer pancreatic enzyme replacement asordered.

Assess for signs of dumping syndrome (seeChapter 40).

Provide support for patient and family and initiate dis-charge planning.

Patient/farnily education

Pain management is an ongoing chaIlenge with panereaticancer and is often the primary determinant of quality of liftThe nurse serves as the patient's advoeate in the health carsystem to establish an effective pain management protoecand continuously adapt it to changes in the patient's condition. The nurse provides careful teaching about the use of narcotic anaIgesics and the inevitable development of tolerancand physicaI dependence (see Chapter 12). Instruetion is alslprovided about expeeted side effeets and their managemen1Other general measures are those provided to any patient witlÍDvasive eaneer (see Chapter 11). Nursing care of the patienundergoing pancreatie surgery is summarized in the Guidelines for Care Box.

aIone has had any positive effeets on the course of the diseaSIbut combination protocols used in research trials appear textend life e>""Pectancyto nearly 1 year.

Stomoch

Jejunum /

Cystic duct

Gollblodder

Management of Persons vvith Problems of the Gallbladder and Exocrine Pancreas chapter42 1393

References1. Ambrose MS, Dreher HM: Pancreatitis-managing a flareup, Nurs-

ing 26(4):33-39,1996.2. Baker CC, Huynh T: Acute pancreatitis-surgical management, Crit

Care Clin 11(2):311-322, 1995.3. Domingues-Munoz JE, Malfertheiner P: Management of severe

acute pancreatitis, Gastroenterologist 4:248-253,1993.4. Everhart JE: Contributions of obesity and weight loss to gallstone

disease, Ann Intern Med 119(10): 1029-1035, 1993.5. Fenster LF, Lonborg R, Thirlby RC, Traverso LW: What symptoms

does cholecystectomy cure? Am J Surg 169(5): 533-538, 1995.6. Forsmark CE, Toskes PP: Acute pancreatitis':-medical management,

Crit Care Clin 11(2):295-306, 1995.7. Gauwitz DF: Endoscopic cholecystectomy: The patient friendly ai-

ternative, Nursing 20(12):58-59,1992.8. Ghiloni BW: Cholelithiasis: current treatment options, Am Fam

Physician 48(5):762-768, 1993.9. Greifzo S, Dest V: When the diagnosis is pancreatic cancer, RN

54(3):38-41,1991.10. Kohn CL, Brozenec S, Foster PF: Nutritional support for the patient

with pancreatobiliary disease, Crit Care Nurs Clin North Am 5(1):37-45,1993.

11. Krumberger 1M: Acute pancreatitis, Crit Care Nurs Clin North Am5(1):185-201,1993.

12. Marshall JB: Acute pancreatitis: a review with an emphasis on newdevelopments, Arch Intern Med 153(6):1185-1193, 1993.

13. McClave SA, Greene LM, Snider HL: Comparison of the safety ofearly enteral vs. parenteral nutrition in mild acute pancreatitis,J Parenter Enteral Nutr 21(1): 14-20, 1997.

14. McConnell E, Lewis LW: Managing the patient with pancreatitis,Nursing 21(11):98-102,1991.

15. Murr MM et al: Pancreatic cancer, CA: Cancer J Clin 44(2):304-314,1994.

16. National [nstitutes of Health: National [nstitutes of Health Consen-sus Development Conference Statement on Gallstones and Laparo-scopic Cholecystectomy, Am J Surg 165(4): 390-398, [993.

17. Ondrusek RS: Cholecystectomy: an update, RN 56(1):28-31,1993.18. Peterson KJ, Solie CJ: [nterpreting lab values in pancreatitis, Am

J Nurs 94(1l):45A-B, 56F, 1994.19. Price P, Hartranft TH: New trends in the treatment of calculus dis-

ease of the biliary tract, J Am Board Fam Pract 8(1 ):22-28, 1995.20. Price TF, Payne RL, Oberleitner MG: Familial pancreatic cancer in

South Louisiana, Cancer Nurs 19(4):272-282, 1996.21. Sidhu SS, Tandon RK: The pathogenesis of chronic pancreatitis,

Postgrad Med 71(2):67-70,1995.22. Smith A: When the pancreas fails, Am J Nurs 91(9):38-48, 1991.23. Spiro HM: Clinicai Gastroenterology, ed 4, New York, 1993, McGraw

Hill.24. Thompson C: Managing acute pancreatitis, RN 55(3):52-54,1992.

• Malabsorption is treated with the use of pancreatic enzymesupplements. Pain management is extremely difficult if thepatient continues to drink alcohol.

• Cancer of the pancreas is insidious and has a very poorprognosis. In rare instances a pancreatoduodenectomymay be performed.

•

PRIMARY SClEROSING CHOLANGITIS• Primary sclerosing cholangitis is usually idiopathic in etiol-

ogy but frequently occurs in conjunction with IBD. There isno treatment, and most patients eventually require livertransplant.

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 byNPO status, and collaborative monitoring for complications.

• Chronic pancreatitis is progressive and usually results fromalcoholism. It is not reversible.

• Chronic pancreatitis results in pain, malabsorption andsteatorrhea and possibly diabetes mellitus.

• Abstinence from alcohol use is the primary treatment ob-jective in patients with chronic pancreatitis.

CARCINOMA OF THE BILlARY SYSTEM• Carcinoma of the biliary system is insidious and can be

asymptomatic until late in the disease.

1 Mrs. Blue has a T-tube present after an abdominalcholecystectomy. What may normally occur after theremova I of her T-tube? What complication should thenurse be alert for? Why? How should he or sherespond?

2 In what ways would your assessment findings for aperson with chronic pancreatitis differ from those fora person with acute pancreatitis?

3 Mr. Ryan 77, is being treated for acute pancreatitis re-lated to biliary obstruction. What aspect of this typeof pancreatitis differs from acute alcohol-inducedpancreatitis?

CHOlE L1THIASIS/CHOlECYSTITIS/CHOlEDOCHOllTHIASIS11 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 thetreatment 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 opencholecystectomy include ineffective breathing pattern,pain, and management of the T-tube.

management pancreas and gallbladder

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