Interventions for Clients with Problems of the Gallbladder and Pancreas
Disorders of the gallbladder and pancreas begin as single-organ processes, but the inflammatory response may extend to other organs if the primary disorder is not treated. This occurs because of the anatomic proximity of the liver, gallbladder, and pancreas and because the flow of bile from the liver through the biliary (gallbladder) ductal system may be impeded. Inflammation of the gallbladder, liver, or pancreas is caused by obstruction in the biliary system from gallstones, edema, stricture, or tumors. For example, gallstones impacted in the cystic duct cause cholecystitis; gallstones lodged in the ampulla of Vater impede the flow of bile and pancreatic secretions, which can result in pancreatitis.
BILIARY DISORDERS
Cholecystitis
OVERVIEW
The two most common problems that occur within the biliary tree are stone formation (cholelithiasis) and associated chronic inflammation (cholecystitis). Cholecystitis may occur as anacute or chronic inflammation of the gallbladder wall (Table 60-1). Chronic inflammation may be complicated by an acute attack if an obstruction is present.
Pathophysiology
ACUTE CHOLECYSTITIS
Acute cholecystitis (inflammation of the gallbladder) usually develops in association with cholelithiasis (gallstones). Either condition may occur singly, but they frequently occur together. Cholelithiasis is discussed in detail later in this chapter (p. 1333).
Acalculous cholecystitis (inflammation occurring in the absence of gallstones) is believed to be due to bacterial invasion via the lymphatic or vascular route. Escherichia coli is the most common causative bacterium found, but group D Streptococcus, Salmonella, and Staphylococcus may also be found.
Acute cholecystitis usually follows obstruction of the cystic duct by a stone, which evokes the inflammatory response. This response may be the result of a mechanical, chemical, or process (Greenberger & Isselbacher, 1998). When the gallbladder is inflamed, trapped bile is reabsorbed and acts as a chemical irritant to the gallbladder wall; that is, the bile has a toxic effect. The presence of bile, in combination with impaired circulation, edema, and distention of the gallbladder, causes ischemia of the gallbladder wall. The result is tissue sloughing with necrosis and gangrene. Perforation (rupture) of the gallbladder wall may occur. If the perforation is small and localized, an abscess may form. Peritonitis may result if the perforation is large.
In some cases, painful episodes of cholecystitis may be the result of organ or bile duct spasticity. The spasticity temporarily prevents the release of an adequate amount of bile for fat digestion.
■ CHRONIC CHOLECYSTITIS
Chronic cholecystitis results, possibly from repeated bouts of acute or subacute cholecystitis, when gallbladder muscle wall disease and inefficient emptying of bile by the gallbladder persist. Gallstones are almost always present. In chronic cholecystitis, the gallbladder becomes fibrotic and contracted, which results in decreased motility and deficient absorption.
Pancreatitis and cholangitis (inflammation of the common bile duct) can occur as complications of cholecystitis. Pancreatitis and cholangitis result from the backup of bile throughout the biliary tract. Bile obstruction leads to jaundice.
Jaundice (yellow discoloration of the skin and mucous membranes) and icterus (yellow discoloration of the sclerae) can occur in clients with acute cholecystitis but is most commonly seen in clients with chronic gallbladder inflammation. Impeded or obstructed bile flow caused by edema of the ducts or gallstones contributes to extrahepatic obstructive jaundice. Jaundice in cholecystitis may also be caused by direct liver involvement. Inflammation of the liver’s bile channels or bile ducts may cause intrahepatic obstructive jaundice, resulting in an increase in circulating levels of bilirabin, the principal pigment of bile.
When the concentration of bilirabin in the blood increases to greater than 2.5 mg/dL, jaundice occurs (Pagana & Pagana, 1998). In a person with obstructive jaundice, the normal flow of bile into the duodenum is blocked, allowing excessive bile salts to accumulate in the skin. This accumulation of bile salts leads to pruritus (itching) or a burning sensation. The bile flow blockage also prevents bilirabin from reaching the large intestine, where it is converted to urobilinogen. Because urobilinogen accounts for the normal brown color of feces, clay-colored stools result. Water-soluble bilirabin is normally excreted by the kidneys in the urine. When an excess of circulating bilirabin occurs, the urine becomes dark and foamy because of the kidneys’ effort to clear the bilirabin.
Etiology
The exact etiology of cholecystitis is unknown. In addition to the formation of gallbladder calculi, causes of acute cholecystitis include the following:
• Trauma
• Inadequate blood supply
• Prolonged anesthesia and surgery
• Adhesions
• Edema
• Neoplasms (tumors)
• Long-term fasting
• Prolonged dehydration
• Gallbladder trauma
• Prolonged immobility
• Excessive opioid use
Any condition that affects the regular filling or emptying of the gallbladder or causes “gallbladder shock” (a decrease in blood flow to the gallbladder) can result in acute cholecystitis. Cholecystitis has also been attributed to anatomic problems such as twisting or kinking of the gallbladder neck or cystic duct resulting in pancreatic enzyme reflux into the gallbladder.
Incidence/Prevalence
More than 20 million persons in the
WOMEN’S HEALTH CONSIDERATIONS The incidence of gallbladder disease is higher in women, especially Caucasian women. By age 60 years, nearly one third of obese women develop biliary disease (Allen & Phillips, 1997).
COLLABORATIVE MANAGEMENT
Assessment
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
Clients with acute cholecystitis frequently present with pain, although clinical manifestations vary in intensity and frequency (Chart 60-1).
The nurse or assistive nursing personnel obtains the client’s height and weight and determines his or her sex, age, race, and ethnic group. The nurse asks about food preferences and determines whether excessive fat and cholesterol are included in the diet. The client is asked whether any foods are not tolerated. The nurse asks whether any of the following gastrointestinal (GI) symptoms occur in relation to the intake of fatty food: flatulence, dyspepsia (indigestion), eructation (belching), anorexia, nausea, vomiting, and abdominal pain or discomfort.
The client is asked to describe the pain, including its intensity and duration, precipitating factors, and any measures that relieve it. The pain may be described as indigestion of varying intensity, ranging from a mild, persistent ache to a steady, constant pain in the right upper abdominal quadrant. The pain may radiate to the right shoulder or scapula. The abdominal pain of chronic cholecystitis may be vague and nonspecific. The usual pattern of more acute pain is episodic. Clients often refer to these episodes as “gallbladder attacks.”
The nurse also asks the client to describe his or her daily activity or exercise routines to determine whether his or her lifestyle is sedentary. The client is questioned whether there is a family history of gallbladder disease, since there is a familial tendency for biliary tract diseases. If the client is female, the nurse also determines whether estrogen replacement therapy (ERT) is being taken, because this therapy may contribute to biliary disorders.
Because of gallbladder tenderness, it is difficult to use abdominal palpation and percussion in assessment of the client with acute cholecystitis. With right subcostal palpation, pain increases with deep inspiration (Murphy’s sign). Guarding and rigidity, as well as rebound tenderness (Blumberg’s sign), are reliable indicators of peritoneal irritation.
Assessment for rebound tenderness and deep palpation are reserved for physicians and advanced-practice nurses. To elicit rebound tenderness, the nurse pushes his or her fingers deeply and steadily into the client’s abdomen, then quickly releases the pressure. Pain that results from the rebound of the palpated tissue indicates peritoneal inflammation. Deep palpation below the liver border in the right upper quadrant may reveal a sausage-shaped mass, representing the distended, inflamed gallbladder. Percussion over the posterior rib cage intensifies localized abdominal pain.
In chronic cholecystitis, clients may have insidious symptoms and may not seek medical treatment until late symptoms such as jaundice, clay-colored stools, and dark urine result from an obstructive process. Steatorrhea (fatty stools) occurs because fat absorption is decreased owing to the lack of bile. Bile is needed for the absorption of fats and fat-soluble vitamins in the intestine. As with any inflammatory process, the client may have an elevated temperature of 99° to 102° F (37° to 39° C), tachycardia, and dehydration from fever and vomiting.
DIAGNOSTIC ASSESSMENT
There are no laboratory tests specific for gallbladder disease. A differential diagnosis must rule out other diseases that may cause similar symptoms, such as peptic ulcer disease, gas-troesophageal reflux disorder, and pancreatitis. Serum levels of alkaline phosphatase, aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) may be elevated, indicating abnormalities in liver function. The direct (conjugated) and indirect (unconjugated) serum bilirubin levels are elevated if an obstructive process is present. An increased white blood cell (WBC) count with a left shift on the differential count indicates inflammation. If there is pancreatic involvement, serum and urine amylase levels are elevated.
Ultrasonography of the right upper quadrant is the best diagnostic test for cholecystitis and has largely replaced the older cholecystogram. It is safe, accurate, and painless. Acute cholecystitis is evidenced by edema of the gallbladder wall and pericholecystic fluid, both of which are determined by the ultrasound (Nahrwold, 1997). The health care provider may also order an upper GI radiographic series to rule out other causes of abdominal pain, such as gastritis and peptic ulcer disease. A cholecystogram may be ordered if other diagnostic tests are inconclusive.
A hepatobiliary scan with cholecystokinin using tech-netium 99mTc disofenin or mebrofenen can be performed to visualize the gallbladder and determine patency of the biliary system. The pretest fasting period for this scan can be as short as 4 hours, making it preferable to a diagnostic study that would require a longer fasting time. Visualization of the gallbladder excludes the diagnosis of acute cholecystitis with a high degree of certainty (Fischbach, 2000).
Interventions
Nonsurgical treatment measures prescribed during the acute phase of cholecystitis are directed at resting the inflamed gallbladder in an effort to reduce the inflammatory process and relieve the pain. Because of the risk of sepsis and perforation, however, acute cholecystitis is generally managed surgically.
NONSURGICAL MANAGEMENT. Nonsurgical measures to relieve pain include diet and drag therapy. The physician, nurse, and dietitian often collaborate when implementing these interventions.
DIET THERAPY. For clients with acute cholecystitis, the health care provider may recommend withholding food and fluids or modifying the diet by avoiding high-fat or high-volume meals. These dietary measures decrease stimulation of the gallbladder and help prevent pain, nausea, and vomiting. For clients with severe nausea and vomiting, decompression of the stomach may be necessary. A nasogastric tube is inserted to empty the stomach contents. (The nurse’s role in caring for a client with a nasogastric [NG] tube is described in Chapter 58.)
The nurse encourages the client with chronic cholecystitis to consume a low-fat diet to decrease stimulation of the gallbladder. Smaller, more frequent meals assist some clients in tolerating food better.
CRITICAL THINKING CHALLENGE
Your client with chronic cholecystitis tells you that she has been avoiding fried foods and eating a low-fat diet butHs still having problems with pain and nausea after meals. You want to determine what she considers to be “low fat.”
• Using a daily caloric intake of 1800 calories, determine how many grams of fat your client can consume to remain at a 20% total dietary fat intake.
• What questions might you ask her to evaluate whether she can determine the percentage of fat in a food item by reading the label?
• Who else might you involve in this client’s care to assist with nutritional needs?
DRUG THERAPY. For clients in severe pain, the health care provider may order opioid analgesics, such as meperidine hydrochloride (Demerol), to relieve abdominal pain and spasm. Traditionally, morphine has not been given, because it can cause spasms of the sphincter of Oddi and increase pain. Meperidine, like all opioids, can increase smooth muscle tone in the biliary tract as well, causing biliary and pancreatic secretions to decrease and bile duct pressure to increase. This can also result in spasms of the sphincter of Oddi (Pasero, 1998). Antispasmodic agents, such as anticholinergics (e.g., dicyclomine hydrochloride [Bentyl, Lomine^), may be used to relax the smooth muscles, preventing biliary contraction. Decreased muscle contraction minimizes secretions and assists in the reduction of pain. The health care provider usually prescribes antiemetics, such as trimethobenzamide hydrochloride (Tigan), to relieve nausea and vomiting.
SURGICAL MANAGEMENT. The usual surgical treatment of clients with acute and chronic cholecystitis is chole-cystectomy, the removal of the gallbladder. Two operative procedures are available to the surgeon for performing a cholecystectomy: the traditional open approach and laparo-scopic laser cholecystectomy.
TRADITIONAL CHOLECYSTECTOMY. Use of the traditional surgical approach has markedly declined during the past decade. The client undergoing this surgery is usually hospitalized for several days following the procedure.
Preoperative Care.
The nurse provides the usual preop-erative care in the operating suite on the day of surgery (see Chapter 17). The nurse reinforces teaching of aggressive measures to prevent respiratory complications. To minimize abdominal/incisional jarring during coughing, deep breathing, and turning, the nurse demonstrates splinting methods using a pillow or folded blanket. These clients, especially older adults and smokers, are also susceptible to postoperative atelectasis. The nurse instructs the client in the use of sustained maximal inspiration (SMI) devices, such as an incentive spirometer.
The importance of early mobilization in preventing complications is also emphasized. The nurse informs the client to expect to get out of bed the evening of surgery.
Operative Procedure. The surgeoot only removes the gallbladder through a right subcostal incision but also often explores the biliary ducts for the presence of stones. If the common bile duct is explored, the surgeon typically inserts a T-tube drain to ensure patency of the duct (Figure 60-1). Trauma to the common bile duct stimulates inflammation, which can impede bile flow and contribute to bile stasis. In addition, the surgeon usually inserts a drainage tube, such as a Jackson-Pratt (JP) drain. This drainage tube is positioned in the gallbladder bed to prevent fluid accumulation. The drainage is usually serosanguinous (serous fluid mixed with blood) and is bile stained in the first 24 hours postoperatively.
Postoperative Care. Postoperative incisional pain relief after a traditional cholecystectomy is usually achieved with meperidine hydrochloride (Demerol) using a patient-controlled analgesia (PCA) pump. The client participates in coughing and deep breathing exercises more readily when pain is minimized. Therefore the nurse plans for the coughing and deep breathing exercises to be performed when pain relief is optimal.
Antiemetics may be necessary for clients with episodes of postoperative nausea and vomiting. The nurse administers the antiemetic early, as ordered, to prevent retching associated with vomiting and thus decrease the incidence of pain related to muscle straining.
The nurse cares for the incision, the surgical drain, and the T-tube. The surgeon typically removes the surgical dressing and drain within 24 to 48 hours after surgery. The T-tube, however, may remain in place for 6 weeks or longer. Chart 60-2 highlights the important nursing care activities associated with the T-tube system.
The client usually receives nothing by mouth (NPO) for about 8 to 24 hours postoperatively. If gallbladder disease is severe, a nasogastric (NG) tube provides stomach decompression during this period. When peristalsis returns, the nurse removes the NG tube as ordered. The physician places the client on a clear liquid diet. The nurse gradually advances the diet from clear liquids to solid foods as tolerated. Within a day or two, the client resumes the ingestion of solid foods and is discharged to home.
The amount of fat allowed in the client’s diet after a chole-cystectomy depends on his or her tolerance of fat. In the early postoperative period, if bile flow is reduced, a low-fat diet may reduce discomfort and prevent nausea. For most clients, a special diet is not required. The nurse advises the client to eat nutritious meals and avoid excessive intake of fat. If the client is obese, the nurse recommends a weight reduction program. The nurse collaborates with the physician and the dietitian in planning the appropriate diet.
LAPAROSCOPIC CHOLECYSTECTOMY. Laparoscopic cholecystectomy, introduced in 1988, has quickly gained in popularity (see the Clinical Pathway on p. 1852). It is now considered the treatment of choice by many surgeons and is performed more often than the traditional open cholecystectomy. From studies involving 4000 clients undergoing a laparoscopic cholecystectomy, data show very positive results, including the following:
· • Complications are very uncommon.
· Conversion to open cholecystectomy is about 5%.
· The death rate is very low (i.e., <0.1%).
· Bile duct injuries are rare.
These data indicate why the laparoscopic approach to gallbladder removal is now considered the “gold standard” (Greenberger & Isselbacher, 1998).
Preoperative Care. The laparoscopic procedure is commonly done on an ambulatory care basis in a same-day surgery suite. The surgeon explains the procedure; the nurse answers questions and reinforces the physician’s instructions. There is no special preoperative preparation for the client. However, the physician typically orders the usual preoperative laboratory tests and requires the client to be on NPO status before the surgery. Chapter 17 describes general preoperative care for the client undergoing anesthesia.
Operative Procedure. The surgeon makes a 10-mm midline puncture at the umbilicus. The abdominal cavity is insufflated with 3 to
Postoperative Care. Removing the gallbladder with the laparoscopic technique reduces the risk of wound complications. Some clients have a problem with “free air pain” from carbon dioxide retention in the abdomen. The nurse teaches about the importance of early ambulation to promote absorption of the carbon dioxide. Far less opioid analgesia is necessary after the laparoscopic procedure than following the open cholecystectomy procedure.
The client is usually discharged from the hospital or surgery center within 1 day. Following laparoscopic surgery, the client can return to usual activities, including work, much sooner than if an open cholecystectomy had been done. Most clients are able to resume usual activities within 1 to 3 weeks.
Community-Based Care
■ HEALTH TEACHING
With a cholecystectomy, discharge teaching for the client and the family may include the following:
· Pain management
· Diet therapy
· Wound, drain, and incision care
· Activity restrictions
· Complication recognition
· Health care follow-up
In postoperative teaching and discharge planning, the nurse should include a supportive spouse, family member, or significant other to provide reinforcement of information and to assist the client in adhering to the treatment plan.
Diet therapy for the client who has undergone a cholecystectomy is based on his or her tolerance of fats. The nurse or dietitian consults with the client to develop a nutrition program that includes nutritious, well-balanced meals that include the client’s preferences, when possible. If the client has a poor tolerance of fats, a low-fat diet is developed and a list of foods to avoid is provided (Table 60-2). The dietitian may provide printed menu-planning guidelines. Some clients need to maintain a low-fat diet for 6 months or longer. They are advised to add fatty foods to the diet slowly and as tolerated.
If the client has problems tolerating three large meals a day, the nurse advises him or her to try smaller, more frequent meals. If the client is obese, a weight reduction diet is recommended and teaching is tailored to provide appropriate dietary guidelines.
Clients are leaving the hospital sooner after traditional open gallbladder surgery than in the past. Since a T-tube is usually left in place for several weeks, clients are sent home with the drainage systems intact. The nurse instructs the client and one or more family members to inspect the incision wound and the T-tube drainage site for signs and symptoms of inflammation. These signs and symptoms include redness, swelling, warmth, extreme tenderness, excessive drainage, and increased incisional pain. Any of these findings should be reported to the health care provider. The nurse provides oral and written instructions for drainage tube care (Chart 60-3).
The client with cholecystitis who either refuses or postpones surgery must be instructed on the signs of potential complications of chronic cholecystitis, including fever, recurrent abdominal pain, and jaundice. If these signs occur, the client should notify the health care provider for prompt medical care.
■ HOME CARE MANAGEMENT
After a traditional cholecystectomy, clients usually need short-term assistance with procuring foods, preparing meals, performing dressing changes, and caring for the T-tube. Clients who have undergone traditional gallbladder surgery may also need transportation to follow-up appointments with the health care provider. The surgeon typically allows these clients to return to their usual activities 4 to 6 weeks after surgery.
HEALTH CARE RESOURCES
For clients at home with a T-tube or for those older adults who cannot manage self-care, a home care nurse may be needed to provide support and follow-up nursing care and teaching. The home care nurse assesses the client’s adaptation to the treatment plan and evaluates wound healing and the integrity of the T-tube drainage system. The home care nurse also determines the need for further wound and skin care interventions and implements these interventions as needed.
Cholelithiasis
OVERVIEW
Cholelithiasis, the presence of one or more gallstones, is the most common disorder of the biliary tract. It is estimated that 16 to 20 million persons in the
Pathophysiology
PATHOLOGIC CHANGES
The exact pathophysiology of gallstone formation is not clearly understood, but abnormal metabolism of cholesterol and bile salts plays an important role in their formation. Contributing factors may include the following:
· Supersaturation of bile with cholesterol
· Excessive bile salt losses
· Decreased gallbladder-emptying rates
· Changes in bile concentration or bile stasis within the gallbladder
Gallstones may lie dormant within the gallbladder or may move to other areas of the biliary tree as the gallbladder empties and refills with bile. Stones may migrate and lodge within the gallbladder neck, cystic duct, or common bile duct, causing obstruction (Figure 60-2). Common bile duct stones are seen in 20% of clients age 65 years or older who undergo a cholecystectomy (Howard & Fromm, 1999). Gallstones interfere with or totally obstruct normal bile flow from the gallbladder to the duodenum, causing vascular congestion as a result of impeded venous return. Edema and congestion occur and contribute to the initial inflammatory process. When bile cannot flow from the gallbladder, the stasis of bile and local irritation from the gallstones lead to cholecystitis (see Acute Cholecystitis, p. 1327).
Cholangitis, usually associated with choledocholithiasis (common bile duct stones), involves infection of the bile ducts. Ascending cholangitis (inflammation of the biliary tree) occurs after bacterial invasion of the ducts. Bacterial invasion can lead to life-threatening suppurative cholangitis when symptoms are not recognized quickly and pus accumulates in the ductal system.
TYPES OF GALLSTONES
The gallbladder provides an excellent environment for the production of gallstones. In particular, the gallbladder only occasionally mixes its normally abundant mucus with its highly viscous, concentrated bile. The constant temperature within the gallbladder also contributes to stone formation by delaying bile emptying, causing biliary stasis.
Gallstones are composed of substances normally found in bile, such as cholesterol, bilirubin, bile salts, calcium, and various proteins. Stones are classified as either cholesterol stones or pigment stones.
Cholesterol stones form as a result of metabolic imbalances of cholesterol and bile salts. They are the most common type found in people in the
Etiology
There appears to be a familial tendency in the development of cholelithiasis, but this may be related to familial dietary habits (excessive dietary cholesterol intake) and familial sedentary lifestyles. Gallstones are seen more frequently in obese clients, probably as a result of impaired fat metabolism or increased cholesterol. Cholesterol-lowering drugs, which lower cholesterol levels in the blood, actually increase the amount of cholesterol secreted in bile. Age is also a factor, with people over 60 years of age more likely to develop stones than younger people. Persons with type 1 diabetes are also at increased risk for the development of gallstones and cholecystitis because of the higher levels of fatty acids (triglycerides) they generally have.
Cholesterol is increased following rapid weight loss, when the liver excretes extra cholesterol into bile (National Institutes of Health [NIH], 1999). The ingestion of low-calorie or liquid protein diets also increases the susceptibility to gallstone development. These diets cause the liberation of cholesterol from tissues; the cholesterol is excreted as crystals in bile. Alcohol abuse may contribute to the formation of pigment stones, but alcohol in moderate amounts appears to reduce the formation of cholesterol stones (Howard & Fromm, 1999). Cholelithiasis is seen with hemolytic blood disorders, with bowel disease such as Crohn’s disease, and after je-junoileal bypass surgery as a treatment of morbid obesity.
WOMEN’S HEALTH CONSIDERATIONS Women who are between 20 and 60 years of age are twice as likely to develop gallstones as men. Obesity is a major risk factor for gallstone formation, especially in women (NIH, 1999). Pregnancy tends to worsen gallstone formation. Pregnancy, as well as drugs such as estrogen and birth control pills, especially the older oral contraceptives, alter hormone levels and delay muscular contraction of the gallbladder, causing a decreased rate of bile emptying. The incidence of gallstones is higher in women who have had multiple pregnancies. Combinations of causative factors increase the incidence of stone formation, especially in women. For example, an obese pregnant woman or an obese woman taking birth control pills may be at higher risk.
Incidence/Prevalence
Cholelithiasis is common and a major source of morbidity in the
CULTURAL CONSIDERATIONS
Gallstones are more prevalent among Native Americans and less prevalent among African Americans and Asians (Howard & Fromm, 1999). There is a lower prevalence of gallbladder disease among both non-Hispanic black men and women than among non-Hispanic whites. Age-standardized prevalence is similar for non-Hispanic white and Mexican-American men, with both having a higher prevalence thaon-Hispanic black men. Among women, the age-adjusted prevalence is highest for Mexican Americans, followed by non-Hispanic whites and non-Hispanic blacks (Everhart et al., 1999).
COLLABORATIVE MANAGEMENT
Assessment
The same historical database may be obtained for clients with cholecystitis and clients with cholelithiasis (see Assessment [Cholecystitis], p. 1328).
■ PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
The severity of pain and presentation of symptoms in the client with cholelithiasis depend on the following:
• Whether the stone is stationary or mobile
• The size and location of the stone
• The degree of obstruction
• The presence and extent of inflammation
Initially, the pain of cholelithiasis is usually a steady, mild ache located in the mid-epigastric area. It may increase in intensity and duration and may radiate to the right shoulder or back.
The severe pain of biliary colic is produced by obstruction of the cystic duct of the gallbladder. When a stone is moving through or is lodged within the duct, tissue spasm occurs in an effort to mobilize the stone through the small duct. This intense pain may be so severe that it is accompanied by tachycardia, pallor, diaphoresis, and prostration (extreme exhaustion).
Any of the clinical manifestations seen in acute or chronic cholecystitis may occur in cholelithiasis (see Chart 60-1). Clients with chronic cholecystitis and acute ductal obstruction may experience the excruciating pain of biliary colic as well. On inspection, the nurse may observe jaundice of the skin, the sclerae, the upper palate, and the oral mucous membranes. If gallstones occlude the common bile duct, prolonged severe inflammation and hepatic damage may also occur.
LABORATORY ASSESSMENT
There are no specific laboratory tests for cholelithiasis. As in cholecystitis, the serum alkaline phosphatase, lactate dehy-drogenase, aspartate aminotransferase, and direct and indirect bilirubin levels may be elevated. Examination of a random stool specimen may reveal absent or low levels of urobilino-gen in the feces, indicating an obstructive process. If pancreatic involvement accompanies gallstone impaction, serum and urine amylase levels are elevated.
RADIOGRAPHIC ASSESSMENT
Calcified gallstones are easily visualized on abdominal x-ray examination. An oral cholecystogram is diagnostic when the stones are radiopaque. The physician may order intravenous (IV) cholecystography (or cholangiography) for clients who are unable to absorb oral contrast agents.
Percutaneous transhepatic cholangiography is a fluoro-scopic examination of the biliary ducts and may be used to diagnose obstructive jaundice and visualize stones located in the ducts. Another procedure that permits radiographic visualization of the common bile duct, pancreas, pancreatic ducts, and biliary tree is endoscopic retrograde cholangiopancre-atography (ERCP). This procedure permits the gastroenterol-ogist to precisely pinpoint the nature of a biliary obstruction (see Chapter 53).
OTHER DIAGNOSTIC ASSESSMENT
Ultrasound of the gallbladder is most commonly used procedure to determine the presence of stones within the biliary system. It is the test of choice to confirm the diagnosis of cholelithiasis and to distinguish between obstructive and nonobstructive jaundice. Ultrasound of the gallbladder is reported to be 95% accurate in detecting gallstones. The exception is a stone found in the common bile duct, which rarely visualizes on ultrasound (McCormick, 1999).
CRITICAL THINKING CHALLENGE
Your client is scheduled to have an ERCP performed in the morning. She asks you how this test can determine what is causing her jaundice and expresses concern about the safety of the procedure.
• What answers will you give this client?
• How does jaundice develop in the biliary tree?
• What does an ERCP detect that other procedures might not?
• What are the risks and benefits of an ERCP?
• What postprocedure assessments and interventions will you need to provide for this client?
• Interventions
The health care provider may institute supportive medical treatment for clients with cholelithiasis as an alternative to or before surgical removal of the gallbladder and gallstones.
NONSURGICAL MANAGEMENT. Two thirds of gallstones are asymptomatic, or silent (Howard & Fromm, 1999). Asymptomatic stones are usually managed conservatively with no medical or surgical intervention. Acute pain occurs when the gallstones partially or totally obstruct the cystic or common bile duct. Measures aimed at resting the inflamed gallbladder are the same as those discussed earlier for cholecystitis, p. 1330. Symptomatic clients require treatment, and laparoscopic cholecystectomy is the accepted first-line therapy (Strasberg, 1999).
DIET THERAPY. In general, the client must adhere to a low-fat diet to prevent further pain of biliary colic. If gallstones are causing an obstruction of bile flow, the health care provider may order replacement of fat-soluble vitamins (such as vitamins A, D, E, and K) and the administration of bile salts to facilitate digestion and vitamin absorption. Food and fluids are withheld if nausea and vomiting occur.
DRUG THERAPY. Pain caused by acute obstruction with gallstones necessitates opioid analgesia with meperidine hy-drochloride (Demerol). Older clients should not be given De-merol, since it can cause acute confusion and nausea (see Chapter 7). Morphine is usually not used, because it is thought to cause biliary spasm and constrict the sphincter of Oddi. Antispasmodic or anticholinergic drugs, such as dicy-clomine hydrochloride (Bentyl, ЬогшпеФ), may be given to relax smooth muscles and decrease ductal tone and spasm. The health care provider orders antiemetics to control nausea and vomiting.
Bile acid therapy has been effective in dissolving gallstones, depending on the type of stones. Chenodeoxycholic acid (CDCA; chenodiol; Chenix) and ursodeoxycholic acid (UDCA; ursodiol; Actigall) reduce cholesterol stones by un-saturating bile. They do this by decreasing coupling of cholesterol to bile acids during bile secretion. Adverse effects of chenodiol are lessened when it is used in conjunction with ursodiol. Ursodiol has also been shown to be effective in preventing gallstone formation after rapid weight loss (Howard & Fromm, 1997).
Chenodiol may be effective in dissolving small stones (less than
Ursodiol has been approved in the
Obstructive jaundice in cholelithiasis is caused by impeded bile flow through the common bile duct as a result of gallstone obstruction. It may lead to excessive accumulation of bile salts in the skin. As a result, severe pruritus may occur. Cholestyramine resin (Questran) binds with bile acids in the intestine, forming an insoluble compound that is excreted in the feces. As a result, excessive bile salts are removed and itching is decreased. The nurse mixes the powder form of the drug with fruit juices or milk. It should be given before meals and at bedtime.
EXTRACORPOREAL SHOCK WAVE UTHOTRIPSY. .Extracorporeal shock wave lithotripsy is a noninvasive procedure that is used for ambulatory treatment of clients with gallstones in some settings. A machine-a lithotriptor-generates powerful shock waves to shatter the gallstones (Figure 60-3). Clients who are eligible for this procedure must have three or fewer cholesterol stones (measuring between 5 and
Eating and drinking are permitted almost immediately after the procedure. The nurse informs the client that right upper quadrant discomfort after the procedure is not uncommon and usually resolves within 2 days. Acetaminophen (Tylenol, Exdol^) often provides enough analgesia to relieve this pain.
PERCUTANEOUS TRANSHEPATIC BILIARY CATHETER INSERTION. The physician may insert a percutaneous transhepatic biliary catheter under fluoroscopic guidance. This procedure decompresses obstructed extrahepatic ducts so that bile can flow (Figure 60-4). It is primarily used for inoperable hepatic, pancreatic, or bile duct carcinoma. It may be a nonsurgical alternative for the treatment of biliary obstruction caused by gallstones and hepatic dysfunction associated with obstructive jaundice and biliary sepsis in high-risk candidates. Nursing care associated with this treatment is outlined in Chart 60-4.
SURGICAL MANAGEMENT. One of several procedures may be indicated in the surgical treatment of cholelithiasis (Table 60-3). Cholecystotomy (an opening into the gallbladder) may be an emergency procedure to remove gallstones. This procedure is often performed for older adults or critically ill clients with life-threatening multisystem problems who may not withstand a prolonged surgical procedure. If the stones are located in the common bile duct, a choledo-cholithotomy (an incision into the common bile duct to remove stones) is necessary. If the common bile duct is explored, the surgeon inserts a T-tube drain into the duct to ensure patency until edema subsides and to allow collection of excessive bile drainage.
A simple, traditional cholecystectomy or laparoscopic cholecystectomy is performed when stones are confined to the gallbladder. The common bile duct and adjacent ducts are explored for the presence of additional stones or stone fragments and crystals in this traditional surgical procedure (see Surgical Management [Cholecystitis], p. 1330).
After a cholecystectomy with T-tube placement, the surgeon may prescribe drugs to stimulate bile production and bile flow from the liver. Bile flow promotes the digestion and absorption of fat, fat-soluble vitamins, and cholesterol in the duodenum. Hydrocholeretic drugs, such as dehydrocholic acid (Decholin, Cholan), which are synthetic bile salts, increase the solubility of cholesterol. Increased solubility prevents the accumulation of cholesterol in bile, thereby decreasing the recurrence of biliary calculi and promoting drainage of (potentially infected) bile through the T-tube drainage system.
A postoperative T-tube cholangiogram can identify retained stones. Direct visualization of the biliary tract with an endoscope (choledochoscopy) enables the removal of calculi retained in the common bile duct. Choledochoscopy is performed through a T-tube or an incision into the common bile duct. An instrument with a small, basket-like attachment is used to snare the stone (Figure 60-5). If this method fails, a fiberoptic endoscope is introduced into the duodenum. An incision into the papillae (papillotomy) allows the stone to pass into the duodenum.
The preoperative and postoperative nursing care measures for the client undergoing gallbladder surgical procedures are the same as those for cholecystectomy (see Surgical Management [Cholecystitis], p. 1330).
An additional therapeutic intervention, used in conjunction with or as an alternative to surgery, is endoscopic retrograde cholangiopancreatography (ERCP). This procedure allows the physician radiographic visualization of the common bile duct, gallbladder, pancreatic ducts, and biliary tree. Since about 10% of clients with gallstone disease also have common duct stones, this can be significant (Nahrwold, 1997). If gallstones are present in the bile ducts, the surgeon may use ERCP in removing them, either before or during gallbladder surgery.
• Community-Based Care
Most often, the client with cholelithiasis has surgery and is discharged to home postoperatively (see Community-Based Care [Cholecystitis], p. 1332). The client may be discharged with a T-tube drainage system intact (see Chart 60-3) and will need instructions as to care of the tube.
The nurse provides information to the client and family about the potential for postcholecystectomy syndrome, in which the clinical manifestations of biliary tract disease occur following cholecystectomy in a small percentage of clients. Postcholecystectomy syndrome is caused by residual or recurring calculi, inflammation, or stricture of the common bile duct.
The nurse instructs the client to report symptoms of biliary tract disease, including jaundice of the skin or sclera, darkened urine, light-colored stools, pain, fever, or chills, to the physician or nurse practitioner.
Cancer of the Gallbladder
OVERVIEW
Primary cancer of the gallbladder is rare and is more common in women than in men (NIH, 1999). Adenocarcinoma and squamous cell carcinoma of the gallbladder account for the majority of gallbladder cancers. They typically infiltrate the liver and ducts, as well as the gallbladder. These rare gallbladder carcinomas appear more frequently in clients with pre-existing chronic cholecystitis and cholelithiasis.
The diagnosis of gallbladder cancer is difficult. Early symptoms, when present, are insidious in onset and similar to those of chronic cholecystitis and cholelithiasis. Characteristic signs and symptoms include the following:
· Anorexia
· Weight loss
· Nausea
· Vomiting
· General malaise
· Jaundice
· Hepatosplenomegaly
· Chronic, progressively severe epigastric or right upper quadrant pain
A moderately tender, irregularly shaped mass may be palpated. Often, gallbladder carcinoma is discovered during other procedures for diagnosis of suspected cholecystitis or during cholecystectomy.
COLLABORATIVE MANAGEMENT
The prognosis for the client with cancer of the gallbladder is poor. Three treatments are used: surgery, radiation therapy, and chemotherapy. Surgical intervention, when performed, is usually extensive. A bile drainage tube (transhepatic biliary catheter) may be inserted to relieve symptoms such as jaundice and itching (see Chart 60-4).
PANCREATIC DISORDERS
Acute Pancreatitis
OVERVIEW
Acute pancreatitis is a serious and, at times, life-threatening inflammatory process of the pancreas. This inflammatory process is brought on by a premature activation of pancreatic enzymes that destroy ductal tissue and pancreatic cells, resulting in autodigestion and fibrosis of the pancreas. The pathologic changes occur in variable degrees. The severity of pancreatitis depends on the extent of inflammation and tissue destruction. Pancreatitis can range from mild involvement evidenced by edema and inflammation to necrotizing hemor-rhagic pancreatitis (NHP). NHP affects approximately 20% of clients diagnosed with pancreatitis and is characterized by diffusely bleeding pancreatic tissue with fibrosis and tissue death.
Pathophysiology
The pancreas is unusual in that it functions as both an ex-ocrine gland and an endocrine gland. The primary endocrine disorder is diabetes and is discussed in Chapter 65. The ex-ocrine function of the pancreas is responsible for secreting enzymes that assist in the breakdown of starches, proteins, and fats. These enzymes are normally secreted in the inactive form and become activated once they enter the intestine. Early activation (i.e., activation within the pancreas rather than the intestinal lumen) results in the inflammatory process of pancreatitis. Direct toxic injury to the pancreatic cells and the production and release of pancreatic enzymes (trypsin, elas-tase, phospholipase A, lipase, and kallikrein) result from the obstructive damage. Following pancreatic duct obstruction, increased pressure within the pancreas and the pancreatic ducts may contribute to ductal rupture, allowing spillage of trypsin and other enzymes into the pancreatic parenchymal tissue. In acute pancreatitis, four major pathophysiologic processes occur: lipolysis, proteolysis, necrosis of blood vessels, and inflammation.
LIPOLYSIS
The hallmark of pancreatic necrosis is enzymatic fat necrosis of the endocrine and exocrine cells of the pancreas caused by the enzyme lipase. Fatty acids are released during this lipoly-tic process and combine with ionized calcium to form a soap-like product. The initial rapid lowering of serum calcium levels is not readily compensated for by the parathyroid gland. Because the body needs ionized calcium and cannot use bound calcium, hypocalcemia occurs.
PROTEOLYSIS
The pathogenesis of pancreatitis involves autodigestion of the pancreatic parenchyma by the enzymes normally produced by the pancreas (Figure 60-6). Trypsin is the key element that activates all other proteolytic enzymes involved in autodigestion.
The agent that triggers the premature activation of trypsin to trypsinogen has not been identified and is being investigated. Proteolysis involves the splitting of proteins by hydrolysis of the peptide bonds, resulting in the formation of smaller polypeptides. Proteolytic activity may lead to thrombosis and gangrene of the pancreas. Pancreatic destruction may be localized and confined to one area or may involve the entire organ.
NECROSIS OF BLOOD VESSELS
Elastase is activated by trypsin and causes elastic fibers of the blood vessels and ducts to dissolve. The necrosis of blood vessels results in bleeding, ranging from minor bleeding to massive hemorrhage of pancreatic tissue. Another pancreatic enzyme, kallikrein, causes the release of vasoactive peptides, bradykinin, and a plasma kinin known as kallidin. These substances contribute to vasodilation and increased vascular permeability, further compounding the hemorrhagic process. This massive destruction of blood vessels by necrosis may lead to generalized hemorrhage with blood escaping into the retroperitoneal tissues. The client with hemorrhagic pancreatitis is critically ill, and extensive pancreatic destruction and shock may lead to death. The majority of deaths in clients with acute pancreatitis result from irreversible shock.
INFLAMMATION
The inflammatory stage occurs when leukocytes cluster around the hemorrhagic and necrotic areas of the pancreas. A secondary bacterial process may lead to suppuration (pus formation) of the pancreatic parenchyma or the formation of an abscess (see later discussion under Pancreatic Abscess, p. 1348). Infected lesions that are mild may be absorbed. When infected lesions are severe, calcification and fibrosis occur. If the infected fluid becomes walled off by fibrous tissue, a pancreatic pseudo-cyst is formed (see Pancreatic Pseudocyst, p. 1349).
THEORIES OF ENZYME ACTIVATION
Several theories explain the triggering mechanisms leading to enzyme activation in acute pancreatitis. The bile reflux (“common channel”) theory proposes that an obstruction of the common channel (the common bile duct and the main pancreatic duct channel) causes reflux of the bile into the pancreatic tissue, resulting in activation of the enzymes. Not all biliary tracts have this common channel. If the common channel is absent, the common bile and pancreatic ducts merge into the duodenum separately.
According to the hypersecretion-obstruction theory, the pancreatic duct ruptures and the resulting disruption or tearing of the cell membrane allows pancreatic secretions and enzymes to leak back into the parenchymal tissue.
The exact mechanism of alcohol-induced changes in pancreatitis is unclear. Alcohol appears to have a direct metabolic effect on the pancreas by stimulating hydrochloric acid and se-cretin production, which in turn stimulates exocrine functions of the pancreas. Alcohol also causes edema of the duodenum and the ampulla of Vater, obstructing the flow of pancreatic secretions. Alcohol may decrease the tone of the sphincter of Oddi and cause sphincter spasm and duodenal reflux.
According to the fourth theory, reflux of duodenal contents can occur from biliary tract disease, gallstones in the bile duct (causing the sphincter of Oddi to dilate), or a generalized loss of tone caused by alcohol ingestion. Duodenal contents can enter the pancreatic duct through the weakened sphincter, activating the pancreatic enzymes.
The generalized abdominal pain of acute pancreatitis is related to peritoneal irritation. Ductal release of digested proteins and lipids into the peripancreatic tissues, along with stretching of the pancreatic tissue, causes the seepage of these substances into the mesentery. The resultant peritonitis stimulates the sensory nerves, contributing to intense pain in the back and flanks.
COMPLICATIONS OF ACUTE PANCREATITIS
Acute pancreatitis may result in severe, life-threatening complications. Jaundice occurs from swelling of the head of the pancreas, which impedes bile flow through the common bile duct. The bile duct may also be compressed by calculi or a pancreatic pseudocyst. The resulting total bile flow obstruction causes severe jaundice. Transient hyperglycemia occurs as a result of the release of glucagon, as well as the decreased release of insulin due to damage to the pancreatic islet cells. Total destruction of the pancreas may occur, leading to type 1 diabetes.
Left lung pleural effusions frequently develop in the client with acute pancreatitis. Amylase effusions probably occur when exudate containing pancreatic enzymes passes from the peritoneal cavity into the pleural cavity via the transdiaphrag-matic lymph channels. Atelectasis and pneumonia may also occur, especially in older clients.
Multisystem organ failure occurs as a sequela to necrotiz-ing hemorrhagic pancreatitis (NHP). The client is at risk for acute respiratory distress syndrome (ARDS). This severe form of pulmonary edema is caused by disruption of the alveolar-capillary membrane and is a serious complication of acute pancreatitis. (See Chapter 32 for a discussion of ARDS.) In acute pancreatitis, pulmonary failure accounts for more than half of all deaths that occur in the first 7 days of the disease.
Coagulation defects are another major potential complication and may result in death. Complex physiologic changes in the pancreas cause the release of necrotic tissue and enzymes into the bloodstream, resulting in altered coagulation. Disseminated intravascular coagulation (DIC) involves hyperco-agulation of the blood, with consumption of clotting factors and the development of microthrombi.
Shock in acute pancreatitis results from peripheral vasodi-lation from the released vasoactive substances and the retroperitoneal loss of protein-rich fluid from proteolytic digestion. Hypovolemia may result in decreased renal perfusion and acute renal failure (Ambrose & Dreher, 1996). Paralytic ileus results from peritoneal irritation and seepage of pancreatic enzymes into the abdominal cavity.
Etiology
In many cases, the cause of pancreatitis is not known. Many factors can produce injury to the pancreas. The most commonly cited factor is biliary tract disease, with gallstones accounting for 45% of the cases of obstructive pancreatitis. Excessive alcohol ingestion is the second leading cause of pancreatitis. Iatrogenic acute pancreatitis may occur as a result of trauma from surgical manipulation after biliary tract, pancreatic, gastric, and duodenal procedures, such as cholecystec-tomy, the Whipple procedure, and partial gastrectomy. The trauma may also originate as a complication of the diagnostic procedure endoscopic retrograde cholangiopancreatography (ERCP).
Other etiologic factors include the following:
· Trauma: external (blunt trauma) or operative
· Pancreatic obstruction: tumors, cysts, or abscesses; abnormal organ structure
· Metabolic disturbances: hyperlipidemia, hyperparathyroidism, or hypercalcemia
· Renal disturbances: failure or transplantation
· Familial, inherited conditions
· Penetrating gastric or duodenal ulcers, resulting in peritonitis
· Viral infections, such as coxsackievirus В infection
Toxicities of drags, including opiates, sulfonamides, thiazides, steroids, and oral contraceptives (The exact mechanism by which these and other drugs cause pancreatitis is unknown.)
Incidence/Prevalence
Steady, heavy alcohol intake for 5 to 10 years is likely to be the causative mechanism for pancreatitis in the middle-aged male population. Episodes of acute pancreatitis usually occur after excessive alcohol consumption. These attacks are especially common during holidays and vacations. Women are affected most often after cholelithiasis and biliary tract disturbances.
Death occurs in approximately 10% of clients with acute pancreatitis, but with early diagnosis and treatment, mortality can be reduced. Death occurs at a higher rate in older adults and in clients with postoperative pancreatitis. The prognosis for recovery is favorable for pancreatitis associated with biliary tract disease and poor if pancreatitis accompanies alcoholism. Mortality rises as high as 60% wheecrosis and hemorrhage occur.
COLLABORATIVE MANAGEMENT
Assessment
HISTORY
The nurse asks the client with acute pancreatitis to indicate why he or she is seeking medical treatment. Most often, the client will indicate that the primary reason is to obtain relief from abdominal pain. The nurse asks whether the abdominal pain is related to alcohol ingestion or to eating a high-fat meal. Information about alcohol usage should be obtained, including the amount of alcohol consumed during what period of time (i.e., years of consumption, how much usually consumed over a particular period). Because of the familial connection, the client is questioned about a family history of alcoholism, pancreatitis, or biliary tract disease. The client is questioned concerning a personal history of any biliary tract problems, such as gallstones. The nurse further determines whether any abdominal surgical interventions, such as chole-cystectomy, or diagnostic procedures, such as ERCP, have been performed recently.
The nurse assesses for the presence of other medical problems known to cause pancreatitis, including peptic ulcer disease, renal failure, vascular disorders, hyperparathy-roidism, and hyperlipidemia. The client is also asked whether any recent viral infections have been experienced and to list all prescription and over-the-counter (OTC) drugs taken recently.
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
Diagnosis of pancreatitis is made on the basis of the clinical presentation combined with the results of diagnostic studies—both laboratory and radiologic. Clinical manifestations of acute pancreatitis vary widely and depend on the severity of the inflammation. Typically, a client is diagnosed after presenting with abdominal pain that localizes in the epigastrium; this is the most frequent symptom. The nurse obtains in-depth data about the pain. The client often states that the pain had a sudden onset, is located in the mid-epigastric area or the left upper quadrant, and radiates to the back, left flank, or left shoulder. The pain is described as intense and continuous, and it is worsened by lying in the supine position. Often the client finds relief by assuming the fetal position (with the knees drawn up to the chest and the spine flexed) or when sitting upright and bending forward. The client may report weight loss resulting from nausea and vomiting.
When performing an abdominal assessment, the nurse may find the following on inspection:
· Generalized jaundice
· Gray-blue discoloration of the abdomen and periumbilical area (Cullen’s sign)
· Gray-blue discoloration of the flanks (Turner’s sign), caused by pancreatic enzyme leakage to cutaneous tissue from the peritoneal cavity
The nurse listens for bowel sounds; absent or decreased bowel sounds usually indicate paralytic (adynamic) ileus. On light palpation, the nurse notes abdominal tenderness, rigidity, and guarding as a result of peritonitis. A palpable mass may be found if a pancreatic pseudocyst is present. Pancreatic ascites creates a dull sound on percussion.
The nurse or assistive nursing personnel takes and records vital signs frequently to assess for elevated temperature, tachycardia, and decreased blood pressure. The nurse uses these data to determine whether complications are occurring. Respiratory complications, such as left lung pleural effusions, atelectasis, and pneumonia, are common in clients with acute pancreatitis. The nurse auscultates the lung fields for adventitious sounds or decreased aeration and observes respirations for dyspnea or orthopnea.
Changes in vital signs may indicate the life-threatening complication of shock. Hypotension and tachycardia may result from pancreatic hemorrhage, excessive fluid volume shifting, or the toxic effects of abdominal sepsis from enzyme damage. The nurse also observes the client for changes in behavior and sensorium that may be related to alcohol withdrawal, hypoxia, or impending sepsis with shock (see Chapter 8).
PSYCHOSOCIAL ASSESSMENT
Excessive alcohol intake, particularly in men, is the most frequent cause of acute pancreatitis. Thus the nurse tactfully explores the client’s alcohol intake history. The nurse and the client should discuss the intake of alcohol and the reasons for overindulging. The nurse asks him or her when increased drinking episodes occur, in particular, whether binges occur during holidays, vacations, or weekends or revolve around particular activities, such as card playing or television viewing. The client is also questioned about any recent traumatic event that may have contributed to increased alcohol consumption, such as the death of a family member or a job loss.
LABORATORY ASSESSMENT
Diagnostic laboratory abnormalities are found in clients with acute pancreatitis (Table 60-4). Elevated serum amylase and lipase levels provide the most reliable and direct evidence of pancreatitis and are considered the cardinal diagnostic signs. Serum amylase levels usually increase within 12 to 24 hours and remain elevated for 3 to 4 days. A level of serum amylase three times greater thaormal is considered diagnostic (Greenberger, Toskes, & Isselbacher, 1998). Persistent elevations of amylase levels may be an indicator of pancreatic abscess or pseudocyst (Lillemoe & Yeo, 1998). Lipase is considered more specific in the diagnosis of acute pancreatitis, and serum levels remain elevated for up to 2 weeks. Because serum lipase levels stay elevated for such a long time, the physician may find this test useful in diagnosing clients who are not examined until several days after the initial onset of symptoms (Hoerner, 1998). Amylase levels in 24-hour urine collections are also elevated as a result of the inflammatory process and remain elevated for up to 2 weeks. However, testing the urine for amylase is no more sensitive than testing serum amylase, yet it costs more. Testing the urine is sometimes useful several days after the onset of symptoms, when serum amylase levels may be normal.
If pancreatitis is accompanied by biliary dysfunction (biliary pancreatitis), serum bilirubin and alkaline phosphatase levels are usually elevated. A sensitive indicator of biliary obstruction in acute pancreatitis is serum alanine aminotrans-ferase (ALT). A threefold or greater rise in concentration offers a 95% probability that the diagnosis of acute biliary pancreatitis is correct (Baillie, 1997). Elevated white blood cell (WBC) count and serum glucose levels are also common in acute pancreatitis (Ambrose & Dreher, 1996).
Decreased serum calcium and magnesium levels are seen with fat necrosis. Calcium levels may fall and remain decreased for 7 to 10 days. Calcium levels that consistently remain below 8 mg/dL are associated with a poor prognosis.
RADIOGRAPHIC ASSESSMENT
Computed tomography (CT) provides a reliable diagnosis of acute pancreatitis. This noninvasive technique may be used to rule out pancreatic pseudocyst or ductal calculi. A chest x-ray film may reveal elevation of the left side of the diaphragm or pleural effusion.
OTHER DIAGNOSTIC ASSESSMENT
In the client with severe pancreatitis, ultrasonography and magnetic resonance imaging (MRI) of the pancreas help confirm an initial clinical impression, assess for the degree of inflammatory resolution, and reveal common bile duct dilation from obstruction or gallstones. The MRI study provides information similar to that of a CT scan but is much more costly and offers no real advantage over the less expensive CT scan. Endoscopic retrograde cholangiopancreatography (ERCP) is the definitive test to locate and assist in removing gallstones, which can cause biliary pancreatitis.
Analysis
В COMMON NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS
The following are priority nursing diagnoses for clients with acute pancreatitis:
1. Acute Pain related to the effects of pancreatic inflammation and enzyme leakage
2. Imbalanced Nutrition: Less Than Body Requirements related to the effects of pancreatic dysfunction, nausea, vomiting, and anorexia
ADDITIONAL NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS
In addition to the commoursing diagnoses, clients with acute pancreatitis may have one or more of the following:
· Deficient Fluid Volume related to pancreatic hemorrhage, fluid loss into the abdominal cavity, nausea and vomiting, and nasogastric suctioning
· Ineffective Breathing Pattern related to the complications of pleural effusion or acute respiratory distress syndrome (ARDS)
· Risk for Activity Intolerance related to debilitation
· Anxiety related to severe illness and a possibly chronic condition
· Disturbed Sleep Pattern related to pain
· • Impaired Health Maintenance related to insufficient knowledge about the illness, its causative factors, and the treatment plan
The client with pancreatitis is also likely to have the following collaborative problems:
· Potential for Hyperglycemia
· Potential for Hemorrhage
· Potential for Fluid and Electrolyte Imbalances
Planning and Implementation
acute pain
PLANNING: EXPECTED OUTCOMES. The client with acute pancreatitis is expected to verbalize a decrease in or absence of abdominal pain, as evidenced by a pain scale measurement.
INTERVENTIONS. Abdominal pain is the prominent symptom of pancreatitis. The main focus of nursing care is aimed at reducing discomfort and pain by the use of interventions that decrease gastrointestinal (GI) tract activity, thus decreasing pancreatic stimulation. Pain assessment to measure the effectiveness of these interventions is a vital nursing activity (see Chapter 7).
NONSURGICAL MANAGEMENT. The health care team initially attempts to achieve pain relief with nonsurgical interventions, which include fasting, drug therapy, and comfort measures.
FASTING. In an effort to rest the pancreas and reduce pancreatic enzyme secretion, food and fluids are withheld in the acute period. The health care provider orders IV fluid administration to maintain hydration. IV replacement of calcium and magnesium may also be needed.
Nasogastric drainage and suction may be necessary to decrease gastric distention and to suppress pancreatic secretion. Gastric decompression prevents gastric digestive juices from flowing into the duodenum. Because paralytic (adynamic) ileus is a common complication of acute pancreatitis, prolonged nasogastric intubation may be necessary. The nurse assesses for the presence of bowel sounds before the nasogastric (NG) tube is removed.
ANALGESIC ADMINISTRATION (Chart 60-5). Pain management for acute pancreatitis should begin with titration of opioids by means of patient-controlled analgesia (PCA). Meperidine hydrochloride (Demerol) is the traditional drug of choice for relieving abdominal pain associated with acute pancreatitis (Pasero, 1998). It has been thought that meperidine hydrochloride causes less incidence of spasm of the smooth musculature of the pancreatic ducts and the sphincter of Oddi than do other analgesics such as morphine. In mild pancreatitis, the pain usually subsides in 3 to 4 days; however, with severe acute pancreatitis, the abdominal pain and tenderness may persist for up to 2 weeks. The nurse individualizes dosages and intervals of medication administration, as ordered, according to the severity of the disease and the symptoms.
DRUG THERAPY. Decreasing the release of secretin reduces pancreatic stimulation. Secretin is an intestinal hormone that stimulates the release of enzymes and bicarbonate from the pancreas when acidic chyme is present in the duodenum. Antacids administered orally or via an NG tube that is clamped for 20 minutes after administratioeutralize gastric secretions. The health care provider orders histamine receptor antagonists, such as ranitidine hydrochloride (Zantac), to decrease hydrochloric acid production so that pancreatic enzymes are not activated by an acidic pH. These interventions are also useful in reducing the occurrence of GI erosion and bleeding. Anticholinergics, such as dicyclomine hydrochloride (Bentyl, Lornine*1), are indicated to decrease vagal stimulation, decrease GI motility, and inhibit pancreatic enzyme and bicarbonate volume and concentration. However, these drugs can cause unwanted side effects for older adults, such as dry mouth, urinary retention, constipation, and acute confusion.
An additional drug that the care provider might prescribe is somatostatin or its synthetic analog, octreotide. This is used in an attempt to decrease pancreatic activity, but the research is still inconclusive about the value of the therapy (Uhl et al., 1999).
COMFORT MEASURES. Helping the client to assume the fetal position (with the legs drawn up to the chest) may decrease the abdominal pain of pancreatitis.
If the client has an NG tube in place, the nurse provides frequent oral hygiene measures to keep mucous membranes moist and free of inflammation or crusting. Because of the drying effect of anticholinergic drugs and the absence of oral fluids, the mouth and oral cavity may be extremely dry, resulting in considerable discomfort.
Lowering the client’s anxiety level may also substantially reduce pain. The nurse provides thorough explanations of procedures. The client is encouraged to express the emotions and responses he or she is experiencing. The nurse also provides reassurance and diversional activities, such as television, music, and reading material, and encourages visitors to direct attention away from the pain.
SURGICAL MANAGEMENT. Surgical intervention for acute pancreatitis is usually not indicated. However, complications of pancreatitis, such as pancreatic pseudocyst and abscess, may necessitate surgical drainage. If pancreatitis is caused by biliary tract obstruction, the physician may perform a laparotomy (abdominal exploration) for common bile duct exploration and the release of obstruction.
PREOPERATIVE CARE. In addition to general preopera-tive care measures, the client usually has an NG tube inserted and begins receiving IV fluids. The client is frequently in pain, a factor that inhibits the learning process, so the nurse provides preoperative teaching in a manner that takes the client’s comfort level into account. Postoperative reminders may be needed to reinforce the preoperative learning. The nurse teaches the client to expect a pancreatic drainage tube and explains its care during the postoperative period. The nurse needs to be certain that the client knows how to promote respiratory function by turning, coughing, deep breathing, and splinting the incision, because the client with an NG tube is at increased risk for postoperative pulmonary complications.
OPERATIVE PROCEDURE. When an abscess or pseudo-cyst is incised and drained with the client under general anesthesia, drainage tubes are inserted, sutured in place, and connected to low suction (
POSTOPERATIVE CARE. Postoperatively, the nurse monitors drainage tubes for patency by assessing for kinks in
the tubes and maintaining the ordered drain suction pressure and system integrity. The nurse records the output amount from the drain and describes the character of the drainage. A sump type of drain is usually inserted. The nurse ascertains that the drain is functioning, as indicated by a hissing noise from the sump lumen.
The nurse provides meticulous skin care and dressing changes. The client is monitored for the first signs of redness or skin irritation because pancreatic enzyme drainage is particularly excoriating to the skin. Skin barriers, such as a Stom-ahesive wafer around the drainage tube, are applied to repel drainage from the skin. The nurse continually assesses for further deterioration of the tissue. The nurse should also collaborate with an enterostomal therapist (ET) for measures to promote skin integrity, such as the use of individualized ostomy appliances and the application of topical ointments.
IMBALANCED NUTRITION: LESS THAN BODY
REQUIREMENTS
PLANNING: EXPECTED OUTCOMES. The client with acute pancreatitis is expected to have sufficient nutritional intake to maintain body weight and a decrease in pancreatic stimulation.
INTERVENTIONS. The client is maintained on NPO status in the early stages of pancreatitis. Clients who have severe pancreatitis and are unable to eat for 7 to 10 days should receive nutritional support in the form of total parenteral nutrition (TPN) (see Chapter 61) or total enteral nutrition (TEN) (see the Evidence-Based Practice for Nursing box on p. 1345). If TPN is used for nutritional support, the nurse assesses for glucose intolerance by monitoring for elevated blood glucose levels. This is extremely important in clients with pancreatitis because pancreatic dysfunction affects the release of insulin. Some clients require insulin administration during an acute episode of the disease. TEN has been shown to produce fewer episodes of glucose elevation and other complications associated with the use of TPN yet has been shown to be as effective in maintaining nutritional status (Scolapio et al., 1999).
When food is tolerated during the recovery phase, the health care provider generally orders small, frequent, moderate- to high-carbohydrate, high-protein, low-fat meals. Foods should be bland with little spice; caffeine-containing foods (tea, coffee, cola, and chocolate), as well as alcohol, should be avoided.
To boost caloric intake, commercial liquid nutritional preparations, such as Ensure and Isocal, supplement the diet. If caloric intake is less than desired, an NG tube may be required for additional nutrition via enteral feedings. The health care provider may also prescribe fat-soluble and other vitamin and mineral replacement supplements.
Community-Based Care
HEALTH TEACHING
Educatioeeds to be started early in the hospitalization period—as soon as the acute episodes of pain have subsided. The nurse assesses the client’s and family members’ or significant others’ knowledge of the disease.
The goals of discharge planning and education are to avoid further episodes of pancreatitis and prevent progression to a chronic disease. The nurse instructs the client to abstain from alcohol to prevent further pain attacks and extension of inflammation and pancreatic insufficiency. The client is told that if alcohol is consumed, pain will be experienced, and further autodigestion of the pancreas will lead to chronic pancreatitis and chronic pain.
The nurse also teaches the client to notify the health care provider after discharge to home if acute abdominal pain or biliary tract disease (as evidenced by jaundice, clay-colored stools, or darkened urine) occurs. These signs and symptoms are possible indicators of complications or disease progression.
HOME CARE MANAGEMENT
Home care preparation will need to be individualized for each client’s circumstances. Some clients with acute pancreatitis may be severely weakened from their acute illness and need to confine activity to one floor, limiting stair climbing and other strenuous activities until they regain their strength.
HEALTH CARE RESOURCES
Clients with acute pancreatitis require visits by a home care nurse if the hospital course was complicated. In these cases, home care may be needed for wound care and assistance with activities of daily living (ADLs). The client requires medical follow-up with the primary care physician or nurse practitioner for monitoring of the disease process. For clients with alcoholism, the nurse provides information about groups such as Alcoholics Anonymous (AA). Family members may attend support groups such as Al-Anon and Al-Ateen.
Evaluation: Outcomes
The nurse evaluates the care of the client with acute pancreatitis on the basis of the identified nursing diagnoses and collaborative problems. The expected outcomes include that the client will:
Experience an alleviation of or reduction in abdominal pain, as indicated by self-report
• Maintain adequate nutritional intake with a decrease in pancreatic stimulation as evidenced by weight maintenance Not experience a recurrence of pancreatitis
Chronic Pancreatitis
OVERVIEW
Chronic pancreatitis is a progressive, destructive disease of the pancreas, characterized by remissions and exacerbations (recurrence). Inflammation and fibrosis of the tissue contribute to pancreatic insufficiency and diminished function of the organ. Chronic pancreatitis usually develops after repeated episodes of alcohol-induced acute pancreatitis. It may also be associated with chronic obstruction of the common bile duct. Chronic pancreatitis may develop in the absence of a known acute disorder. Relief of pain, prevention of recurrence of attacks, prevention of complications, and nutritional support are the principal interventions.
Pathophysiology
К TYPES OF CHRONIC PANCREATITIS
Alcohol-induced chronic pancreatitis is also known as chronic calcifying pancreatitis (CCP). Protein precipitates that plug the ducts and lead to ductal obstruction, atrophy, and dilation characterize CCP. As the protein plugging becomes diffuse, the epithelium of the ducts undergoes histologic changes, resulting in metaplasia (cell replacement) and ulcer-ation. This inflammatory process causes fibrosis of the pancreatic tissue. Intraductal calcification and marked pancreatic parenchymal destruction develop in the late stages. Cystic sacs containing pancreatic secretions and enzymes form on the pancreas. The organ becomes hard and firm as a result of acinar cell atrophy and pancreatic insufficiency.
Chronic obstructive pancreatitis develops from inflammation, spasm, and obstruction of the sphincter of Oddi. Inflammatory and sclerotic lesions occur in the head of the pancreas and around the ducts, causing an obstruction and backflow of pancreatic secretions (see Complications of Acute Pancreatitis, p. 1340).
PATHOLOGIC CHANGES
Pancreatic insufficiency in chronic pancreatitis is characterized by the loss of exocrine function. Pancreatic exocrine secretion is divided into two components: aqueous bicarbonate and enzymes.
The aqueous component neutralizes the duodenal contents and pancreatic enzymes that are essential to normal digestion and absorption. Most clients with chronic pancreatitis have a decreased output of pancreatic secretion and bicarbonate. Pancreatic enzyme secretion must be reduced by more than 80% to produce steatorrhea resulting from severe malabsorp-tion of fats. These characteristic stools are pale, bulky, and frothy and have an offensive odor. The action of colonic bacteria on unabsorbed lipids and proteins is responsible for the foul odor. On inspection of the stools, the fat content is visible. In severe chronic pancreatitis, stool fat output may exceed 40 g/day.
Fat malabsorption also contributes to weight loss and muscle wasting (a decrease in muscle mass) and leads to general debilitation of the client. Protein malabsorption results in a “starvation” edema of the feet, legs, and hands caused by decreased levels of circulating albumin.
The loss of pancreatic endocrine function is responsible for the development of frank diabetes mellitus in clients with chronic pancreatic insufficiency. (See Chapter 65 for a complete discussion of diabetes mellitus.)
The client with chronic pancreatitis may have pulmonary complications, such as pleuritic pain, pleural effusions, and pulmonary infiltrates. Pancreatic ascites may impede diaphragmatic excursion and decrease lung expansion, resulting in impaired ventilation. In the ill client with chronic pancreatitis, acute respiratory distress syndrome (ARDS) may develop.
Etiology
The cause of chronic calcifying pancreatitis is persistent excessive alcohol intake that results in repeated episodes of acute pancreatitis. The most common cause of chronic obstructive pancreatitis is cholelithiasis and biliary tract disease, which results in persistent inflammation. Other etiologic factors include pancreatic pseudocyst, postoperative ductal scarring, and cancer of the pancreas or duodenum. All of these factors can produce obstruction of the pancreatic duct. Prolonged starvation and prolonged use of parenteral feedings for nutritional support can result in pancreatic atrophy, causing pancreatic insufficiency.
Incidence/Prevalence
Approximately 75% of clients with chronic pancreatitis are alcoholics (Price & Wilson, 1997). Alcohol-induced pancreatitis is predominantly found in men, but the incidence in women is increasing. In women, chronic pancreatitis occurs more commonly among those with biliary tract disease (cholecystitis and cholelithiasis). The age at occurrence of chronic pancreatitis is variable but is usually between 45 and 60 years.
COLLABORATIVE MANAGEMENT
Assessment
Clinical manifestations of chronic pancreatitis differ from those of an acute inflammation, although, as with acute pancreatitis, abdominal pain is the major clinical manifestation (Chart 60-6). The client with chronic pancreatitis typically describes the pain as a continuous burning or gnawing dullness with periods of acute exacerbation. The pain is intense and relentless. The frequency of acute exacerbations may increase as the pancreatic fibrosis develops.
The nurse performs the same abdominal assessment as for clients with acute pancreatitis, but the findings may not be as significant. Abdominal tenderness is less intense. A mass may be palpated in the left upper quadrant, which is indicative of a pancreatic pseudocyst or abscess (see Pancreatic Pseudocyst, p. 1349). Massive pancreatic ascites may be present, producing dullness on abdominal percussion. Because respiratory complications can accompany the condition, the nurse auscultates the lung fields for adventitious sounds or decreased aeration and observes for dyspnea or orthopnea.
The client is asked to collect a random stool specimen, if able, or is asked to describe the stools. The nurse or assistive nursing personnel collects the stool specimen for diagnostic studies. The specimen may show the presence of steatorrhea (foul-smelling fatty stools that may increase in volume as pancreatic insufficiency progresses and lipase production decreases). The nurse observes the client’s anal area for excoriation resulting from frequent defecation.
The client may also experience weight loss, muscle wasting, jaundice, dark urine, and the signs and symptoms of diabetes mellitus, such as polyuria, polydipsia, and polyphagia.
In chronic pancreatitis, significant laboratory findings include normal or moderately elevated serum amylase and lipase levels. Obstruction of the intrahepatic bile duct can cause elevated serum bilirubin and alkaline phosphatase levels. Transient elevations in serum glucose levels are common and can be detected by blood glucose monitoring, both fasting and nonfasting.
The only definitive diagnostic test for chronic pancreatitis is the identification of calcification of pancreatic tissue in a biopsy specimen. If direct evidence of chronic pancreatitis is needed, the health care provider may order a secretin test. This test is the most sensitive and specific for chronic pancreatitis, other than histology (Amann, DiMagno, & Rubin, 1997). Secretin is an intestinal hormone that stimulates hepatic and pancreatic secretion. In this test, the client swallows a double-lumen gastrointestinal (GI) tube. The tip should reach the duodenum, with the proximal lumen port located in the stomach. Gastric and duodenal contents are aspirated before and after IV administration of secretin. An abnormal volume of enzymes and bicarbonate in the GI contents may indicate chronic pancreatitis.
Abdominal ultrasonography is also a helpful diagnostic tool, especially to reveal pseudocysts. Endoscopic retrograde cholangiopancreatography (ERCP) may reveal ductal system abnormalities, such as calcification and strictures, or it may delineate the presence of pancreatic pseudocyst.
Interventions
The focus of caring for the client with chronic pancreatitis is to manage pain, assist in maintaining a sufficient nutritional intake, and prevent recurrence.
NONSURGICAL MANAGEMENT. Nonsurgical interventions primarily include drug and diet therapy.
DRUG THERAPY.
The major intervention for the pain of chronic pancreatitis is drug therapy. In addition, the nurse teaches the client to avoid ingesting irritating substances that can precipitate pain.
Analgesic Administration (see Chart 60-5). The nurse medicates the client, as ordered, according to the assessment of the level and intensity of pain and evaluates the effectiveness of the drug intervention. Opioid analgesia with meperi-dine hydrochloride (Demerol) is most frequently used, but opioid dependency may become a problem. Nonopioid analgesics may be tried to relieve pain. (See Chapter 7 for other interventions for chronic pain.)
If drug dependency becomes a problem, behavior modification programs and drug and alcohol counseling will be necessary. The health care provider may need to admit these clients to drug and alcohol dependency programs.
Enzyme Replacement. Pancreatic enzymes (non-enteric-coated preparations) are essential dietary supplements (Chart 60-7). These are given with meals or snacks to aid in digestion and absorption of fat and protein. Drugs such as pan-creatin (Donnazyme) and pancrelipase (Cotazym, Viokase, or Pancrease) are prescribed in capsule, tablet, or powder form and contain amylase, Hpase, and protease. Cotazym also contains calcium carbonate to increase depleted calcium levels. The nurse mixes the powder form in applesauce or fruit juice to make it more palatable. Enzyme preparations should not be mixed with foods containing proteins, because the enzymatic action dissolves the food into a watery substance. The nurse advises the client to wipe his or her lips with a wet towel to prevent the skin irritation and breakdown that residual enzymes can cause.
The dosage of pancreatic enzymes depends on the severity of the malabsorption and maldigestion. The nurse records the number and consistency of stools per day to monitor the effectiveness of enzyme therapy. If pancreatic enzyme treatment is effective, the stools should become less frequent and less fatty.
Insulin Therapy. If the client has diabetes, the health care provider prescribes insulin or oral hypoglycemic agents for glucose control. Clients maintained on total par-enteral nutrition (TPN) are particularly susceptible to labile glucose levels and may require regular insulin additives to the solution. The nurse closely monitors blood glucose levels so that hyperglycemia is controlled and insulin or diabetic shock is prevented. The use of glucometers allows frequent assessment of glucose levels during the critical insulin dosage adjustment period. The nurse, laboratory technician, or assistive nursing personnel checks glucose levels every 2 to 4 hours.
Other Drugs. The health care provider may also prescribe histamine receptor antagonists, such as ranitidine hydrochloride (Zantac), to decrease gastric acid. Gastric acid destroys the Hpase needed to break down fats. Controlling the acidity of the stomach with H2 blockers or proton pump inhibitors or neutralizing stomach acid with oral sodium bicarbonate may enhance the effectiveness of the non-enteric-coated enzyme therapy. Subcutaneous octreotide (Sandostatin), a growth hormone similar to somatostatin, is ordered by some physicians if pain and diarrhea persist (Amann, DiMagno, & Rubin, 1997).
DIET THERAPY. Protein and fat malabsorption results in significant weight loss and decreased muscle mass in the client with chronic pancreatitis. Therefore the nutritional interventions for acute pancreatitis are also relevant for the chronic phase of pancreatitis. The client often limits food intake to avoid the recurrent pain, which is exacerbated by eating. For this reason, nutrition maintenance is often difficult to achieve, and clients are provided with TPN or total enteral nutrition (TEN), including vitamin and mineral replacement.
For long-term dietary management, the client needs an increased number of calories, up to 4000 to 6000 calories/day, to maintain weight. Foods high in carbohydrates and protein also assist in the healing process. Foods high in fat are avoided because they cause or increase diarrhea.
SURGICAL MANAGEMENT. Surgery is not a primary intervention for the treatment of chronic pancreatitis. However, it may be indicated for intractable abdominal pain, incapacitating relapses of pain, or complications such as abscesses and pseudocysts.
The underlying pathologic changes determine the procedure indicated. The surgeon incises and drains an abscess or pseudocyst. Cholecystectomy or choledochotomy (incision of the common bile duct) may be indicated if biliary tract disease is an underlying cause of pancreatitis. If the pancreatic duct sphincter is fibrotic, the surgeon performs a sphinctero-tomy (incision of the sphincter) to enlarge it.
In pancreaticojejunostomy, the pancreatic duct is opened and anastomosed to the jejunum to relieve obstruction. This procedure relieves pain and preserves pancreatic tissue and function. The preoperative and postoperative care is similar to that for clients undergoing the Whipple procedure (discussed under Surgical Management [Pancreatic Carcinoma], p. 1352). A partial pancreatectomy (resection of the pancreas) may be performed for clients with advanced pancreatitis or disabling pain. Vagotomy with gastric antrectomy is done to alter nerve stimulation and decrease pancreatic secretion. (See Chapter 56 for a discussion of nursing care.)
In a few cases, pancreas transplantation may be done. However, this procedure is performed most often for clients with severe, uncontrolled diabetes. Chapter 65 discusses pancreas transplantation.
• Community-Based Care
The care of the client with pancreatitis usually involves a case manager or discharge planner. A community-based case manager may continue to follow the client while he or she requires health care in the home or other community-based setting.
В HEALTH TEACHING
Because there is no known cure for chronic pancreatitis, client and family education is aimed at preventing further acute exacerbations of this chronic disease, providing long-term care, and promoting health maintenance (Chart 60-8).
DIET THERAPY. The nurse instructs the client to avoid known precipitating factors, such as the ingestion of caf-feinated beverages and alcohol. The dietitian elicits the participation of the family or significant other in diet planning and food preparation. Diet teaching focuses on eating bland, low-fat, frequent meals and avoiding rich, fatty foods. The nurse and dietitian stress the importance of dietary compliance and the need for increased nutritional intake to prevent acute exacerbations of this chronic illness. Written instructions on diet and pancreatic enzyme replacement therapy are essential.
The nurse instructs the client and family members or significant others on the importance of adhering to the pancreatic enzyme replacement treatment. The client must take the prescribed enzymes with meals and snacks to aid in the digestion of food and promote the absorption of fats and proteins. The nurse teaches the client to take the enzymes at the beginning of the meal and to report to the health care provider any increase in the occurrence of foul-smelling, frothy, fatty stools; abdominal distention; and cramping so that pancreatic enzyme replacement may be increased as needed. The client should report any skin excoriation or breakdown so that therapeutic interventions to promote skin integrity can be instituted.
SKIN CARE. The frequency of defecation (whether continent or incontinent) poses challenging skin care problems. The nurse instructs the client to keep his or her skin dry and free of the abrasive fatty stools, which are excoriating to the skin. The skin should be cleaned thoroughly after each stool and a soothing emollient, such as Sween, applied. To prevent breakdown and maintain skin integrity, a skin barrier may be needed. Many products on the market, such as zinc oxide cream, actively repel stool from the skin.
DRUG THERAPY. The client and family members must be able to state the desired effect of the prescribed drugs, the schedule for drug administration, and potential side effects. The nurse provides written guidelines as reinforcement.
If the client develops diabetes mellitus as a result of chronic pancreatitis from endocrine dysfunction, management of elevated glucose levels after discharge from the hospital may necessitate oral hypoglycemic agents or insulin injections. If this is the case, the client and the family require in-depth teaching concerning diabetes, its signs and symptoms, medical management, insulin administration, dietary management, urine and blood glucose monitoring, and general care information. (See Chapter 65 for a discussion of diabetes.)
HOME CARE MANAGEMENT
Client with chronic pancreatitis are usually discharged to home, but some may require care in a long-term care setting. If the client is discharged to home, the activity area should be limited to one floor until he or she regains strength and can increase activity. Toilet facilities must be easily accessible because of chronic steatorrhea and frequent defecation. If toilet facilities are not available in the immediate rest area, a bedpan or bedside commode is obtained for the home.
HEALTH CARE RESOURCES
Chronic illnesses are devastating for families. The high costs of medical insurance, medical treatment, and drug therapy cause serious financial problems. Often the client with chronic pancreatitis is unable or unwilling to work. Case management to coordinate care and manage resources should be instituted during hospitalization and continue throughout the course of the illness.
The client may require home visits by nurses and a dietitian, depending on the severity of the chronic health problems and home maintenance and support needs. The home care nurse assesses the client for pain management, compliance with dietary guidelines and alcohol abstinence, the effectiveness of pancreatic enzyme therapy, and psychosocial adaptation to a chronic illness.
The nurse or case manager refers the client to a counselor or a self-help group, such as Alcoholics Anonymous, if appropriate.
Pancreatic Abscess
OVERVIEW
Pancreatic abscesses are the most serious complication of pancreatitis. If untreated, they are always fatal. After surgery, the recurrence rate is higher than 30%. The abscesses form from collections of purulent liquefaction of the necrotic pancreas.
Pancreatic abscesses occur after severe acute pancreatitis, exacerbations of chronic pancreatitis, or biliary tract surgery. The development of either a single abscess or multiple abscesses results from extensive inflammatory necrosis of the pancreas that is readily invaded by infectious organisms such as Escherichia coli, Klebsiella, Bacteroides, Staphylococcus, and Proteus. They can erode through the retroperitoneum into the bowel mesentery, the mediastinum, the pleural space, or the pelvis.
COLLABORATIVE MANAGEMENT
Clients with pancreatic abscesses often appear more seriously ill than clients with pseudocysts. Clinical manifestations are similar; however, the temperature in clients with abscesses may spike to as high as 104° F (40° C). Blood cultures are helpful in revealing the infective organism. Pleural effusions commonly accompany these abscesses. Ultrasonography and computed tomography (CT) cannot differentiate between pancreatic pseudocysts and abscesses.
Pancreatic abscesses that are not surgically drained carry 100% mortality. Drainage should be performed as soon as possible to prevent sepsis. Antibiotic treatment alone does not resolve the abscess. Mortality remains as high as 60%, even after surgical drainage. Many clients require multiple drainage procedures for recurrent abscesses.
CRITICAL THINKING CHALLENGE Your client has indicated that he does not intend to alter his alcohol consumption after he is discharged; in fact, he plans to stop for a drink at his favorite bar on the way home after his release later today.
• What is the connection between alcohol consumption and chronic pancreatitis?
• What questions should you ask to determine if the client fully understands the connection between alcohol consumption and recurrence of pancreatitis?
• What resources are available to him to assist with his alcohol problem?
» What nursing diagnoses are appropriate for this client?
Pancreatic Pseudocyst
OVERVIEW
Pancreatic pseudocysts develop as a complication of acute or chronic pancreatitis. Pseudocysts occur in pancreatitis caused by alcoholism, biliary tract disease, or abdominal or surgical trauma. Pseudocysts develop in 10% to 20% of all people with pancreatitis, and mortality is reported at approximately 10%. Pancreatic pseudocysts, or false cysts, are so named because, unlike true cysts, they do not have an epithelial lining. Pseudocysts are encapsulated saclike structures that form on or surround the pancreas. The pseudocyst wall is inflamed, vascular, and fibrotic. It may contain up to several liters of straw-colored or dark-brown viscous fluid, the enzymatic ex-udate of the pancreas.
COLLABORATIVE MANAGEMENT
A pseudocyst can be palpated as an epigastric mass in approximately 50% of cases. The primary presenting symptomis epigastric pain radiating to the back. Other common clinical manifestations include abdominal fullness, nausea, vomiting, and jaundice.
Pseudocysts are diagnosed, and their growth and resolution monitored, by serial abdominal ultrasonographic examination or CT.
Complications of pseudocyst formation include the following:
· Hemorrhage
· Infection
· Obstruction of the bowel, biliary tract, or splenic vein Abscess
· Fistula formation
· Pancreatic ascites
Pseudocysts may spontaneously resolve, or they may rupture and produce hemorrhage. Surgical intervention is necessary if the pseudocyst does not resolve within 6 weeks or if complications develop. To accomplish internal drainage, the surgeon creates an opening (ostomy) between the pseudocyst and the stomach (cystogastrostomy), the jejunum (cystojejunostomy), or the duodenum (cystoduodenostomy). To provide external drainage, the surgeon inserts a sump drainage tube to remove pancreatic secretions and exudate. Pseudocysts recur in almost 10% of cases. Pancreatic fistulas are common after surgery, and skin breakdown from corrosive pancreatic enzymes presents a major nursing care challenge (see earlier discussion under Postoperative Care [Acute Pancreatitis], p. 1344).
Pancreatic Carcinoma
OVERVIEW
Cancer of the pancreas is one of the leading causes of cancer-related mortality, accounting for 2% to 3% of the new cancer cases each year and for high costs of care (see the Cost of Care Box on p. 1350) (Sauter & Coleman, 1999).
Pathophysiology
Pancreatic tumors usually originate from epithelial cells of the pancreatic ductal system. If the tumor is discovered in the early stages, the tumor cells may be localized within the glandular organ; however, this is highly unlikely. Most often, the tumor is discovered in the late stages of development and may be a well-defined mass or is diffusely spread throughout the pancreas.
The tumor may be a primary cancer, or it may result from metastasis from cancers of the lung, breast, thyroid, or kidney or from skin melanoma. Primary pancreatic tumors are generally adenocarcinomas and grow in well-differentiated glandular patterns. Pancreatic adenocarcinoma grows rapidly and spreads to surrounding organs (stomach, duodenum, gallbladder, and intestine) by direct extension and invasion of lymphatic and vascular systems. This highly metastatic lesion may eventually invade the lung, peritoneum, liver, spleen, and lymph nodes.
Clinical manifestations depend on the site of origin or metastasis. The head of the pancreas is the most common site of pancreatic carcinoma. Pancreatic tumors are usually small lesions with poorly defined margins. Jaundice results from tumor compression and obstruction of the common bile duct and from gallbladder dilation, causing the organ to enlarge.
Carcinomas of the body and tail of the pancreas are usually large and invade the entire tail and body. These tumors may be palpable abdominal masses, especially in the thin client. Through metastatic spread via the splenic vein, metastasis to the liver may cause hepatomegaly (enlargement of the liver up to two to three times its normal size). Carcinomas of the body and tail spread more extensively than do pancreatic head carcinomas, with invasion of the retroperitoneum, vertebral column, spleen, adrenal glands, colon, or stomach. Regardless of where it originates, pancreatic cancer spreads rapidly through the lymphatic and venous systems to other organs.COST OF CARE
PANCREATIC CANCER
Cost of Care
• Pancreatic cancer ranks eleventh in incidence and fifth in
cancer deaths.
• Total annual costs are $4.9 billion (men: $3.0 billion; women:
$1.9 billion).
• Total direct costs are $881.3 million.
Seventy-one percent of total direct costs ($627.1 million/ $881.3 million) are for those over 65 years of age.
Total hospital costs are 77% ($679.5 million/$881.3 million) of total direct costs.
• Total indirect costs are $4 billion.
Sixty-three percent of total indirect costs ($2518.43 million/$4018 million) are for those ages 45 to 64 years.
Mortality costs are $3.7 billion—93% ($3739 million/$4018 million) of indirect costs.
Implications for Nursing
Pancreatic cancer has a very low 5-year survival rate, with fewer than 20% of those diagnosed with the disease living longer than 1 year after diagnosis.
Because of the cost of pancreatic cancer, it is important that nurses recognize the role they might play in the disease process. This role might include education about the risk factors and prevention, the signs and symptoms, and the treatment of this cancer.
Currently there is no known diagnostic test to predict the individual’s susceptibility to this type of cancer, nor is the exact cause of the cancer known.
Nurses need to identify who might be at higher risk to develop pancreatic cancer: some possible links have been shown with alcohol and caffeine consumption and with a diet high in fat and protein. Smoking is known to be the single most significant risk factor for the development of pancreatic cancer. These actual and potential risk factors are modifiable.
Thrombophlebitis is a common complication of pancreatic carcinoma. It is attributed to an increase in the levels of thromboplastic factors in the blood. Necrotic products of the pancreatic tumor are believed to have thromboplastic properties, resulting in the blood’s hypercoagulable state. Thrombophlebitis is due to the client’s confinement to bed and extensive surgical manipulation.
Etiology
The exact cause of pancreatic carcinoma is unknown. The single most prevalent risk factor for pancreatic cancer is smoking. A diet high in protein and fat, and high coffee or alcohol consumption have also been investigated for possible linkage to the disease, but current studies do not show a substantial direct association (Sauter & Coleman, 1999). Research does support the theory that there might be a genetic link in the development of pancreatic cancer (McEwen et al., 1996).
Incidence/Prevalence
Approximately 28,000 people develop pancreatic cancer each year, and an equal number of people die from the disease each year. Fewer than 20% of persons diagnosed with pancreatic cancer survive longer than 1 year after diagnosis (Sauter & Coleman, 1999).
CONSIDERATIONS FOR OLDER ADULTS
BBS The incidence of pancreatic cancer increases with age. The highest rates of incidence are in people between 60 and 70 years of age, and pancreatic cancer rarely develops before the age of 50. The disease appears to be somewhat more common in men than in women, but the difference is slight (Mayer, 1999; Sauter & Coleman, 1999).
CULTURAL CONSIDERATIONS
Cancer of the pancreas occurs in developed countries. A slightly higher incidence among African Americans has been reported (Sauter & Coleman, 1999).
COLLABORATIVE MANAGEMENT
Assessment
Pancreatic cancer often presents in an insidious manner. The presenting symptoms depend somewhat on the location of the tumor. The first clue to the presence of pancreatic carcinoma may be the appearance of jaundice, which is a late sign (Chart 60-9). Jaundice appears as the initial sign in two thirds of all cases because the gallbladder and liver are commonly involved. As the tumor spreads, the green-gold skin color associated with obstructive jaundice progressively worsens. On noting the jaundice, the nurse asks the client whether the color of the stool and urine has changed. As a result of the obstructive process, the stool is clay colored and the urine is dark and frothy. The nurse inspects the skin for dryness and scratch marks, indicating pruritus from jaundice. The nurse also assesses the sclerae for icterus and the mucous membranes for signs of jaundice.
By the time jaundice appears, the pancreatic carcinoma is usually in an advanced stage. The nurse may be able to palpate the enlarged gallbladder and liver. In advanced cases of pancreatic carcinoma, the tumor may be palpated as a firm, fixed mass in the left upper abdominal quadrant or epigastric region.
The most common complaint, often misinterpreted by even the client, is fatigue. This fatigue is described as a diminished energy level and an increased need for rest disproportionate to the level of activity. The client notices an inability to perform usual physical or intellectual activities (Sauter & Coleman, 1999).
The nurse questions the client about abdominal pain, which may be described as a vague, constant dullness in the upper abdomen and nonspecific in nature. Pain, a common early complaint in clients with pancreatic carcinoma, is also present in the advanced stages of the disease. Pain may be related to eating or activity.
In addition, the nurse asks the client whether he or she is experiencing pain in other areas of the body. Referred back pain may be caused by pressure on the nerve plexus. Some clients have leg or calf pain with swelling and redness as a result of thrombophlebitis, a complication of pancreatic carcinoma.
The nurse or assistive nursing personnel weighs the client and determines the extent of weight loss and whether it has occurred rapidly. The client is questioned about food intake and intolerances. Anorexia accompanied by early satiety, nausea, flatulence, and vomiting is common. Gastrointestinal (GI) bleeding may develop from esophageal or gastric varices caused by the tumor pressing on the portal vein. A new diagnosis of diabetes is found in some clients.
The nurse performs a general abdominal assessment. In particular, the nurse percusses the abdomen for dullness, which may indicate the presence of ascites. Pancreatic ascites occurs in the advanced stages of the disease process.
There are no specific blood tests to diagnose pancreatic carcinoma. Serum amylase and lipase levels, as well as alkaline phosphatase and bilirubin levels, are elevated. The degree of elevation depends on the acuteness or chronicity of the pancreatic and biliary damage. Elevated carcinoembryonic antigen (CEA) levels occur in 80% to 90% of clients with pancreatic carcinoma. This test may provide early information about the presence of tumor cells. CA 19-9, another tumor marker, has been found to be the most useful serologic test for monitoring a proven diagnosis and for continuing surveillance of the cancer for potential spread or recurrence (Sauter & Coleman, 1999).
Computed tomography (CT) can confirm the presence of a tumor and can differentiate the tumor from a cyst. Biopsy of pancreatic tissue by needle aspiration reveals malignant cells. Ultrasonographic examinations do not distinguish pancreatic carcinoma from other pancreatic disorders. Endoscopic retrograde cholangiopancreatography (ERCP) visualization and cytologic study of aspirate provide the most definitive diagnostic data. An alternative to ERCP is a percutaneous trans-hepatic biliary cholangiogram with placement of a percutaneous transhepatic biliary drain (PTBD). This drain decompresses the blocked biliary system by draining bile, either internally or externally (Sauter & Coleman, 1999). Aspiration of pancreatic ascitic fluid by abdominal paracentesis may reveal malignant cells and elevated amylase levels. When the secretin test is performed (see Assessment [Chronic Pancreatitis], p. 1346), duodenal or gastric aspirate may reveal malignant cells.
Interventions
Management of the client with pancreatic carcinoma is geared toward preventing tumor spread and decreasing pain. These measures are not curative, only palliative (see the Evidence-Based Practice for Nursing box above). The cancers are often multifocal and recur despite treatment.
NONSURGICAL MANAGEMENT. As in other types of cancer, chemotherapy or radiation is used to relieve pain. (See Chapter 25 for nursing interventions associated with these treatment modalities.)
DRUG THERAPY. In an effort to keep the pain under control, the nurse medicates the client, as ordered, with opi-oid analgesics (usually morphine) and provides comfort measures before the pain escalates and reaches a peak. Because of the poor prognosis, drug dependency is not a consideration. High doses of opioid analgesics may be needed for the intense abdominal and back pain that occurs in the late stages of the disease.
Chemotherapeutic interventions for pancreatic carcinoma have had limited success. Combining agents such as fluo-rouracil (5-fluorouracil [5-FU]) and carmustine (BCNU) has been more successful than single-agent chemotherapy. 5-FU is an antimetabolite that interferes with deoxyribonucleic acid (DNA) synthesis in rapidly dividing cells. Two other drugs prescribed are mitomycin (Mutamycin), an antitumor antibiotic that inhibits synthesis of ribonucleic acid (RNA), and streptozocin (Zanosar), a nitrosourea that interferes with the replication of DNA. The nurse provides the client with symptomatic relief and comfort measures for the adverse effects of chemotherapeutic agents, such as nausea and vomiting. Gem-citabine, a new cytotoxic agent, is now standard therapy for the treatment of clients whose cancer is nonresectable or whose cancer has metastasized. The major benefit to the client is pain management, with shrinkage of tumor size and prolonged survival a secondary benefit (Sauter & Coleman, 1999).
RADIATION THERAPY. Intensive external beam radiation therapy to the pancreas may offer pain relief by shrinking tumor cells, alleviating obstruction, and improving food absorption; it does not improve survival rates. Implantation of radioactive iodine (125I) seeds, in combination with systemic or intra-arterial administration of floxuridine (FUDR), has also been used. The client may experience discomfort during and after the radiation treatments. Supportive nursing interventions for the relief of symptoms are indicated.
SURGICAL MANAGEMENT. Complete surgical resection of the pancreatic tumor offers the individual with pancreatic cancer the only effective treatment, but the surgery is only possible in a small percentage of cases. The mean survival rate for clients with nonresectable pancreatic cancer is 6 months after diagnosis (Mayer, 1999). Clients with tumors confined to the head of the pancreas are candidates for curative resection. Clients with tumors of the body and tail generally are not candidates for surgery, because in most cases their tumors have spread to other organs. The surgeon may perform either a total pancreatectomy or the Whipple procedure (pan-creaticoduodenectomy).
PREOPERATIVE CARE. The client with pancreatic carcinoma is a poor surgical risk because of malnutrition and debilitation. A nasogastric (NG) tube for decompression is inserted, and the administration of IV fluids or total parenteral nutrition (TPN) is typically started before surgery.
The client experiences anorexia with early satiety and often experiences nausea and vomiting, making the oral intake of nutrition difficult to maintain. Management is geared toward providing optimal nutrition preoperatively and postoperatively.
Tube Feedings. As long as intestinal function is adequate, the client may be maintained nutritionally with enteral tube feedings. When tube feedings are tolerated, a small-lumen sili-cone feeding tube, such as a Dobbhoff tube, is inserted to avoid the complications of larger-lumen tubes, such as sinusitis and nasal irritation. Commercially prepared products chosen by the health care provider or dietitian provide specific nutrients. Feedings are given by bolus or continuous infusion, depending on the client’s tolerance and residual volumes.
Often, in the late stages of pancreatic carcinoma or during the Whipple procedure, the physician inserts a small catheter
into the jejunum (jejunostomy) so that enteral feedings may be given. This feeding method is preferred to prevent reflux and to facilitate absorption. Feedings are initiated in low concentrations and volumes and are gradually increased as tolerated. The nurse delivers feedings by means of a tube-feeding pump to maintain a constant volume and assesses for diarrhea frequency as a means of measuring tolerance (see Chapter 61).
Total Parenteral Nutrition. For optimal nutrition, hyper-alimentation by TPN may be necessary in addition to tube feedings or as a single measure to provide nutrition. When central venous access is required, a Hickman catheter or other type of catheter may be necessary. Meticulous IV line care is an important nursing measure to prevent catheter sepsis. Sterile dressing changes and site observation are extremely important (see Chapter 14). The nurse also performs finger sticks to obtain blood for glucose measurements. These measurements help to monitor the client’s pancreatic function and tolerance of dextrose in the solution. Additional nursing care measures for the client receiving TPN are given in Chapter 61.
OPERATIVE PROCEDURES. The Whipple procedure (radical pancreaticoduodenectomy) involves extensive surgical manipulation and is used to treat cancer of the head of the pancreas. The procedure entails removal of the proximal head of the pancreas, the duodenum, a portion of the jejunum, the stomach (partial or total gastrectomy), and the gallbladder, with anastomosis of the pancreatic duct (pancre-aticojejunostomy), the common bile duct (choledochoje-junostomy), and the stomach (gastrojejunostomy) to the jejunum (Figure 60-7). In addition, the surgeon may remove the spleen (splenectomy).
POSTOPERATIVE CARE. In addition to routine postoperative care measures, the client who has undergone a radical pancreaticoduodenectomy requires intensive nursing care and is usually admitted to a surgical critical care unit. The nurse assesses for potential complications of the Whipple procedure (Table 60-5).
Gastrointestinal Drainage Monitoring. The monitoring of gastrointestinal (GI) drainage and NG tube patency is an important aspect of postoperative nursing care. Drainage tubes are strategically placed during surgery to remove drainage and secretions from the area and to prevent stress on the anastomosis sites. The nurse assesses the tubes and drainage devices for undue stress or kinking and maintains the drainage tubes in a dependent position. The suction pressure gauge is checked frequently to maintain the desired suction level. Most often,
The nurse monitors the drainage for color, consistency, and amount. The drainage should be serosanguineous; the appearance of clear, colorless, bile-tinged drainage or frank blood with an increase in output may indicate disruption or leakage of an anastomosis site. Most of the disruptions of the anastomosis site occur within a week to 10 days after surgery. Hemorrhage can occur as an early or late complication.
If the NG tube is obstructed, the nurse instills air first. If this method does not keep the drainage lumen open, irrigation with 10 to 20 mL of normal saline is gently performed. If the problem continues, the nurse may need to notify the physician for additional interventions.
The development of a fistula (an abnormal passageway) is the most common and most serious postoperative complication. Biliary, pancreatic, or gastric fistulas result from partial or total breakdown of an anastomosis site. The secretions that drain from the fistula contain bile, pancreatic enzymes, or gastric secretions, depending on which anastomosis site is ruptured. These secretions, particularly pancreatic fluid, are corrosive and irritating to the skin, and internal leakage causes a chemical peritonitis. Peritonitis (inflammation and infection of the peritoneum) necessitates treatment with multiple antibiotics.
Positioning. The nurse places the client in the semi-Fowler’s position to reduce stress on the suture line and anastomosis site, as well as to optimize lung expansion. Stress on the gastric suture line can be minimized by maintaining NG tube drainage at a low suction level to keep the remaining stomach (if a partial gastrectomy is done) or the jejunum (if a total gastrectomy is done) free of excessive fluid buildup and pressure. The NG tube is also used to reduce stimulation of the remaining pancreatic tissue.
Assessment of Fluids and Electrolytes. Because the Whipple procedure is extensive and can take 6 to 10 hours to complete, maintaining fluid and electrolyte balance can be difficult. Clients tend to experience significant intraoperative blood loss and postoperative bleeding. The intestine is exposed to air for long periods, and evaporation of fluid occurs. Significant losses of fluid and electrolytes occur from NG and other drainage tubes. In addition, these clients are usually malnourished and have low serum levels of protein and albumin, which maintain colloid osmotic pressure within the circulating system. Reduction in the serum osmotic pressure makes the client susceptible to third spacing of body fluids, with fluid moving from the intravascular to the interstitial space, resulting in shock.
For these reasons, the nurse closely monitors vital signs for decreased blood pressure and increased heart rate, decreased vascular pressures with a central venous line or pulmonary artery catheter (Swan-Ganz catheter), and decreased urine output to detect early signs of hypovolemia and prevent shock. The nurse is also alert for pitting edema of the extremities, dependent edema in the sacrum and back, and an intake that far exceeds output. Nutritional repletion via hyperalimentation and the administration of albumin promote the shift of fluid from the interstitial space back into the intravascular space.
Maintenance of ordered IV fluid volume replacement is important. The nurse monitors hemoglobin and hematocrit values to assess for blood loss and the need for blood transfusions. Electrolyte values are reviewed for decreased serum levels of sodium, potassium, chloride, and calcium. IV fluid concentrations must be altered to correct these electrolyte imbalances. The physician orders replacement of electrolytes as needed.
CRITICAL THINKING CHALLENGE
Your client had a Whipple procedure performed 3 days ago, and he has come to your unit from the surgical intensive care unit. He still has an NG tube to low suction and a wound drain in place.
• What physical assessments need to be made initially on placement in your care unit?
• Which postoperative complications would you assess the client for at this point?
• What changes iasogastric output might signify a complication? What should the normal output look like?
Glucose Monitoring. Immediately after the Whipple procedure, the client may have transient hyperglycemia or hypoglycemia as a result of stress and surgical manipulation of the pancreas. Most of the endocrine cells (islets of Langerhans, responsible for insulin and glucose secretion) are located in the body and tail of the pancreas. In most clients, up to half of the gland remains, and diabetes does not develop; however, a large number of clients are diabetic before surgery. The nurse monitors glucose levels frequently during the early postoperative period and administers insulin injections, as prescribed.
Community-Based Care
The client with pancreatic cancer is usually followed by a case manager, both in the hospital and in the home or other community-based setting. The role of the case manager is to ensure that the client receives cost-effective treatment and that his or her biopsychosocial needs are met.
Ш HEALTH TEACHING
When the client is discharged to home, many of the care measures are palliative and aimed at providing relief of symptoms such as pain. Care measures and teaching information are similar to those for clients with chronic pancreatitis.
In many cases, the diagnosis of pancreatic cancer is made a few months before death occurs. The client needs time to adjust to the diagnosis, which is usually made too late for cure or prolonged survival. The nurse helps the client identify what needs to be done to prepare for death. For example, the client may want to write a will or see family members and friends whom he or she has not seen recently. The client needs to make specific requests for the funeral or memorial service known to family members or significant others. These actions help the client prepare for death in a dignified manner. Chapter 9 discusses anticipatory grieving and preparation for death in detail.
В HOME CARE MANAGEMENT
The stage of progression of pancreatic carcinoma and available home care resources dictate whether the client can be discharged to home or whether additional care is needed in a skilled nursing facility or hospice. Home care preparations depend on the client’s physical and activity limitations and should be tailored to his or her needs. The nurse needs to coordinate care with the client and whoever will be used as the care provider after discharge from the hospital—home care provider, hospice care provider, or extended care provider.
The client and family need emotional support to deal with issues related to this illness. The nurse assists family members in ascertaining realistically and objectively the amount of physical care required for the client. The family members must be told that their own physical and emotional health is at risk during this stressful period and that supportive counseling is indicated. If the family does not have a religious affiliation or a spiritual leader (e.g., a minister or a rabbi) to provide support, the nurse suggests alternative counseling options. It is appropriate for the nurse to make the initial contact or appointment according to the client’s or family’s wishes.
HEALTH CARE RESOURCES
Regular home care nursing and assistive nursing personnel visits are scheduled to assist the client and family by providing physical, psychologic, and supportive care. The nurse supplies information about local hospice care (see Chapter 9) and cancer support groups.
