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

I

alternatives for biliary tract disease.

3

Describe the nursing care needs of patients with disorders of the biliary system"

4

List the causes of acute and chronic pancreatitis.

5 Explain the pathophysiological and pancreatic tumors. 6 Discuss management 7

basis for signs and symptoms

approaches

of acute and chronic pancreatitis

for acute and chronic pancreatitis.

Develop nursing diagnoses, patient outcomes, and plans of interventions for patients who have acute or chronic pancreatitis or cancer of the pancreas or who have had pancreatic surgery.

PROBLEMS OF THE GALLBLAOOER The biliary system is affected by stones and obstruction, inflammation and infection, and cancer. Gallbladder disorders are extremely common and affect millions of adults every year. CHOLELlTHIASIS/CHOLECYSTITISI CHOLEOOCHOLITHIASIS Etiology Gallstones can occur anywhere

in the biliary tree. The term in the gallbladder and represents the most common biliary disorder. Either acute or chronic inflarnrnation, termed cholecystitis, can result, usually precipitated by the presence of stones. When stones form in or migrate to the common bile duct the condition is termed choledocholithiasis. Figure 42-1 illustrates common sites for gallstones. Eighty percent of gallstones are composed of cholestereI. 19The remaining 20% are pigmented stones, which are further classified as black or brown.'9 Although the precise etiology of gallstones is unknown, the basic component of supersaturation of the bile v,ith êholesterol is widely accepted. Because most healthy individuals experience supersaturation of the bile at various times without developing gallstones, it is clear that other factors are operational as well. Risk factors for gallstones have been well identified and include various clinical states associated with changes in cholesterol formation and excretion (Research Box). The risk factors for cholesterol gallstones are listed in the Risk Factors Box on the next page. The development of pigmented stones is linked to disease states such as cirrhosis, hemolytic disease, and chronic small bowel disease.19

cholelithiasis refers to stone formation

Epidemiology Cholelithiasis is a common health problem in the United States. Stones affect about 10% of men and 15% of women older than 55 years of age. An estimated 20 to 25 million adults have gallstones, and 1 million new cases are diagnosed annually.'9 Many, if not most, patients are asymptomatic, and it is theorized that a large number of cases remain undiagnosed. Ten percent of persons with gallstones develop symptoms within 5 years of diagnosis, and greater than 500,000 surgical procedures are performed each year at an annual treatment cost in excess of five billion dollars.16 These figures make cholelithiasis and its associated disorders the most common and costly digestive disease. Cholelithiasis is two times more

research'~i, Relerence: Everhart JE: Contributions 01 obesity and weight loss to gallstone disease, Ann Intern Med 119(10):1029-1035,1993.

Obesity and the process of rapid weight loss are typically identified as significant risk factors for the development of gallstone disease. This study involved a data review of studies related to the prevalence of gallstone disease from 1966 to 1992. The data showed that obesity was a strong risk factor for gallstones in women, particularly during periods of rapid weight loss. Between 10% and 25% of obese persons will develop gallstones within a few months of beginning a very low-calorie diet, with perhaps one third of the total becoming symptomatic. The risk is less strong in men and most strong in persons with the highest body mass index and most rapid weight 1055. Treatment with ursodeoxycholic acid (ursodiol) during weight 1055 effectively prevented the development of stones. The effect of various diets on the incidence of stone formation was not explored.

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common in women, occurs most frequently in midclle-aged and older persons, and affects American Indians, Mexican Americans, and whites more frequently than African Americans and Asians, although the incidence in Asians is increasing. Pathophysiology Bile is primarily composed of water plus conjugated bilirubin, organic and inorganic ions, smali amounts of proteins, and three lipids-bile salts, lecithin, and cholesterol. When the balance of these three lipids remains intact, cholesterol is held in solution. If the balance is upset, cholesterol can begin to precipitate. Cholesterol gallstone formation is enhanced by the production of a mucin glycoprotein, which traps cholesterol particles. Supersaturation of the bile with cholesterol also impairs gallbladder motility and contributes to stasis. Cholesterol stones are hard, white or yellow-brown in color, radiolucent, and can be quite large (up to 4 cm). The stones most frequently occur in multipIes but can be solitary. The process of stone formation is sIow. Stones are theorized to grow steadily for 2 to 3 years and then stabilize in size.

Small bile duct

Eighty-five percent of ali stones are Iess than 2 cm in diameter. Most are found in the galibIadder, but it is estimated that 15% to 60% of persons oIder than age 60 who undergo surgery for galistones also have stones in the common bile duct.8 Black pigmented stones form as the result of an increase in unconjugated bilirubin and calcium with a corresponding decrease in bile salts. GalibIadder motility may also be impaired. Brown stones develop in the intra- and extrahepatic ducts and are usualiy preceded by bacterial invasion. Although most persons with gallstones are asymptomatic, choIecystitis can develop at any time, usualiy from a blockage of the cystic duct by the stone or from edema and spasm initiated by the presence or passage of the stone. In acute cholecystitis the galibladder is enIarged and tense. A secondary bacterial infection can occur within several days and is the cause of most of the serious consequences of the disease. Classic clinicaI manifestations of symptomatic galistones include pain in the right upper quadrant (RUQ) of the abdomen, which is described as severe and steady. The pain frequently radiates to the right scapula or shoulder, has a sudden onset, and persists for about 1 to 3 hours.8 It may awaken the patient at night or be associated with the consumption of a large or highfat meal. Some patients experience nausea and vomiting and may be febrile. Chills and fever are more likely with acute choIecystitis. Patients are rareIy jaundiced. Bowel sounds may be absento Palpation of the RUQ causes a severe increase in pain and temporary inspiratory arrest (Murphy's sign). The episode of choIecystitis usualiy subsides in 1 to 4 days. Clinical manifestations of choIecystitis are summarized in Box 42-1. The diagnosis of galistones is fairIy straightforward when the classic symptoms are present. The diagnosis is more difficult when the symptoms are milder or reflect simply general dyspepsia. It is estimated that up to 25% of patients with irritable bowel syndrome or peptic ulcer disease also have galistones, and the exact etiology of the patient's symptoms needs to be determined if possible.8 Researchers theorize that many patients with "poor outcomes" after gallbladder surgery may actualiy reflect situations where the gallbladder was not really the source of the patient's dyspepsia.8•19

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

" .. ÇJl1S

i Cholecystitis figo

42-1

Common

sites

of gallstones.

risk'act rs Cholesterol

Gallstones

Obesity Middle age Pregnancy, multiparity, and the use of oral contraceptives Rapid weight loss (-5 pounds/wkl Hypercholesterolem ia, use of anticholesterol medications Diseases of the ileum Gender (approximately twice as common in women)

Sudden onset pain in the RUO of the abdomen Severe and steady in quality Frequently radiates to the right scapula or shoulder Persists for about 1 to 3 hours May awaken the patient at night May be associated with consumption of a large or fatty meal , Anorexia, nausea, and possibly vomiting Mild to moderate fever Decreased or absent bowel sounds Acute abdominal enderness and a positive Murphy's sign Elevated white blood cell count, slightly elevated serum bilirubin and ai a 'ne phosphatase leveis

=

e Gallbladder

- - 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 not see' help unril jaundice or other complications develop. Figure 42-2 shows the relationship between stone formation and associated outcomes in uncomplicated gallbladder disease. Collaborative

Diagnostic

Care Management

tests

Ultrasonography is the primary diagnostic tool for identifying cholelithiasis. If the results of ultrasonography are inconclusive, oral cholecystography may be performed (Figure 42-3). Laboratory tests include white blood cell count, serum bilirubin, alkaline phosphatases, and liver function. Any additional diagnostic testing is performed to rule out other causes of gastrointestinal (GI) discomfort.

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Treatments

Extracorporeal shock wave lithotripsy was pioneered in Germany and adapted to the treatment of gallstones. Lithotripsy uses shock waves to disintegrate the stones. Extensive selection criteria limit the use of this treatment to a small number of patients with gallstones.19 Patients must also undergo oral dissolution therapy after treatment to dissolve the stone fragments. Recurrence is a problem, and the treatment, including follow-up drug therapy, is tive times more expensive than surgery. It is rarely a cost-effective option.8 Percutaneous drainage may be used as a primary treatment for patients .with acute cholecystitis or to relieve inflammation and infection before surgery. The drainage tube is placed percutaneously using sonographic guidance. An operating scope may be introduced by dilating the tract to remove a stone. The procedure has good short-term results, but since the gallbladder remains intact, recurrence rates run as high as 50%.19 Surgical management

Medications

Oral dissolution therapy with ursodeoxycholic acid (Actigall) may be prescribed for patients who are poor surgical risks or who refuse surgery. The drug gradually desaturates the bile, which allows space for the reuptake of the cholesterol in the stones. The treatment is only effective when stones are less than 1.5 to 2 cm in diameter. A full course of treatment takes from 1 to 3 years and is extremely expensive. Up to 50% of patients experience recurrences within 5 years.19 Direct dissolution therapy with methyl-tert-butyl ether is occasionally used in high-risk surgical patients. The drug is instilled through a percutaneous catheter, which is monitored fluoroscopically. Multiple drug instillations are required over 12 to 24 hours, which makes the treatment labor intensive for the physician and extremely expensive.

Cholecystectomy was first performed in Berlin in 1882 and evolved into a procedure with excellent effectiveness and extremely low associated morbidity and mortality. lt is the

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

CholedodTOlithiasis

I Asymptomatic.1

figo 42-2 The development cystitis.

of uncomplicated

chole-

figo 42-3 (arrollVs)

Oral cholecystogram. Radiolucencies are caused by gallstones.

I II

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second most common surgical procedure performed in the United States following cesarean section and serves as the standard against which other gallstone treatments are measured.8 The main advantage of cholecystectomy is the fact that it stops the disease. The recurrence rate is zero. The main disadvantage has always been that it is major abdominal surgery with a11of the associated pain and disability. Hospital stays averaged 3 to 7 days and recovery required 4 to 6 weeks. Laparoscopic cholecystectomy was first performed in France in 1987and in the United States in 1988,and by the early 1990s had revolutionized the care of patients with gallbladder disease.16 Laparoscopic cholecystectomy offers several real advantages over traditional surgery. It is less invasive,which allows a shorter healing and recuperation time; there is less scarring; and, most important1y, the pain associated with the

follow a low-fat diet and eat sma11meals until definitive therapy is completed. After treatment they can resume a normal diet. Activity

There are no activity restrictions for persons with cholelithiasis, cholecystitis, or choledocholithiasis. Referrals

Referrals would not general1ybe required for the management of uncomplicated gallstones unless a serious comorbid condition necessitated the involvement of additional professionals.

proceáure ís sígnífjcantIy reduced. The hospital stay is less than

NURSING MANAGEMENT

24 hours, and patients can return to normal activities in 2 to 3 days. It is conservative1y estimated that at least 80% of all cholecystectomies are being performed laparoscopically today, and the number continues to increase as surgical techniques improve. Acute infection is the only remaining contraindication. When the laparoscopic cholecystectomy was first introduced, the ability to explore the common bile duct was limited. This limitation necessitated the use of open cholecystectomy procedures with placement of a T-tube for drainage whenever stones were present or suspected to be present in the common bile duct. Surgical techniques have continued to improve, however, and laparoscopic approaches are now being successfully combined with endoscopic exploration and sphincterotomyto effective1ytreat patients with common bile duct stones. Laparoscopic cholecystectomy is performed under general anesthesia. The procedure consists of the creation of four 1/2-inch incisions made at the umbilicus, midJine in the epigastric region, in the right upper quadrant at the midclavicular line, and at the anterior axillary line. Three to 4 L of carbon dioxide gas are introduced to insufflate the abdomen and permit adequate visualization and the introduction of instruments. The operative field is magnified and projected on a videoscreen, and a laser or cautery is used to dissect the gallbladder. The gallbladder is deflated and removed through the umbilical incision. The CO2 is removed at the end of the procedure. lf problems develop during the procedure, it can be rapidly converted to an open cholecystectomy. The ski11of the surgeon is the primary determinant of outcomes. The slight1yhigher rate ofbile duet injury associatedwith the procedure is usual1yattributable to inexperience with the technique. Laparoscopiccholecysteetomytakes about 90minutes and is more expensivethan traditional open surgery.The short hospital stayand tremendous patient satisfactionwith the procedure, however, clearly outweigh the higher surgical costs. The mild shoulder pain that patients may experiencefor up to 1week is attributed to nerve irritation from distention and the CO2 gas,but the discomfort is easilymanaged with mild analgesics.

OF THE PATIENT UNDERGOING LAPAROSCOPIC CHOLECYSTECTOMY

Diet

No diet is known to prevent the formation of gallstones. Patients who are experiencing symptoms are encouraged to

• PREOPERATIVE

CARE

Patients will complete their preoperative preparation at home before their arrival on the day of surgery. The nurse will verify that the patient has had nothing by mouth (NPO) and completed any required bowe1 preparation. Preoperative teaching includes reviewing the scope and nature of the surgi cal procedure and the care that will be provided in the immediate postoperative period. The nurse also ensures that the patient understands that the expected pain is mild to moderate and can be successfu11ymanaged with standard analgesics. • POSTOPERATIVE

CARE

The patient will be close1ymonitored in the immediate postoperative period, and pain control will receive priority attention. A left side-lying Sims position can he1p to move the retained gas pocket of CO2 away from the diaphragm and decrease irritation. Deep breathing is encouraged. Foley catheters and nasogastric tubes are common1y inserted during the procedure and will be removed in the postanesthesia care unit. As soon as the patient is sufficient1yalert, he or she will be encouraged to sip clear fluids and get out of bed. Dressings over the small incisions are monitored for bleeding. Healthy patients with adequate home support may be discharged when they are fu11yalert and have successfu11yvoided. Patient/Family

Education

Discharge instructions are straightforward. The patient is instructed to slowly resume normal activity over the next 2 to 3 days and consume a light diet. The patient is advised to limit the intake of fatty and fried foods for the first few weeks after surgery until tolerance is established. The incisions require minimal care, and the dressings can usually be removed the next day. The patient is instructed to report the development of redness, swellin ,or discharge from any incision, as we11as the onset of feyer.pain, or tenderness in the abdomen. Heavy lifting should e a ·oided.

II Management

of Persons with

Problems

of the Gallbladder

A ClinicaI Pathway for the patient undergoing laparoscopic cholecystectomy is shown below. The Guidelines for Care Box summarizes the care provided to a patient who undergoes traditional open cholecystectomy. GERONTOLOGICAL CONSIDERATIONS Gallbladder disease is seen more frequently with advancing age but is treated in the same manner. Elderly persons may have

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more subtle symptoms and signs in the presence of cholecystitis. Thus they can develop baeterernia before they seek help. Because of the normal decrease in immune function with aging, they are at greater risk for septic shock. Elderly patients have more risks with surgery just because of their age.The laparoscopic cholecystectomy procedure is particularly effective in this agegroup as it decreases the period of immobility and recovery substantially. Wound healing needs to be carefully monitored .

.',clinicai pa1:hway . Laparoscopíc Cholecystectomy DAY OF SURGERY DAY OF ADMISSION DAY 1

Diagnostic Tests

Pancreas

Wíthout Complícatíons DAY OF DISCHARGE DAY 2

Preoperative: CSC, UA Postoperative: Hgb and Hct PAR: IVs decreased to saline lock after nausea subsides; IV analgesic, then PO

Disc saline lock; PO analgesic

Treatments

PAR: 1&0 q shift; VS q4hr x 4, then q8hr; assess bowel sounds q4hr; check drainage on bandages q2hr

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

Diet

NPO until nausea subsides, then c1ear liquids; advance to full liquids, low fat

Regular diet, low fat

Activity

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

Up ad lib, OK to shower

edications

Consultations

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

guidelines

for care

The Person Undergoing Open Cholecystectomy Preoperative Teach patient the importance of frequent deep breathing and use of incentive spirometer because the high incision and RUO pain predispose the patient to atelectasis and right lower lobe pneumonia. Explain the types of biliary drainage tubes that are anticipated, if any. Teach patient about the pain control plan to be used in the postoperative period. Postoperative Place patient in low Fowler's position; assist to change position frequently. Urge patient to deep breathe at regular intervals (every 1 to 2 hours) and to cough if secretions are present until ambulating well. Assist patient to effectively splint the incision. Encourage use of incentive spirometer. 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 believed to minimize spasms in the bile ducts, but morphine is being used with increasing frequency.

Maintain a dry, intact dressing; usually a drain is inserted near the stump of the cystic duct; some serous fluid drainage is normal initially. Encourage progressive ambulation when permitted. Increase diet gradually to regular with fat content as tolerated (appetite and fat tolerance may be diminished if there is externai biliary drainage). Biliary Drainage Connect any biliary drainage tubes to closed gravity drainage. See Figure 42-4 and the Guidelines for Care Box on p. 1378 for care of a T-tube. Attach sufficient tubing 50 the patient can move without restriction. Explain to patient the importance of avoiding kinks, clamping, or pulling of the tube. Monitor the amount and color of drainage frequently; measure and record drainage at least every shift. Report any signs of peritonitis (abdominal pain, rigidity, or fever) to the physician immediately. Monitor color of urine and stools; stools will be grayishwhite if bile is flowing out a drainage tube, but the normal color should gradually reappear as externai drainage diminishes and disappears.

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SPECIAL ENVIRONMENTS Criticai

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FOR CARE

Care Management

Critical care management would not .be anticipated for any phase of routine gallstone management. The surgical procedures have an excellent safety record and are associated with a less than 7% incidence of morbidity from any cause. Home

Care Management

Cholecystectomy is the foundation of care for gallstones, and the procedure has become essentially same-day or overnight surgery. Self-care management at home is therefore expected. Most patients have no specific home care needs beyond routine monitoring of wound healing and the progressive return to usual activities.17 For more complex procedures patients may be discharged from the hospital with a T-tube in place. Teaching concerning T-tube care is included in the Guidelines for Care Box. Elderly patients may need some additional as-

'guide'ines Managing

for care

sistance at home when they undergo same-day surgery. These needs are ideally identified and arranged before surgery. COMPLlCATIONS Transient mild diarrhea is the only adverse outcome that has been consistently linked to cholecystectomy. The most common complication of nonsurgical management of gallstone disease is recurrence, and it is clear that undiagnosed or inadequately treated gallbladder disease can result in serio and even life-threatening complications, including overwhelming sepsis and peritonitis. Chronic dyspepsia and subclinical malabsorption are often included as possible complications of cholecystectomy, but there is no concrete evidence that the reduction in the pool of bile salts and the loss of the reservoir funetion of the gallbladder increase the incidence of duodenal reflux or an alkaline shift in the gastric pH.16 Some researchers suggest that these so-called "complications" may actually reflect situations in which the patient's original digestive symptoms were never related to the gallstones and therefore were not improved by their rem oval (Research BOX).5

a T-Tube

Purpose

PRIMARY SCLEROSING CHOLANGITIS

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

Inflammation and scarring of the biliary tree occur most commonlyas a result of gallstones and bile duct infection. Parasites are a common source of chronic duct infection in Asia and developing countries. When no cause for the bile duct injury can be found, the process is called idiopathic or primary sclerosing cholangitis (PSC).

General

Etiology/Epidemiology

Care

Attach the tube to gravity drainage. Ensure that sufficient tubing is in place to prevent pulling and restriction of movement. Check drainage every 2 hours on the first day ànd at least once per shift on subsequent days. Record output carefully. Initial drainage may be as much as 500 to 1000 ml per day, but this amount should steadily decrease as healing occurs. Follow physician's order for initiating clamping of the tube. Monitor patient's response to c1amping and record incidence of distress. Unclamp the tube promptly if distress occurs. Monitor the color of the stool. Stool is initially claycolored but regains pigmentation as bile again flows into the duodenum. Keep the skin clean and protected from bile drainage as bile is extremely irritating to the skin. Teach the patient to empty the bag and convert it to a leg bag if discharge with the T-tube is planned. Provide self-care teaching: A daily shower is usually permitted. A sterile dressing should be reapplied to the T-tube entry site each day. Zinc oxide may be used to protect the skin from irritation. Redness, swelling, or drainage from the site and the development of fever should be promptly reported to the physician.

42-4 Section o' T- ube emerging from stab vvound may be placed over roll of gauze anchored to skin vvith adhesive spe to prevent its lumen from being occluded b p'essure.

figo

anagement

of Persons

vvith Problems

of the

The prevalence of PSC is unknown. Both genetic and immunological mechanisms are suspected in its development. The disease may occur alone but is generally associated with other disorders, most of which have a strong immunological component. The closest link is with inflammatory bowel disease (IBD), particularly ulcerative colitis. Of patients with PSC 70% have IBD, although PSC only occurs in 2% to 4% of all patients with IBDY The PSC may precede the diagnosis of IBD or follow it from 1 to 20 years late r. The patients are usually male, and PSC is diagnosed in early or middle adulthood, typically by the age of 45. PSC is the cause for about one third of all patients needing liver transplantation. Pathophysiology

Primary sclerosing cholangitis causes changes in and around the large bile ducts from inflammation, obstruction, and intraand extrahepatic fibrosis. Strictures can usually be found in multiple locations. These strictures are short and diffusely distributed and alternate with normal or dilated segments of the ducts to create a beadlike appearance on x-ray. It is unusual for the gallbladder or cystic duct to be involved. Liver biopsy shows the combination of inflammation, fibrosis, proliferation, and duetal obliteration that confirms the presence of the disease. The disease proceeds in stages, and by stage 4, biliary cirrhosis is present (Chapter 37), making the diagnosis complexo Many patients are asymptomatic in early stages. Others are seen with a combination of fatigue, fever, jaundice, abdominal pain, and weight loss. Persistent severe pruritis can be a particularly difficult aspect of the disease. Patients may experience recurrent attacks of cholangitis. Collaborative

Care Management

The diagnosis of PSC is not easily established and is usually made as part of a workup for cholecystitis or general nonulcer dyspepsia. PSC causes elevated liver enzymes and serum bilirubin levels, but the elevations in alkaline phosphatase are

Gallbladder

and

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Pancreas

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considered to be a hallmark feature. Endoscopic retrograde cholangiopancreatography (ERCP) (Chapter 38) is used to visualize the biliary tree. Liver biopsy helps rule out other causes of the symptoms and assists in estimating the severity of the liver damage. The prognosis of PSC largely depends on its clinicai course, which can be highly unpredictable. The aggressiveness of the disease is influenced by the number and severity of infections and the development of complications related to cirrhosis. Death is usually the result of liver failure, bleeding, or sepsis, but timely intervention with a liver transplant can significantly alter the outcomes.23 Survival is typically about 10 years. Drug therapy is aimed at reducing biliary tree infiarnmation and preventing the scarring that leads to obstruction. Steroids and other immunosuppressive agents have not been effective, but the use of ursodeoxycholic acid has shown promise even though its mechanism of action in PSC remains unknown. Surgical procedures other than transplant have been effective for diffuse disease. Endoscopic treatment to remove stones, relieve obstruction, dilate ducts, and place stent tubes is ongoing but primarily in the form of clinicai trials. Liver transplantation is the primary treatment option. Patient/fami/y

education

The uncertain nature of PSC is one of its most difticult characteristics. Patients are instructed about the disease and its possible outcomes and are prepared for the possibility of the eventual need for liver transplant. Persistent jaundice may negatively affect body image, and chronic severe pruritis can be a daily nightmare. Some patients respond to cholestyramine resin, which theoretically binds the itch-triggering elements in the bile. The nurse also suggests that the patient experiment with common interventions that may lessen itching. Possible strategies are summarized in the Guidelines for Care Box. A low-fat diet is recommended to patients who develop problems with diarrhea or steatorrhea, and the fat

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

This study attempted to evaluate the effectiveness of cholecystectomy in relieving presenting GI problems. Data were colleeted from 225 patients who underwent laparoscopic cholecystectomy. Eighty-two percent had documented gallstones before surgery, 91% experienced biliary-related pain, and 77% had both. Eighty-two percent also experienced related GI symptoms, e.g., bloating, gas, indigestion, and intolerance to fatty foods. The study results showed that documented gallstone-related pain was universally relieved by surgery, but pain was only relieved in 52% of those without documented gallstones (acalculous cholecystitis). And, although nonpain symptoms were extremely common in this population, surgery only relieved the related symptoms in approximately 44% of the patients.

guide'ines Strategies

to Control

for care

Pruritis

Avoid irritating clothing (wool or restrictive clothing). Use tepid water for bathing rather than hot. Experiment with nonirritating soaps and detergents. Pat skin dry after bathing or showering; do not rub. Apply emollient creams and lotions to dry skin regularly. Maintain a cool environment and ensure adequate amounts of humidity in the air. Avoid activities that increase body temperature or cause sweating. Experiment with treatments sueh as oatmeal baths. Keep the fingernails short and eonsider use of cotton gloves at night to minimize skin damage from seratehing. Use antipruritie medieations as ordered.

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

PROBLEMS OF THE PANCREAS ACUTE PANCREATITIS

CARCINOMA OF THE BILlARY SYSTEM Etiology/Epidemiology Primary tumors of the gallbladder are extremely rare in clinical practice, and their incidence may be declining beca use of prompt surgical intervention for gallbladder disease. The etiology is unknown. Gallbladder cancer occurs almost exclusively in persons older than 60 years of age and is twice as common in women.23 High-risk groups for gallbladder disease in general have a slightly increased risk of gallbladder canceI. Cancer can also develop in the bile ducts. This disease process also typically affects patients between 50 and 70 years of age. It demonstrates a striking link with the presence of inflammatory bowel disease. Pathophysiology

Alcoho/-re/ated

Carcinoma can occur anywhere in the biliary system. It has a very insidious onset and can metastasize by direct extension, through the lymphatics, and through the blood. Most patients have no symptoms that are referable to the gallbladder. Others have symptoms similar to those seen with cholelithiasis and cholecystitis because of obstruction and inflammation. Intermittent pain in the upper abdomen is the most common symptom. Anorexia, nausea, vomiting, weight loss, and jaundice may also be present. The patient may have a palpable abdominal mass. Signs and symptoms indica tive of metastasis to the liver or pancreas may also be present.23 By the time gallbladder cancer produces symptoms it is usually incurable. Collaborative Care Management Surgery is the primary treatrnent for cancer of the gallbladder. If the disease is diagnosed incidentally, it may be confined to the gallbladder and be curable with surgery. Cholecystectomy with wedge resection of 3 to 5 cm of normal liver plus lymph no de dissection is usually performed. Survival for those with invasive disease is usually less than 2 years. Neither radiotherapy nor chemotherapy has thus far improved patient outcomes. Treatment of bile duct cancer focuses on maintaining bile flow. Surgery may be used to divert bile flow to the jejunum, or stent tubes may be placed to attempt to maintain duct patency. When bile flow can be maintained, patients may live for several years after diagnosis. Pat:ient:/family

Etiology Acute pancreatitis occurs when obstruction of the outflow of pancreatic secretions triggers acute inflammation in the gland. The obstruction can progress to necrosis of the pancreatic exocrine and endocrine cells and can involve either the large or small pancreatic ducts or both. The two major causes of acute pancreatitis in the United States are gallbladder disease and alcohol abuse."·23 Together they account for about 80% of all cases. Acute pancreatitis may be similar in presentation to chronic pancreatitis, but it represents a different pathological process.1I Other rare causes of pancreatitis include abdominal or surgical trauma, obstruetion of the gland by neoplastic growth, drug effects, a variety of infectious diseases, and other chronic diseases of the GI tract.

educat:ion

Nursing intervention is focused on asslstmg the patient to self-manage the symptoms and possibly care for bile drainage systems (see the Guidelines for Care Box on p. 1378). The remainder of care and teaching is generally supportive as the patient and family face an uncertain haure and poor prognosis. General care of the cancer patient is discussed in Chapter 11.

pancreatitis

The role of alcohol in the development of acute pancreatitis is well recognized clinically but remains poorly explained. Alcohol is presumed to have a direct toxic effect on the pancreas in selected persons, probably through some genetic enzymatic abnormality. Extensive amounts of aIcohol over a minimum period of several years are probably required to initiate the processo Alcohol also weakens cell membranes and makes the acinar cells more vulnerable to injury. It is also known to decrease the amount of trypsin inhibitor available, which again increases the susceptibility of the pancreas to injury. Alcohol is believed to initiate an asymptomatic pancreatitis in the organ before the first acute episode. Alcoholic patients also typically develop chronic disease once an acute episode has occurred, and the presence of chronic pancreatitis appears to make the pancreas even more vulnerable to the damaging effects of alcohol.12·21.23Recurrent episodes of acute pancreatitis are common. Biliary

pancreatitis

Transient obstruction of the ampulla ofVater by a gallstone is considered to be a major cause ofbiliary pancreatitis. Stones were found in the stool of more than 90% of patients with gallstone pancreatitis in some studies. The obstruction does not have to be prolonged to initiate acute inflammation. How the obstruction activates the pancreatic enzymes is not understood. The presence of tiny gallstones (microlithiasis or biliary sludge) toa small to be identified by imaging studies, is believed to play a role. There is also considerable evidence that structural abnormalities that lead to narrowing at the sphincter of Oddi can be considered a cause of biliary pancreatitis. It is theorized that the various forms of obstruction can reverse the normal pancreatic pressure gradient. This would permit reflux of bile or duodenal contents into the pancreatic ducts and possibly even cause small duct rupture.1I Biliary pancreatitis begins acutely, but is likely to be mild in course and followed by rapid recovery. It can, however, in selected situations trigger rnassive pancreatic necrosis and lead to death. It rarely leads to cnronic disease.

Management

of Persons with

Problems

of the Gallbladder

Epidemiology

The incidence of acute pancreatitis has increased in recent years, but this increase may represent improved diagnostic capabilities rather than a true increase in cases. The current annual incidence is estimated to be 0.1 to 0.5 cases per 1000population. Patients with biliary pancreatitis are likely to be 55 to 65 years of age and predominantly female, whereas patients with alcohol-related pancreatitis are usually slightly younger and predominantly male. Acute pancreatitis may take a mild, severe, or fulminant course. Pancreatitis has a fulminant course in approximately 5% to 15% of all patients, and 20% to 60% of these patients will either die or face potentially lethal complications.6 The overall mortality rate for pancreatitis remains at about 10% despite improved diagnosis and more aggressive treatment. Pathophysiology

The two major pathological varieties of acute pancreatitis are the (1) acute interstitial form and (2) acute hemorrhagic formoAlthough either form can be fatal, the interstitial form is often a mi!der disease. The defining characteristic of acute interstitial pancreatitis is a diffusely swollen and inflamed pancreas, which retains its normal anatomic features. There are minimal or no areas of hemorrhage or necrosis in the gland. The interstitial spaces become grossly swollen by extracellular edema, and the ducts may contain purulent material. The acute hemorrhagic disease presents with a very different picture. The gland readily shows acute inflammation, hemorrhage, and marked tissue necrosis. Extensive fat necrosis is present in patients with fulminant disease, not just in the pancreas but throughout the abdominal and thoracic cavities and subcutaneous tissues.23

and Exocrine

Pancreas

chapter42

ecrosis of vessels can cause significant loss of blood, and abscesses and infection form in areas of walled off necrotic tissue. Systemic complications such as fat emboli, hypotension, shock, and fluid overload are common. Pancreatic juice normally contains only inactive forms of the proteolytic enzymes. The pancreas secretes a trypsin inhibitor specifically to prevent activation within the gland, because once trypsinogen is activated to trypsin it can then activate the other enzymes as well. Activation of the pancreatic enzymes before they reach the duodenum has long been recognized as a major component of the diseaseprocessoThe mystery of acute pancreatitis is how that pathological sequence is initiated. The etiológical roles of alcohol and bi!iary disease have been discussed, but they fai! to fully explain the disease process.22 Enzyme activation overwhelms all of the normal protective mechanisms of the pancreas and initiates a massive attack on the pancreatic tissues. Pancreatic autodigestion is initiated. 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 disseminated intravascular coagulation • Increased permeability causing massive movement of fluids, which leads to circulatory insufficiency • Releaseof myocardial depressant factor, which further compromises cardiac function • Activation of the renin-angiotension network, which impairs renal function in conjunction with circulatory insufficiency Figure 42-5 outlines the major pathological events that can occur in acute pancreatitis .

. Ihterper-itoneol. soponificotíon oF calcium

figo 42-5

Summary of major pathological

1381

events that occur in acute pancreatitis.

, 382 unit viii

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in Digestion

and

Elimination Collaborative Care Management

The clinical manifestations of acute pancreatitis vary somewhat according to the severity of the attack. Acute pain in the epigastric region is the hallmark feature of the disease. The pain is usually steady in nature and may radiate to the back. It is typically worsened by lying supine, and patients may curve their backs and draw their knees up toward the body in an attempt to dirninish its intensity. The pain is variously attributed to stretching of the pancreatic capsule, obstruction of the biliary tree, and/or chemical burning of the peritoneum by activated enzymes. In more severe forms of the disease the pain may be agonizing. Vomiting is a second common feature of acute pancreatitis. The severity of the vomiting varies and is typically worsened by the ingestion of food or fluido Vomiting does not relieve the pain and may become protracted. Physical findings for patients with severe pancreatitis include abdominal tenderness and rigidity, progressive abdominal distention, and decreased bowel activity. Fever is common, but it rarely exceeds 39° C. Fulminant disease may progress to hypovolemic shock, ascites, acute tubular necrosis, and respiratory failure. The clinical manifestations of mild and severe pancreatitis are summarized in Box 42-2.

'.I.IIf·· .

Diagnostic

L"" ~.&: • l_, Iça,l~nJ,,-est-a1;!Qn

Acute Pancreatitis PAIN

Steady and severe in nature, excruciating in fulminant cases Located in the epigastric or umbilical region; may radiate to the back Worsened by Iying supine; may be lessened by flexed knee, curved back positioning

I ~~:~~~~~:::::~~ I ,

o'"".

ABDOMINAL

I.'

FINDINGS

•

I f

". Rigidity, tenderness, guarding Distention Decreased or absent peristalsis.

r: ADDITIONAL

ISymptoms

FEATURES OF FULMINANT

Medications

li

~~r~~~~N~verity but is usually protracted Worsened by ingestion of food or fluid

~I'~.':".

tl

DISEASE

of hypovolemic shock Oliguria: acute tubular necrosis • Ascites Jaundice Respiratory failure i Grey Turner's sign (bluish discoloration along the flanks)* Cullen's sign (bluish discoloration around the umbilicus)*

*NOTE: These signs indicatethe accumulationof bloodinthese areas and represent the presence of hemorrhagicpancreatitis.

tests

The diagnosis of acute pancreatitis is made initially from the measurement of the serum amylase level, which rises within a few hours of the onset of the disease. In mild disease it may only remain elevated for a few days. There is no apparent relationship between the severity of the disease and the height of the enzyme levels.18 The levels of urinary amylase may also be measured if the patient sustains adequate kidney function. Serum lipase elevations are also diagnostic and persist for up to 5 to 7 days.J8 Neither amylase nor lipase elevations are exclusive to pancreatic disease, which complicates diagnosis in questionable cases. Other laboratory findings commonly seen with acute pancreatitis include leukocytosis, hyperglycemia, which may reach leveIs as high as 500 to 900 mg/dl, and elevated liver function tests. Hypocalcemia may develop from the sequestering of calcium by fat necrosis in the abdomen, and this is usually a poor prognostic signo It may occur in conjunction with low levels of both albumin and magnesium, especially in chronic alcoholics. Computed tomographic (CT) scanning has become the gold standard for diagnosing acute pancreatitis, although it is actually not needed except for patients with severe disease and suspected complications. CT scans can estimate the size of the pancreas; identify cysts, abscesses, and masses; and with contrast medium can clearly diagnose hemorrhagic disease. Early in the diagnostic process abdominal x-rays may be taken to rule out ulcer perforation, and ultrasonography may be used to rule out the presence of gallstones.

r !leI

~ ~j

i ~;

f

t

There is no drug treatment for acute pancreatitis. Drug therapy to reduce pancreatic secretion with somatostatin, histamine H2-receptor antagonists, anticholinergic agents, and glucagon has not been shown to have any therapeutic effect. Pain management is the primary consideration, and patients may require substantial amounts of opioids. Synthetic narcotics such as meperidine (Demerol) have traditionally been used because they do not cause spasm in the sphincter of Oddi." Morphine, however, is now believed to have minimal sphincter effects and is an extremely effective analgesic. Fluid and electrolyte replacement is criticaI since the loss of intravascular fluid through membrane leakage averages 4 to 6 L and can easily exceed these levels in severe cases.3,23 Prevention of hypovolemic shock necessitates aggressive fluid management. Urinary output should remain at or above 30 to 50 ml/hr. Potassium losses can also be significant in both vomitus and pancreatic fluids, and serum leveIs need to be maintained. Hypocalcemia develops frequently and is carefully monitored. Replacement of calcium is initiated if the patient becomes symptomatic.23 Exogenous insulin may be needed in severe disease, but it is used cautiously because these patients are very vulnerable to severe hypoglycemia from decreased glycogen and glucagon reserves.

Management

of Persons

with

Problems

of the

Gallbladder

Treatments

and

Exocrine

Pancreas

chap~er42

1383

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

There are no known treatments for pancreatitis. Medical therapy is direeted at general supportive care for most patients with mild to moderate disease. The patient is generally given NPO. Nasogastric suctioning has frequently been used, but is probably not necessary unless the patient develops ileus or experiences persistent vomiting. More aggressive and invasive interventions are available for patients who are at high risk for complications. The course of acute pancreatitis is not readily apparent, and several clinical prognostic rating scales have been developed to help clinicians identify patients at greatest risk. The older system uses the criteria of Ransom applied at admission and again within the first 48 hours. The modified Glasgow criteria are easier to apply clinically. These prognostic scoring systems are presented in Table 42-l. Peritoneallavage has been used in patients with severe pancreatitis in the attempt to remove toxic substances. Clinical trials have involved small numbers of patients, and results have been somewhat inconsistent, but a trend toward a decrease in deaths related to pancreatic infection has been observed. The removal of retained gallstones by ERCP reduces overall morbidity in the select group of patients in whom an obstructing stone can be identified.

Diet

The patient is given nothing by mouth until the abdominal pain has subsided, and amylase levels return to normal. This practice, in theory, rests the pancreas and limits or stops the secretion of enzymes. Most patients do recover without complications or sequelae.IO Oral tluids and feedings can usually be resumed within 3 to 7 days and gradually advanced to a normal diet once peristalsis is reestablished. There is no clinical proof of the need for a low-fat diet or any other dietary restrictions during recovery except for abstinence from alcoho1.6 Total enteral or parenteral nutrition may be implemented for patients who are unable to eat for extended periods of time (Research Box). The early use of total parenteral nutrition (TPN) does not appear to affect outcomes of patients with mild pancreatitis, but its use significantly decreases morbidity and mortality in severe and fulminant disease.11 Efforts are made to keep plasma albumin levels above 3.5 gld and total protein values above 6.5g/d, thereby maintaining a positive nitrogen balance. Ii Activity

Surgical management

Bedrest is maintained during the acute phase of disease management to decrease the body's overall metabolic demands. Once the patient's condition has stabilized, activity can

Surgery is not a routine part of the management of acute pancreatitis, but some procedures may be necessary to control related gallbladder problems, pseudocyst, or abscesso Necrotic tissue may also be resected. Patients requiring

research\~il Relerence: McClave SA et ai: Comparison 01 the salety 01 early enteral vs. parenteral nutrition in mild acute pancreatitis. J Parent Ent Nutr21(1l:14-20.1997.

Tvvo Representative Prognostic Scoring Systems Used in Acute Pancreatitis ~..,-~~~

.~

~

RANSOM

ADMISSION

. Age >55 years WBC >20,000 cell/mm3 LDH >350 IU/L AST >250 IU/L Glucose >200 mg/dl INITIAL 48 HR

Hematocrit decrease >10% BUN increase >5 mg/dl Calcium <8 mg/dl Po, <60 mm Hg Base deficit >4 Estimated fluid sequestration >6 L

••

~

.•....•

:z=:""

~~~

GLASGOW

WITHIN48HR OF ADMISSION

Age >55 years WBC >15,000 Glucose >180 mg/dl BUN >45 mg/dl Po, <60 mm Hg Albumin <3.2 g/dl Calcium <8 mg/dl LDH >600 IU/L

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

't !

This study was designed to compare the safety, cos!, and effectiveness of two methods of nutrition support for patients with mild acute pancreatitis. The study involved 30 patients who were admitted with mild acute pancreatitis documented by the presence of pain and elevated serum amylase and lipase leveis. Patients were randomly assigned on admission to receive either total enteral nutrition (TEN) via a nasointestinal tube or total parenteral nutrition (TPN) by central or peripheral catheter. Nutrition support was initiated within 48 hours of admission. No differences were noted between the groups on admission in mean age, Ransom criteria, APACHE score. or other prognostic screening tool. No deaths occurred in either group. No differences were found in serial pain scores, the number of days before normalization of blood values occurred, serum albumin leveis, or the incidence of nosocomial infection. The cost of TPN, however, was more than four times greater than the cost of TEN, and stress-induced glucose leveis were significant in the TPN group. The study concluded that isocaloric/isonitrogenous TEN via nasointestinal tube appears to be a cost-effective alternative to intervention with TPN in this population.

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

Presence of Grey Turner's or Cullen's signs: bluish discoloration on flanks and/or around umbilicus Jaundice

Referrals

Patients with acute pancreatitis are severely ill and may require the expertise of a variety of specialists during the treatment and recovery periods. Fulminant illness may necessitate critical care monitoring and consultation. This is particularly true for patients who develop respiratory complications such as adult respiratory distress syndrome (ARDS) or respiratory failure and require intubation and mechanical ventilation. The nutrition support team will be involved if TPN is initiated. Any number of medical specialists may be consulted to manage emergency complications. The surgeon is often needed to drain abscesses, relieve obstruction, or debride necrotic tissue. An enterostomal therapist may be consulted if draining wounds are left open to heal by secondary intention. In many patients alcohol abuse is the etiological stimulus of acute pancreatitis, and continuation of alcohol use will increase the risk of recurrent acute pancreatitis and chronic pancreatitis in the future. The nurse needs to be knowledgeable about resources available in the local community for supporting individuals who want to become and remain abstinent from alcohol. The severe nature of acute pancreatitis may serve as a stimulus for lifestyle change in some individuals. It is important to use this opportunity to refer the person for alcohol treatment if possible.

NURSING MANAGEMENT • ASSESSMENT Subjective

Data

Subjective data to be collected to assess the patient with acute pancreatitis include: Pain: steady and severe in nature and quality; located in the epigastric or umbilical region, may radiate to back; worsens when patient is supine Nausea and vomiting, usually severe and protracted; worsens by the ingestion of food or fluid; vomiting does not relieve pain History of gallbladder disease; long-term high alcohol intake

• NURSING DIAGNOSES Nursing diagnoses are determined from analysis of patient data. Nursing diagnoses for the person with acute pancreatitis may include but are not limited to: Diagnostic Title Pain Fluid volume deficit Nutrition, aItered: less than body requirements Risk for impaired home maintenance management HeaIth maintenance, aItered

Data

Objective data to be collected to assess the patient with acute pancreatitis include: General affect: patient looks distressed; sits with knees pulled toward abdomen Fever, generally <39 C Abdominal rigidity, distention, guarding, and tenderness Diminished or absent bowel sounds Signs of dehydration: falling urine output, decreased skin turgor, dry or sticky mucous membranes Vital signs: evidence of hypovolemia; tachycardia, tachypnea, normal to low blood pressure, restlessness, and anxiety 0

Lack of knowledge about disease process and therapeutic regimen UnhealthY lifestyle patterns, including aIcoholism

• EXPECTED PATlENT OUTCOMES Expected patient outcomes for the person with acute pancreatitis may include but are not limited to: I. States that pain is controlled and does not appear to be in pain (does not display distressed appearance, limited body movement, or limited activity). 2. Will have adequate fluid volume as demonstrated by normal blood pressure, absence of orthostatic changes, normal skin turgor, moist mucous membranes, and adequate urine output. 3. Will gradually resume a normal oral diet without discomfort and regains lost weight . 4. Patient and significant others will be able to: a. Describe the disease and the purpose of various interventions. 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., controls alcoholism if present as an etiological condition of acute pancreatitis). .INTERVENTIONS Controlling

Objective

Possible Etiological Factors Inflammation of pancreas or peritoneum Vomiting, fluid shifts in abdomen Nausea and vomiting; pain

Pain

Control of pain is a major priority, and either morphine or meperidine (Demerol) may be used. Critically ill patients may receive a continuous infusion of N narcotics supplemented by boluses as needed for breakthrough pain. Patientcontrolled analgesia should be used if feasible to allow for successful pain management.14 The nurse will regularly and frequently assess the patient's levei of pain and response to interventions. The physician will be consulted for needed changes in the regimen. An attitude occasionally encountered in caring for patients with alcohol-induced pancreatitis is that the patient is somehow "getting what he or she deserves," especially on repeat admission for recurrent disease. The nurse must serve as the patient's advocate in the system, document-

Management

of Persons with

Problems

of the Gallbladder

ing the severity of the pain and ensuring that an effective plan is in place to manage it. Some patients find that the pain is decreased if they assume a sitting position with the trunk flexed, or a side-Iying, knee-chest position with their knees drawn up to the abdomen. Epidural analgesia can be used if pain is persistent and not relieved by routine narcotic administration. Although the research is currently inconclusive most patients will be given nothing by mouth to "rest" the pancreas and decrease the autodigestive processoA nasogastric (NG) tube will be inserted to keep the stomach decompressed if vomiting is severe. The nurse will also explore the use of a variety of nonpharmacological pain relief strategies with the patient, including distraction, imagery, massage, or back rub. The environment should also be kept quiet, comfortable, and conducive to restoThese measures are used in addition to, and not in place of, narcotic administration for pain control. Maintaining Fluid and Electrolyte Balance

AB soon as the patient is admitted, the nurse should institute monitoring related to fluid and electrolytestatus, cardiac output, and renal status. It is a critical need. Monitoring includes intake and output, vital signs, daily weights, abdominal girth, and all routine laboratoryvalues with particular emphasis on potassium and calcium levels.Physicalassessment will include assessing for signsofhypokalernia and hypocalcernia (see Chapter 15). An indwelling Foley catheter may be necessary, since decreased renal function can occur in association with hypotension and shock. Monitoring parameters and frequency of monitoring will depend on the stability of the patient's condition. Fluids, electrolytes, colloids, or blood will be given as necessary. Aggressive fluid replacement will necessitate establishing and maintaining large bore IV access. The nurse is responsible for administering the fluids and for monitoring the patient's response. The development of hypovolemic shock is of particular concern in the early days of the disease, and the nurse watches carefully for the early signs that could indicate the development of shock (see Chapter 17).The patient also is monitored for hyperglycemia, and checks of blood glucose should be performed four times a day. If severe hyperglycemia occurs, it may be treated with insulin. Promoting Adequate Nutrition

The patient will be given nothing by mouth and often has a nasogastric tube in place. Good oral hygiene will be necessary to decrease discomfort from NPO status and from the nasogastric tube. TPN may be used during the criticaI phase of the illness for patients with severe disease. When the acute symptoms decrease (3 to 5 days), oral fluids and food are restarted. The patient is given clear liquids and then slowly advanced toward a regular diet. Tolerance for oral feedings is carefully assessedas is the possibility of the return of pain. Frequent small mealsare usually better tolerated in the early refeeding period. The only diet restriction that needs to be followed after discharge is the avoidance of alcohol.

and Exocrine

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Patient/Family Education

Teaching the patient and significant others will be ongoing. At the beginning of hospitalization, the patient and significant others need basic information about the disease, the diagnostic tests, and the treatment. Because of the pain and the distress acute pancreatitis causes and because of the severity of the disease process, the patient and family may be experiencing tremendous anxiety. Therefore explanations and instructions should be brief and as simple as possible and may need to be repeated. Support and continuity of care also need to be provided to help decrease anxiety. Education will be directed toward preventing future attacks and maintaining a nutritious diet. The patient must know that any recurrence of signs and symptoms should be reported immediately. Follow-up care must be explained in detail. Health Promotion/Prevention

If unhealthy lifestyle patterns such as alcoholism are a cause of acute pancreatitis, the nurse must work with the patient on the problems. This care will not be instituted until the patient's condition is stabilized, but it must be introduced before the patient leaves the hospital. See Chapter 14 for further information on coping with alcoholism. If the patient's pancreatitis is related to biliary diseasé,it will be important to stress the importance of treatrnent for gallstones.The episode of pancreatitis is frightening and could make the patient reluctant to undergo any further medical or surgical treatrnent. The nurse will reinforce the etiological role of biliary disease in the development of pancreatitis and encourage the patient to follow through on recommended treatrnent. • EVALUATION

To evaluate the effectiveness of nursing interventions, compare patient behaviors with those stated in the expected patient outcomes. Successful achievement of patient outcomes for the patient with acute pancreatitis is indicated by: la. States no pain. b. Does not splint, grimace, and breathe shallowly. 2. Has hemodynamic measures within normal limits and shows intake equal to output. 3a. Maintains NPO status as appropriate. b. Consumes a well-balanced diet without nausea, vomiting, or pain by discharge. c. Returns to normal weight. 4a. Appropriately describes the disease, tests, and planned interventions. b. Appropriately describes the relationship between etiological factors and the disease. c. Appropriately describes and selects well-balanced diet. 5a. Correctly identifies planned follow-up treatrnent for biliary disease. b. Makes commitment to treatment for alcoholism. GERONTOLOGICAL CONSIDERATIONS

Biliary disease becomes increasingly common as people age, and biliary disease-related pancreatitis is most likely to occur in the elderly patient. The severity of the disease is difficult to

1386

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predict, but elderly patients with acute pancreatitis may become critically ill faster because of comorbid problems. Elders are also more likely to develop complications related to their disease-enforced immobility as well as to the pancreatitis. Respiratory complications are of particular concem, and the elderly patient needs frequent respiratory assessment and aggressive pulmonary hygiene during the acute stage of the disease. Infection is a common complication of pancreatitis (see discussion under Complications), and elderly patients are less able to withstand the stress imposed on the body by sepsis. The same is true for the development of hypovolemia and fluid shifts. These factors strain the cardiovascular system and may overwhelm the elderly patient's ability to adapt and respondo SPECIAL ENVIRONMENTS Criticai

Care

FOR CARE

Management

Although most patients with pancreatitis recover without any residual dysfunction, a minority experience life-threatening disease. These patients will be managed in a criticaI care unit. The nurse's major roles are collaborative with the physician and involve ongoing monitoring of all systems and the prevention or identification of complications. Routine interventions will include hemodynamic monitoring and aggressive fluid support. Critically ill patients may also need cardiac support with drugs such as dopamine. A pulmonary artery catheter may be inserted to assess perfusion adequacy. Left ventricular dysfunction is a common problem. The airway is compromised in several ways. Severe pain limits diaphragmatic excursion, and both shock and sepsis place extraordinary metabolic demands on the respiratory system that can progress into full-blown ARDS in some patients. Prompt intubation and mechanical ventilation will be crucial. Hypercoagulability increases the risk of pulmonary embolism. Management includes supplemental oxygen, suctioning as needed, and aggressive chest physiotherapy. Assessment is conducted hourly. Respiratory failure accounts for a disproportionate number of pancreatitis-related deaths. In addition to the concems addressed above, the critically ill patient with pancreatitis will receive TPN to support a pósitive nitrogen balance and may undergo peritoneal lavage through a peritoneal catheter. Other interventions will be directed at specific complications as they arise.

make referrals to community programs for alcohol treatment if the patient agrees. It is important to recognize, however, that the decision to continue drinking is a matter of personal choice. The nurse's role is to be certain that the patient has all of the information that he or she needs to make an informed decision about the future. A positive outcome cannot be guaranteed. COMPLlCATIONS About 25% of patients who have acute pancreatitis will develop complications, and most deaths associated with the disease occur in that group of patients. Complications may be local or systemic. The systemic complications tend to occur within the first week and have largely been discussed within the context of the fulminant disease processo These include complications such as hypovolemic shock, sepsis, renal failure, and ARDS. The major complications of acute pancreatitis are summarized in Box 42-3. Pseudocysts

Pancreatic fluid or exudate forms in up to 50% of patients with acute pancreatitis.6 Pseudocysts are rounded collections of fluid enclosed in a fibrous capsule. This process occurs in only 5% to 10% of all patients.6 Many pseudocysts resolve spontaneously over time, and intervention is not always warranted. However, pseudocysts can also become life threatening if they obstruct neighboring structures, rupture or hemor-

., •• ~~~.s~~._:a;;:"

Major Complicatians af Acute Pancreatitis .._~:,;;~=:l;t=.f'",.......,;.

CARDIOVASCULAR

Hypotension/shock albuminemia

from hypovolemia

or hypo-

HEMATOLOGICAL

Leukocytosis from generalized inflammation or secondary infections, anemia from blood loss, disseminated intravascular coagulation (OIC) from unknown causes RESPlRATORY

Atelectasis, pneumonia, tory distress syndrome

pleural effusion, adult respira(AROS)

GASTROINTESTINAL Home

Care

Management

Most patients with acute pancreatitis recover spontaneously and can be discharged from the hospital within 1 to 2 weeks. Patient needs for home care will be minimal if complications did not develop. Normal activities are gradually resumed as strength and activity tolerance increase. Patients with alcoholism present a unique challenge as even the pain and anxiety of acute pancreatitis may not be sufficient motivation for them to abstain from alcohol. The nurse will discuss the importance of abstinence with the patient and

GI bleeding PANCREATIC

Pancreatic pseudocysts, pancreatic necrosis or phlegmon, pancreatic abscesses, pancreatic ascites RENAL

Oliguria and acute tubular necrosis METABOLIC

Hyperglycemia,

hypocalcemia,

hyperlipidemia

Management

of Persons with

Problems

of the Gallbladder

rhage, or become infected. A "wait and see" policy is generally followed, and the cysts are monitored regularly. Inflammatory exudate from the pancreas may form into an inflamed mass, which is called a phlegmon. Intervention is again not indicated unless bleeding or infection develops. As with pseudocysts the pWegmon may be drained, surgically debrided, or resected as needed. Pancrea~icInfec~ion As treatment for systemic complications has improved, pancreatic infection has become the most frequent cause of serious morbidity and mortality associated with acute pancreatitis. Infection typically appears 8 to 20 days after the onset of pancreatitis and has a 100% mortality rate if untreated.2 Infection usually develops in the are as of necrosis created by fulminant disease. The initial diagnosis of infection can be complicated by the fact that acute pancreatitis itself manifests with the common symptoms of inflammation and infection. Infection-related fever, however, typically exceeds 39° C, and the patient's clinical condition deteriorates. CT scanning allows for the accurate identification of areas af necrosis, which can then be aspirated by CT-guided needle aspiration. Gram stain and culture can then identify the specific organisms responsible for the infection. Broad-spectrum antibiotics are initiated immediately, but definitive therapy requires percutaneous drainage or surgical debridement. Attempts to prevent the development of infection with the routine use of antibiotics have not proven to be effective, although irnipenem (Primaxin) is able to effectively penetrate the capsule of the pancreas and shows promise. Percutaneous drainage is used most effectively with infected pseudocysts because there is minimal particulate matter present that can clog the tubes. The traditional surgical approach had been to excise as much necrotic material as possible and then place multiple large-bore sump drains in the operative areas to remove infected material.2 Continuous saline infusion and suction were needed to maintain tube patency. Many surgeons now recommend an open method in which the resected are as are packed, and the dressings are changed under anesthesia every 2 to 3 days until granulation is well underway. The abdomen is left open and eventually doses over an absorbable mesh barrier. A feeding tube is placed once granulation is underway. The development of fistulae can complicate the healing processo Chronic Pancreatitís Patients with alcohol-induced acute pancreatitis are believed to already have asymptomatic chronic disease when they experience their first acute episode. If the patient continues to drink, the likelihood of recurrence is extremely high. Chronic pancreatitis is discussed below. CHRONIC PANCREATITIS Etiology/Epídemiology Chronic pancreatitis is present when recurrent bouts of inflammation lead to progressive injury and scarring of pan-

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1387

creatic tissue with gradual fibrous replacement of the normal tissue.21·23The progressive degeneration of the gland makes chronic pancreatitis a separate disorder from recurrent acute pancreatitis in which pancreatic function essentially returns to normal when the inflammation subsides.'·23 Chronic pancreatitis occurs almost exclusively in alcaholics and is more common in men. Other potential causes of chronic pancreatitis include neoplasms, structural problems, and, rarely, inflammatory problems such as inflammatory bowel disease and primary sclerosing cholangitis. Biliary tract disease remains the primary causative facto r in acute recurrent pancreatitis. Pathophysiology The basic pathological change of chronic pancreatitis is destruction of the exocrine parenchyma and replacement with fibrous tissue. This process is associated with varying degrees of duct dilatation. Scarring and fibrotic changes may occur throughout the pancreas or be limited to selected areas. Calcium salts may be deposited in both the ducts and the parenchyma, usually in areas of fat necrosis. Ductal obstruction occurs secondarily. The factors that influence the solubility of calcium in the calcium-rich pancreatic secretions are not well identified. As the process becomes increasingly severe the islets of Langerhans are also involved and destroyed. The role of alcohol in both acute and chronic pancreatitis remains obscure. Alcohol appears to act as a direct toxin, but since only a minority of heavy drinkers develop problems, some genetic defect must also exist that allows alcohol to have such detrirnental effects. The pathological nature of the alcohol-induced injury is believed to be similar to that occurring in acute pancreatitis. In addition there is evidence of small protein plugs in the acinar ductules. Secretions are more viscous and tend to form calcium-containing stones. Trypsinogen and other proteases are activated by poorly understood mechanisms. The patient with chronic pancreatitis may initially have signs and symptoms identical to those described for the patient with acute pancreatitis, with pain being the major manifestation. The pain occurs in the right or left upper quadrant, in the back, or throughout the total abdomen. It is severe and constant and is not relieved by food ingestion or antacids. Nausea, vomiting, and abdominal distention may be present, but they are usually secondary to the pain. In the alcoholic patient it is very difficult to decide where acute pancreatitis leaves off and chronic disease begins. Theoretically the dense fibrosis can entrap and alter the pancreatic nerves, affecting both sensory and motor functions.1 It is possible that much of the pain is eventually related to this nerve entrapment, although the pain is not different in nature or severity from that which accompanies acute pancreatitis.' It is frequently worsened by eating and needs narcotic administration for control. Pancreatic insufficiency begins once 80% of the pancreatic tissue is destroyed. Symptoms include diarrhea, which is

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in Digestion

and Elimination

often steatorrhea, and marked weight loss. Diabetes is common and mayprecede other clinicai symptoms. Unique metabolic derangements in glucose metabolism create a strong vulnerability to hypoglycemia and a smaller need for insulin. Oral hypoglycemic agents are not effective. Malabsorption leads to clinicai deficiency in vitamins E and B12 and other fat-soluble vitamins, but patients rarely develop overt symptoms of deficiency. A history of acute pancreatitis is the best diagnostic connection to chronic disease. Amylase and lipase levels will ris e during recurrent attacks, and both fasting and postprandial hyperglycemia are usually present. Stool examination can quantify the severity of the steatorrhea and malabsorption. CT scanning is the basis of diagnosis and can demonstrate fibrosis, atrophy, duct dilatation, and calculi. Collaborative Care Management Effective management of abdominal pain is the greatest challenge with chronic pancreatitis. Patients who continue to drink alcohol will continue to have pain, and even abstinence is eventually no guarantee of relief. Patients can usually adapt to the malabsorption and steatorrhea, but the persistent pain may lead to drug dependence and motivate the patient to undergo risky surgical procedures, which are frequently accompanied by poor outcomes and multiple complications. Flare-ups of chronic pancreatitis are managed just like acute disease. Bowel rest is maintained, and attention is paid to managing the acute pain. Ongoing care involves the use of a low-fat diet and supplemental pancreatic enzymes. These extraets will increase the patient's body weight and improve absorption, inereasing the patient's general sense of wellbeing. The recommended diet is high in protein and carbohydrates and may provide as much as 3000 to 6000 calories/day. The use of medium-chain triglycerides to improve the patient's 'nutritional state is being evaluated in several research trials. Fat-soluble vitamin replacement may also be indicated, and the management of diabetes often requires the use of insulin. Chronic pancreatitis affects the small ducts of the pancreas and is not amenable to surgical correction. Surgical intervention is frequently used to attempt to relieve the chronie abdominal pain, but there are no proven surgical solutions. Extensive pancreatic resection or pancreatectomy may be performed in patients who are unable to refrain from drinking alcoho!. Sympathectomy is occasionally performed to release the entrapped nerves. The nurse serves as the patient's advocate in the search for eomfort. Concerns about drug dependenee must not be allowed to prevent the patient from receiving adequate and necessary analgesia. Health care providers can easily become exasperated with patients who are unable or unwilling to stop drinking and can begin to consider the pain of chronic pancreatitis as appropriate retribution for the patient's addiction. This attitude can seriously eompromise the patient's care. In some instances the patient has had negative experiences with pain management during previous hospitalizations for

exacerbations and thus believes that analgesics are not being given because the health team does not care about him or her. The involvement of a pain management team is desirable if such services are available. See Chapter 12 for further discussion of pain management. Patient/falTJi/y

education

The role of alcohol in the etiology and progression of chronic pancreatitis is unequivocal, and yet many alcoholics find themselves unable or unwilling to abstain from alcohol use. The nurse consults with a substance abuse specialist to develop a consistent and appropriate approach for the patient's care and ensures that the patient has ali the data necessary to make informed decisions about his or her present and future. Information coneerning community resources for alcohol treatment should be current and accurate and offered to the patient. The involvement of the family is encouraged if the dynamics are supportive. Family members and health care workers need to be helped to understand and accept that ultimately it is the patient's right to make fundamental decisions about his or her own care, even when these decisions do not appear to be in the patient's own best interests. The patient also needs to learn how to modify the diet and use pancreatic enzyme replacement effectively to control diarrhea and maintain a stable weight. Timing of the medications is critica!. The nurse teaches the patient to take the eapsules 1 to 2 hours before, during, or after meals. Powders can be mixed directly with food. Patients are informed that these products frequently produce a bad taste and may alter the taste of foods. The patient is instructed to monitor the body's response to the supplements and consistently track weight changes. The anorexia and poor eating habits commonly associated with long-term alcohol use makes adherence to a high-protein, high-calorie diet difficult. The use of vitamin supplements is encouraged if recommended by the physician. Patients who continue to drink alcohol will always be just one step away from their next flare-up or complication. The nurse provides the patient with written material that outlines the symptoms of complications and encourages the patient to adhere to the plan for continued follow up. A Nursing Care Plan for the patient with chronic pancreatitis is found on p. 1389. CANCER OF THE PANCREAS Etiology/Epidemiology Cancer of the panereas may arise from any of the elements of the pancreas, although most involve the ductal epithelium and are adenocarcinomas. Both benign and malignant tumors can also arise from the islet cells but these are rare.1S Tumors of the islet cells usually retain some endocrine functions and tend to have a better prognosis than adenoeareinomas. Pancreatic cancer usually occurs in persons older than 50 years of age, but it can develop at any point in the lifespan. It is much more common in men. The etiology is unknown, but an association has been noted with cigarette smoking and

•

•

•

Person with Chronic Pancreatitis

DATA Mr. 1. is a 52-year-old self-employed accountant with a 12-year history of acknowledged alcoholism. He experienced his first attack of acute pancreatitis 4 years ago and chronic pancreatitis has since been diagnosed. He is admitted now with another flare-up of the disease. Mr. 1. has made several efforts to stop drinking and has even undergone inpatient alcohol treatment. His longest period of sobriety has been about 6 months. Some life stressor has always precipitated his descent into alcohol dependency. His wife accompanies him to the hospital but is quick to say"I don't think that I can take much more of this. He's killing himself and nothing I say or do is changing that. I don't think I can stay around any longer watching him die. It hurts toa much." Mr. T.'s admission assessment shows a thin, poorly nourished man who appears older than his stated age. He reports the presence of: • Acute abdominal pain that is generally localized in the midepigastric region and radiates to the back. He rates the pain as an 8 on a 10-point scale in severity. • Steady and protracted vomiting that began late yesterday afternoon. He has had nothing to eat or drink for more than 12 hours. Large, 50ft, and foul-smelling stools that have been increasing in frequency and severity over the last few weeks. He has lost 12 pounds. • A history of decreased alcohol use over the last 3 months. Mr. T says "I know no one will believe me but I've really been drinkNURSING

DIAGNOSIS

Acute pain related to distention

States pain is effectively controlled with pharmacological and nonpharmacological methods.

• •

• • • • • • • •

of pancreatic capsule and activation of pancreatic enzymes

1. Assess pain leveis frequently, especially before and after administration of analgesics. a. Document pain leveis on flow sheet.

2. Administer needed.

I

ing much less. The pain starts so quickly when I drink that [ have really been steadily decreasing my intake. I don't understand why this should happen now. What's the use? The doctor said the pain would stop if I stopped drinking so much and look at me now. Maybe I should just drink myself to death and get it over with." Other data on admission include: Blood pressure is 94/60, pulse is 92, and respirations are 22 and shallow. Temperature is 99.8° F. Bloodwork shows the following abnormalities: hemoglobin of 10.2 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 1000 ml of 5% dextrose in li, N saline with 20 mEq of KCI at 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 vomiting persists past 4 PM Accucheck 4 times daily per protocol, cal! house officer if glucose> 160 Monitor c10selyfor hypovolemic shock, e1ectrolyte imbalance, delirium tremens (DTs) Call substance abuse resource counselor for DT protocol initiation if needed

meperidine

q3h as

a. Encourage patient to use analgesics on a regular rather than PRN basis. b. Validate your acceptance ofthe reality ofthe patient's pain and its severity. c. Evaluate effectiveness of the narcotic order. Collaborate with physician to make adjustments in dose or drug as needed. 3. Collaborate with Mr. T to determine the nonpharmacological methods that help to reduce his pain. a. Position him in a mid to high Fowler's position with his knees flexed. b. Explore his experience with strategies such as distraction, massage, relaxation, and guided imagery.

1. Frequent assessment is essential to validate the nature and severity of the patient's pain experience. a. Recording on a flow sheet allows for a pattem of pain to be established and the effectiveness of pain control to be evaluated. 2. Synthetic narcotics are effective analgesics and do not cause spasm in the sphincter of Oddi. a. A regular time schedule of drug use allows for a steady blood levei to be established. b. Patients with chronic pancreatitis are frequently labeled "drug seekers" by staff. c. Acute pain can be immobilizing. Morphine may be substituted for meperidine. 3. Nonpharmacological methods allow the patient a degree of control of the pain experience. a. This position is theorized to reduce tension on the abdomen. b. Ali of these can be effective methods of pain control, but the patient must have an open mind and be willing to experiment with new strategies.

Continued

I

j

I

II

-

1390

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Alterations

in Digestion

and

Elimination

Person with Chronic Pancreatitis-cont'd NURSING DIAGNOSIS increased capillary permeability

Risk for f1uid volume deficit related to vomiting,

Maintains balance of fluids and electrolytes; intake and output are balanced; weight is stable.

NPO status, hyperglycemia,

1. Assess fluid and electrolyte status each shift. a. Maintain accurate intake and output. b. Weigh daily. c. Assess skin turgor and status of mucous membranes each shift. d. Monitor cardiovascular response to fluid replacement. e. Measure abdominal girth daily or as ordered. 2. Monitor blood glucose 4 times daily. a. Administer sliding-scale insulin per protocol.

3. Monitor for hypokalemia and hypocalcemia: muscle weakness, cramping numbness and tingling in fingertips or around mouth; positive Chvostek's and Trousseau's sign NURSING DIAGNOSIS Altered nutrition: less than body requirements malabsorption caused by loss of function of pancreatic enzymes

Receives sufficient nutrients by mouth or TPN to maintain stable body weight, keeps albumin leveis above 3.8 g/dl, and produces normal stools.

2. Assess current nutritional nation status.

1. Patient is at risk for hypovolemic shock and dehydration. May lose 4 to 14 L of fluid into the abdomen. Fluid replacement is based on estimates of losses. A urine output of 30 to 50 ml/hr is essential to prevent the onset of acute tubular necrosis. Fluid and gas accumulation in GI tract can result in significant abdominal distention. 2. Destruction of the beta cells and islets of Langerhans produces severe hyperglycemia. Because of the risk of labile hypoglycemia, insulin is not given unless glucose levei continues to rise. 3. Large amounts of potassium are lost through vomiting and in the pancreatic secretions; calcium is believed to bind with free fats and can drop to leveis that increase neural excitability.

related to vomiting,

1. Maintain NPO status and bed rest until patient's condition stabilizes.

and elimi-

3. Monitor daily weight and serum protein and albumin leveis. 4. initiate TPN if NPO status needs to be protracted.

5. Reinitiate oral feedings once abdominai pain is controlled and amylase/lipase leveis stabilize.

6. Offer small, frequent feedings to the patient's tolerance; assess patient response. a. Restrict fat in diet if steatorrhea persists. 7. Evaluate composition and volume of stools. Adjust dose of pancreatic enzymes to achieve normal elimination.

and

NPO status, and

1. NPO status is theorized to reduce the secretion of pancreatic enzymes. Bed rest decreases the body's metabolic rate. 2. Patients with chronic pancreatitis are often malnourished before the attack from alcoholism and malabsorption. 3. These parameters provide the best ongoing data about nutritional status. 4. If pain is not controlled promptly the rapid catabolism of the disease must be counteracted by TPN to prevent life-threatening complications. 5. Once pain and enzyme leveis are stable there is no contraindication to oral feeding, and the severity of malabsorption needs to be established. 6. This feeding pattem minimizes distention and malabsorption symptoms. a. Malabsorption primarily affects digestion of fats. 7. Malabsorption manifests itself as large-volume, greasy, foul-smelling stools. Adequate enzyme replacement will restore the stool to near normal. Continueo

Management

,íJ;

of Persons

with

Problems

of the

Gallbladder

and

Exocrine

Pancreas

chapter42

1391

Person wíth Chroníc Pancreatítís-cont'd

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

01

•

Verbalizes understandíng of disease process, role of alcohol, and pharmacological management of symptoms. Makes commitment to abstain from alcohol.

1. Assess

patient's current understanding of the disease process and the role of alcohol in its recurrence. 2. Assess patient's interest and commitment to abstain from alcohol. a. Assess knowledge of community resources for treatment and supporto Refer as appropriate. 3. Assess for symptoms of DTs during first 48 to 72 hours. Consult with substance abuse specialist if needed. 4. Teach patient correct use of pancreatic enzymes: • Take with each meal and snack. Monitor weight and stool consistency to judge need for dosage adjustment. 5. Teach patient about the nature and planned management of diabetes. a. Teach symptoms to report: Hyperglycemia: frequent urination, thirst, lethargy, abdominal cramping • Hypoglycemia: anxiety, tachycardia, diaphoresis 6. Encourage patient to make commitment to changing his lifestyle and gaining control of his disease and his life.

research

to abstain

1. This establishes

a baseline for planning and intervention.

2. Patient has stated his attempts to decrease alcohol use. Wife has stated the end of her tolerance for his continued use 01 alcohol. 3. Patient may not be truthful about current levei of use. Withdrawal carries a high mortality in acutely ill patients and necessitates specialty asisstance .. 4. Malabsorption is permanent, and patient will develop serious nutrient deficiencies if enzymes are not adequately replaced. Dosage adjustments can be safely made by a well-informed patient. 5. Insulin may be needed to control the diabetes of chronic pancreatitis, but hypoglycemia must be prevented. Patient will remain hyperglycemic but must know how to recognize ketoacidosis.

6. Patients with chronic pancreatitis often have given up hope on themselves and their ability to inlluence the future.

~

Reference:PriceTF,PayneRL,OberletinerMG: Familialpancreatic cancer in SouthLouisiana,Cancer Nurs 19(4):275-282, 1996. This study explored a possible familial predisposition to pancreatic cancer among a Cajun heritage population in the Acadiana region of Louisiana. The study was descriptive in nature and used a questionnaire to explore cancer incidence and risk lactors. Thirty-eight patients or family surrogates were enrolled from among the 140 possible cancer patients documented during the year of study. Sampling was difficult as patients rapidly beca me extremely ill or died. Of the sample sixty-five percent reported Cajun ancestry. They reported a total 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 hereditary component (Research Box). A link with chronic pancreatitis has been suggested but remains unproven. Pathophysiology

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

pancreatic cancer. This represented an incidence rate lar above national norms where pancreatic cancer accounts for only 2% of ali new cancer diagnoses. The sample incidence rate was comparable to that of lung cancer. African Americans had the highest incidence (32 per 100,000 versus 17 per 100,000 nationwide). The incidence rate was also significantly increased for whites (18 per 100,000 versus 10 per 100,000 nationwide). Heavy prolonged cigarette smoking was shown to be a clear risk facto r, which has been true in ali samples. Although flawed by sampling difficulties, the study does appear to confirm the presence of a significant familial risk for pancreatic cancer in this unique population.

tumor is usually deeply encased in normal tissue and is poor1y demarcated. The common duct is often obstructed and distended by the presence of the tumor. Metastasis has almost always occurred before the tumor produces its first symptoms beca use there is no capsule surrounding the pancreas to prevent the growth and spread of the tumor. Direct extension of the lesion may cause its spread to the posterior wall of the stomach, the duodenal wall, the colon, and the

1392

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Alterations

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and Elimination

eommon bile dueto Vital blood vessels in the are a are also frequently involved. Pain is the earliest and most eommon symptom of panereatie eaneeI. The pain is usually deseribed as epigastric in location and steady and severe in character. It occurs or is worsened by lying down and bears no relationship to meals. The pain is relentlessly progressive in nature. Weight loss frequently accompanies the pain and can be dramatic. Anorexia is also common. ]aundice and pruritis will typically develop when bile duet obstruetion oecurs. Diarrhea and/or steatorrhea develop fairly late in the disease. Diabetes may aIso develop. Collaborative

Care Management

The diagnosis of pancreatic eancer is often first ma de based on the pattem of symptoms and then is confirmed through CT scanning. Guided needJe biopsy may be performed at the same time. A histological diagnosis is important in planning eare.9 Cancer of the panereas is usually fatal within 6 months regardJess of treatment. Less than 2% of patients survive 2 years. The treatment is generally surgical, aIthough surgery has not been proven to improve survival. Obstruction is a common problem with large tumors involving the pancreatie head, and surgi cal bypass is frequently attempted. Procedures include gastrojejunostomy to bypass the duodenurn and choledochojejunostomy to relieve biliary obstruction. Endoseopic placement of stent tubes to support biliary drainage is increasingly considered as an altemative to surgery. Stents may be placed internally or inserted for externaI drainage. Surgeons who are attempting curative procedures may use the more aggressive Whipple proeedure or total pancreatectomy (Figure 42-6). Neither radiotherapy nor ehemotherapy

Cystic duct

Gollblodder

Stomoch

Jejunum

/

figo 42-6 Pancreatoduodenectomy dure) vvith anastomosis.

(Whipple's proce-

aIone has had any positive effeets on the course of the diseaSI but combination protocols used in research trials appear t extend life e>""Pectancyto nearly 1 year. Patient/farnily

education

Pain management is an ongoing chaIlenge with panereati cancer and is often the primary determinant of quality of lift The nurse serves as the patient's advoeate in the health car system to establish an effective pain management protoec and continuously adapt it to changes in the patient's condi tion. The nurse provides careful teaching about the use of nar cotic anaIgesics and the inevitable development of toleranc and physicaI dependence (see Chapter 12). Instruetion is alsl provided about expeeted side effeets and their managemen1 Other general measures are those provided to any patient witl ÍDvasive eaneer (see Chapter 11). Nursing care of the patien undergoing pancreatie surgery is summarized in the Guide lines for Care Box.

guide'ines ~or carE The Person Undergoing Preoperative

Pancreatic

Surgery

Care

Provi de thorough teaching about planned surgical procedure and expected postoperative care. Monitor prothrombin time and other clotting studies; vitamin K and other c10tting factors may be administered. Assess nutritional status. Administer TPN if ordered. Postoperative

Care

Monitor vital parameters every hour. Criticai care placement is usualiy necessary. Check vital signs, intake and output, and hemodynamic parameters. Perform blood gas, oxygen saturation. and routine blood studies. Se alert to signs of bleeding or shock. Maintain urine output at 30 to 50 ml/hr. Initiate pulmonary hygiene every hour with deep breathing, coughing as needed, and use of incentive spirometry. Establish effective pain management regimen. Monitor every hour. Monitor dressings and drainage tubes. Keep skin clear of drainage. Maintain nutritional support with TPN. Initiate oral feedings with clear Iiquids. Advance as tolerated. Monitor blood glucose and administer insulin as ordered. Monitor patient's weight and the development of steatorrhea. Administer pancreatic enzyme replacement as ordered. Assess for signs of dumping syndrome (see Chapter 40). Provide support for patient and family and initiate discharge planning.

Management

of Persons

vvith

Problems

of the

• 1 Mrs. Blue has a T-tube present after an abdominal cholecystectomy. What may normally occur after the remova I of her T-tube? What complication should the nurse be alert for? Why? How should he or she respond? 2 In what ways would your assessment findings for a person with chronic pancreatitis differ from those for a person with acute pancreatitis? 3 Mr. Ryan 77, is being treated for acute pancreatitis related to biliary obstruction. What aspect of this type of pancreatitis differs from acute alcohol-induced pancreatitis?

CHOlE L1THIASIS/CHOlECYSTITIS/ CHOlEDOCHOllTHIASIS 11 Cholelithiasis and cholecysitis are common health problems. Risk factors include obesity, female gender, multiparity, use of birth control pills, and middle age. • Biliary tract surgery by laparoscopic cholecystectomy is the treatment of choice for gallbladder disease. If acute cholecystitis occurs, pain, nausea, and vomiting, and fluid and electrolyte problems may be of concern. • Patient problems requiring nursing attention after open cholecystectomy include ineffective breathing pattern, pain, and management of the T-tube. PRIMARY SClEROSING CHOLANGITIS • Primary sclerosing cholangitis is usually idiopathic in etiology but frequently occurs in conjunction with IBD. There is no treatment, and most patients eventually require liver transplant. CARCINOMA

OF THE BILlARY SYSTEM

• Carcinoma of the biliary system is insidious asymptomatic until late in the disease.

and can be

PANCREATIC DISORDERS • Pancreatitis may be acute or chronic. • Acute pancreatitis can result in criticai fluid and electrolyte problems, metabolic disturbances, and pain. • Most cases resolve spontaneously, but the mortality from hemorrhagic forms is high. • Care in acute pancreatitis focuses on pain management, fluid resuscitation to prevent shock, resting the pancreas by NPO status, and collaborative monitoring for complications. • Chronic pancreatitis is progressive and usually results from alcoholism. It is not reversible. • Chronic pancreatitis results in pain, malabsorption and steatorrhea and possibly diabetes mellitus. • Abstinence from alcohol use is the primary treatment objective in patients with chronic pancreatitis.

Gallbladder

and

Exocrine

Pancreas

chapter42

1393

• Malabsorption is treated with the use of pancreatic enzyme supplements. Pain management is extremely difficult if the patient continues to drink alcohol. • Cancer of the pancreas is insidious and has a very poor prognosis. In rare instances a pancreatoduodenectomy may be performed.

References 1. Ambrose MS, Dreher HM: Pancreatitis-managing a flareup, Nursing 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 aiternative, 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):3745,1993. 11. Krumberger 1M: Acute pancreatitis, Crit Care Nurs Clin North Am 5(1):185-201,1993. 12. Marshall JB: Acute pancreatitis: a review with an emphasis on new developments, Arch Intern Med 153(6):1185-1193, 1993. 13. McClave SA, Greene LM, Snider HL: Comparison of the safety of early 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 Consensus Development Conference Statement on Gallstones and Laparoscopic 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 disease 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.