Joseph J. Kishel
LEARNING OBJECTIVES
Upon completion of the chapter, the reader will be able to:
1. Describe the pathophysiology of acute and chronic pancreatitis.
2. Differentiate the signs and symptoms of acute from chronic pancreatitis.
3. Discuss the clinical implications of pancreatic fluid collections, pancreatic abscess, and pancreatic necrosis in acute pancreatitis.
4. Formulate care plans for managing acute pancreatitis.
5. Identify pharmacologic and nonpharmacologic means of preventing repeat episodes of chronic pancreatitis.
6. Choose appropriate pancreatic enzyme supplementation for patients with chronic pancreatitis.
KEY CONCEPTS
The most common causes of acute and chronic pancreatitis in adults are ethanol abuse and biliary stones.
Pancreatic necrosis occurs within the first 2 weeks of acute pancreatitis and develops in 10% to 30% of patients with acute pancreatitis.
Therapy of acute pancreatitis is primarily supportive unless a specific etiology is identified. Supportive therapy involves fluid repletion, nutrition support, and analgesia.
Medications aimed at decreasing pancreatic enzyme release (e.g., somatostatin), nasogastric suction, and anticholinergic medications have all failed to show benefit in the treatment of acute pancreatitis.
Long-term sequelae of chronic pancreatitis include dietary malabsorption, impaired glucose tolerance, cholangitis, and potential addiction to opioid analgesics.
Treatment of chronic pancreatitis is aimed at removing the cause (ethanol abuse or biliary stones), providing analgesia, supplementing with pancreatic enzyme preparations, and implementing dietary restrictions.
INTRODUCTION
The pancreas is a gland in the abdomen lying in the curvature of the stomach as it empties into the duodenum. The pancreas functions primarily as an exocrine gland, although it also has endocrine function. The exocrine cells of the pancreas are called acinar cells that produce an alkaline fluid known as pancreatic juice that contains various digestive enzymes. The pancreatic juice is released through the ampulla of Vater into the duodenum to aid in the digestive process as well as buffer acidic fluid released from the stomach (Fig. 23–1).
These enzymes are produced and stored as inactive proenzymes within zymogen granules to prevent autolysis and digestion of the pancreas. The zymogen granules are also responsible for enzyme transport to the pancreatic duct. Amylase and lipase are released from the zymogen granules in the active form, whereas the proteolytic enzymes are activated in the duodenum by enterokinase. Enterokinase triggers the conversion of trypsinogen to the active protease, trypsin. Trypsin then activates the other proenzymes to their active enzymes. The pancreas contains a trypsin inhibitor to prevent autolysis.
FIGURE 23–1. Anatomic structure of the pancreas and biliary tract. (From Berardi RR, Montgomery PA. Pancreatitis. In: DiPiro JT, Talbert RL, Yee GC, et al., eds. Pharmacotherapy: A Pathophysiologic Approach, 7th ed. New York: McGraw-Hill, 2005:660, with permission.)
ACUTE PANCREATITIS
EPIDEMIOLOGY AND ETIOLOGY
In the Western hemisphere, acute pancreatitis is caused mainly by ethanol use/abuse and gallstones (cholelithiasis). Other common causes of acute pancreatitis include hypertriglyceridemia, endoscopic retrograde chol-angiopancreatography (ERCP), pregnancy, and autodigestion due to early activation of pancreatic enzymes. Numerous medications have also been implicated as causes of acute pancreatitis (Table 23–1).
PATHOPHYSIOLOGY
Ethanol abuse may cause precipitation of pancreatic enzymes in the ducts of the pancreas, leading to chronic inflammation and fibrosis resulting in loss of exocrine function. Ethanol itself may be directly toxic to the pancreatic cells, compounding this effect. Gallstones may obstruct the ampulla of Vater causing pancreatic enzymes or bile to move in a retrograde fashion into the pancreas. This retrograde movement maybe responsible for pancreatic autolysis.1
Table 23–1 Selected Medications Associated With Acute Pancreatitis
Autolysis of the pancreas can occur when zymogens are activated in the pancreas before being released into the duodenum. Acute pancreatitis can result from the initial injury to the zymogen-producing cells, which is followed by neutrophil invasion of the pancreas and further activation of enzymes within the pancreas. This cascade of events is destructive to the pancreas and harmful to the patient.
Acute pancreatitis can progress to several distinct consequences. A pancreatic fluid collection (or pancreatic pseudocyst) is a collection of tissue, pancreatic enzymes, and blood that forms weeks after acute pancreatitis. Many pancreatic pseudocysts resolve spontaneously, but some require surgical drainage.2 Rupture of a pancreatic pseudocyst with associated erosion and hemorrhage of major abdominal blood vessels can have a mortality approaching 60%; thus, continued monitoring of a pseudocyst is prudent.3
Pancreatic necrosis is a diffuse inflammation of the pancreas with infectious etiology. Pancreatic necrosis occurs within the first 2 weeks of acute pancreatitis and develops in 10% to 30% of patients with acute pancreatitis.The necrotic pancreas can become secondarily infected with enteric gram-negative bacteria (such as Escherichia coli), and disseminated infection may result from pancreatic necrosis.4,5
Pancreatic abscess is a collection of pus that forms in the pancreas 4 to 6 weeks after acute pancreatitis. Pancreatic abscess is usually less life-threatening than pancreatic necrosis or pancreatic pseudocyst and can be managed with percutaneous drainage.2 Pancreatic fluid collections and pancreatic abscesses can form during the course of acute pancreatitis. Pancreatic necrosis can occur when pancreatic enzymes damage the pancreatic tissue or when pancreatic abscesses become secondarily infected. This infection is usually due to bacteria that are normally found in the GI tract, including E. coli, Enterobacteriaceae, Staphylococcus aureus, viridans group streptococci, and anaerobes.
CLINICAL PRESENTATION AND DIAGNOSIS
A patient with acute pancreatitis may develop many severe local and systemic complications. Abdominal pain and distention may be due to local complications such as fluid collection, necrosis, or abscess in the pancreas. Hypotension, tachycardia, and fever may result from systemic complications, which can affect virtually any organ system but tend to target the pulmonary and cardiovascular systems and the kidneys. Multiorgan failure is a poor prognostic indicator. Acute respiratory distress syndrome (ARDS) is a life-threatening syndrome of acute lung injury with resulting hypoxia. ARDS may be due to the systemic release of pancreatic enzymes causing destruction of pulmonary surfactant, which is required for proper lung function.7 Circulating pancreatic enzymes can cause cardiovascular shock. Acute renal failure may result from hypovolemia.8
Patients at greatest risk for mortality from acute pancreatitis are those who have multiorgan failure (e.g., hypotension, respiratory failure, or renal failure), pancreatic necrosis, obesity, volume depletion, above 70 years of age, and an elevated Acute Physiology, Age, and Chronic Health Evaluation (APACHE) II score.9–10
Clinical Presentation and Diagnosis of Acute Pancreatitis
Symptoms
• Abdominal pain radiating to the back is the most common presenting symptom. Pain can be due to intestinal immobility or chemical peritonitis induced by pancreatic enzymes.
• Other common symptoms include nausea, vomiting, and abdominal pain.
Signs
• Tachycardia, hypotension, fever, and abdominal distention may be present.
• There may be a positive Cullen’s sign (bluish discoloration of the periumbilical skin indicating blood in the peritoneum).
• After 2 to 3 days of acute hemorrhagic pancreatitis, there may be a positive Turner’s sign (local areas of discoloration [bruising] and induration of the skin near the umbilicus due to extravasation of blood).
Laboratory Tests
• The serum amylase can be elevated three times the upper limit of normal within the first 12 hours of the onset of acute pancreatitis. The degree of elevation does not predict the severity of disease.
• As acute pancreatitis progresses, serum lipase and colipase become elevated.6
• Other possible laboratory abnormalities include elevated WBC count, hyperglycemia, hypocalcemia, hyperbilirubinemia, elevated serum lactate dehydrogenase (LDH), and hypertriglyceridemia.
DIAGNOSIS
Diagnosis of acute pancreatitis is based on the patient’s history and presenting signs and symptoms. Evaluation of laboratory results, specifically the serum lipase, aids in diagnosis. Serum amylase is elevated early in the disease process but may return to normal within 12 hours.8 Although an elevated serum amylase had been the diagnostic standard, its utility is limited by lack of specificity. Serum lipase and colipase are now the gold standards for laboratory testing due to greater than 90% specificity for acute pancreatitis. Serum lipase will remain elevated for days after the acute event and may be more useful for diagnosis depending on when the patient presents for evaluation.8,11 CT is more complicated than abdominal radiography or ultrasound, but it is the most useful tool for diagnosis and staging of acute pancreatitis.12
Patient Encounter, Part 1
A 32-year-old woman in her second trimester of pregnancy presents to the emergency department complaining of sharp persistent pain in the RUQ of the abdomen. The pain started 3 days ago and has progressed to become severe. She was nauseated at home and has vomited twice in the emergency department. The patient is at normal weight for this stage in her pregnancy. All prenatal visits were normal. The patient does not smoke or consume ethanol but does have a history of cholelithiasis.
What information about the patient presentation is consistent with acute pancreatitis?
What risk factors does the patient have for acute pancreatitis?
What additional laboratory tests would you recommend?
The patient’s history will identify risk factors for acute pancreatitis, such as age above 70 years or history of alcohol abuse. Finally, CT scan or ultrasound of the abdomen can help identify pancreatic fluid collections.12 The APACHE II score is a rating scale of disease severity in critically ill patients. The CT severity index has the highest sensitivity and specificity in the diagnosis of acute pancreatitis.
TREATMENT
Desired Outcomes
The goals of treatment for acute pancreatitis include: (a) resolution of nausea, vomiting, abdominal pain, and fever; (b) ability to tolerate oral intake; (c) normalization of serum amylase, lipase, and WBC count; and (d) resolution of abscess, pseudocyst, or fluid collection as measured by CT scan.
Nonpharmacologic Therapy
Many medications can precipitate an attack of acute pancreatitis. If a medication is determined to be the cause of acute pancreatitis, it should be discontinued and an alternative therapy be considered.13,14
Therapy of acute pancreatitis is primarily supportive unless a specific etiology is identified (Fig. 23–2). Supportive therapy involves fluid repletion, nutrition support, and analgesia. Patients with acute pancreatitis are administered IV fluids to maintain hydration and blood pressure. Fluids may be given in the form of crystalloids (e.g., 0.9% sodium chloride for infusion) or colloids (e.g., dextran or albumin for infusion).15 Sodium chloride 0.9% for infusion (normal saline) at a rate of 50 to 100 mL/h is reasonable for patients with mild to moderate fluid depletion. However, as much as 200 mL/h may be required for patients with severe fluid losses.16 Electrolytes such as potassium and magnesium may be added to the infusions if necessary. Hyperglycemia can be managed with insulin-containing IV infusions.
FIGURE 23–2. Algorithm for evaluation and treatment of acute pancreatitis. (ERCP, endoscopic retrograde cholangiopancreatography.) (From Berardi RR, Montgomery PA. Pancreatitis. In: DiPiro JT, Talbert RL, Yee GC, etal., eds. Pharmacotherapy: A Pathophysiologic Approach, 7th ed. New York: McGraw-Hill, 2008:664, with permission.)
It is common practice to discontinue oral feedings during an attack of acute pancreatitis. In theory, discontinuation of oral intake will decrease the secretory functions of the pancreas and minimize further complications from the disease. Some patients can be fed with minimal oral intake, even in severe acute pancreatitis. Tube feeding delivered via a nasojejunal tube will feed the patient beyond the ampulla of Vater, minimizing stimulation of the pancreas.15,16 If oral intake is discontinued for a protracted period, total parenteral nutrition must be used to maintain adequate nutrition.17,18
If pancreatic necrosis has been identified, surgical debridement is necessary because mortality approaches 100% without drainage or surgical intervention. Percutaneous drainage is an option for managing pancreatic necrosis but is best used only in unstable patients as a bridge to surgery. Repeated surgery may be required in patients with a protracted or progressing disease state.2,19
Pharmacologic Therapy
Analgesics
Meperidine has historically been the most popular analgesic in acute pancreatitis because it is purported to cause less spasm and resulting pain in the sphincter of Oddi than other opioids. However, the clinical importance of this phenomenon is unclear.15,20 As a result, patients with acute pancreatitis should be given the most effective analgesic. Hydromorphone and fentanyl are reasonable alternatives to meperidine and may be more desirable due to other adverse effects associated with meperidine. Refer to Chapter 30 on pain management for guidance in selecting an analgesic dose.
Antibiotics
Empiric antibiotics are not necessary if the patient has mild disease or a noninfectious etiology of acute pancreatitis. Antibiotics have not been shown to prevent the formation of pancreatic abscess or necrosis when given early in the course of acute pancreatitis.
Antibiotics may be appropriate for pancreatic necrosis, which can be infected initially or be susceptible to a secondary infection; however, published data yield conflicting results regarding mortality and infection rate in this setting.16,21,22 As such, the decision to use antibiotics is highly individualized. Selected intravenous antibiotic regimens are shown in Table 23–2. If necrosis is confirmed, antibiotics are insufficient as sole therapy; surgical debridement is necessary for cure.
Broad-spectrum antibiotics with activity against enteric gram-negative bacilli are appropriate. It is often difficult to narrow the spectrum of activity of the antibiotic choice since the infections are usually polymicrobial. As such, patients may receive long courses of broad-spectrum antibiotics such as meropenem and may develop superinfections due to more resistant bacteria or bacteria not susceptible to meropenem. Antifungal agents such as fluconazole may be considered if peritonitis or GI perforation develops due to the presence of fungi such as Candida alicans in the GI tract.23
Patient Encounter, Part 2: Medical History, Physical Exam, and Diagnostic Tests
PMH: Gravida 2, para 1; cholelithiasis
Allergies: No known allergies
FH: Father and mother alive and well
SH: No ethanol currently, but one to two drinks per night before pregnancy; no tobacco
Meds: No prescription medications; multivitamin one tablet orally once daily; ferrous sulfate 324 mg orally once daily; calcium carbonate 500 mg orally twice daily
ROS: Positive for sharp RUQ abdominal pain radiating to the back, nausea, vomiting, negative for chest pain, or shortness of breath
PE:
VS: Wt 80 kg (176 lb), ht 5’5” (165 cm), BP 110/60 mm Hg, p 120 bpm, RR 18 per minute, T 37.9°C (100.2°F)
CV: Regular rate and rhythm, no murmurs
Abd: Pregnant, (+) rebound tenderness, (+) bowel sounds, no hepatosplenomegaly
Labs: Amylase 50 units/L (0.83 μKat/L), lipase 1,000 units/L (16.7 μKat/L)
Abdominal Ultrasound: Results pending
Given this additional information, what is your assessment of the patient’s condition?
Why is the amylase low and the lipase high?
Table 23–2 Selected IV Antimicrobial Regimens for Pancreatic Necrosis
Ineffective Therapies
Several pharmacologic therapies have been proven to be ineffective in reducing morbidity or mortality from the disease. Ineffective therapies include: reducing pancreatic secretion by administering somatostatin or atropine, reducing gastric acidity and decreasing pancreatic secretion with histamine2 -receptor antagonists, inhibition of pancreatic enzymes using protease inhibitors such as aprotinin, probiotics, and immunomodulation.11–24,27 Nasogastric suction has only been effective in patients with ileus or persistent vomiting.28
Patient Encounter, Part 3: Treatment and Monitoring
The patient acutely decompensates upon leaving the CT scanner and is therefore transferred to the surgical intensive care unit for mechanical ventilation, blood pressure support, and surgical evaluation. A diagnosis of acute pancreatitis with pancreatic necrosis is made.
Formulate a care plan for this patient.
What are some possible causes of respiratory failure and hypotension in this patient? Are these findings poor prognostic indicators?
What is the recommended treatment for pancreatic necrosis?
What empiric antibiotic regimen would be a reasonable choice in this patient? Provide a drug, dose, route, and frequency.
Suppose a surgeon requested clindamycin 600 mg IV every 8 hours for this patient. Would this be a reasonable choice? Why or why not?
OUTCOME EVALUATION
Given the severity of acute pancreatitis, patients are monitored closely in the intensive care setting. Patients with mild disease can be managed more conservatively with observation and supportive care. Critically ill patients may require surgery and aggressive life support measures.16,29
CHRONIC PANCREATITIS
EPIDEMIOLOGY AND ETIOLOGY
The incidence of chronic pancreatitis is approximately one in 10,000 people. The most common cause of chronic pancreatitis in adults in Western countries is ethanol abuse. The most common cause in children is cystic fibrosis due to pre-existing pancreatic insufficiency inherent in the disease. Gallstones can occur at the same time as chronic pancreatitis but are not often implicated as the cause. Unlike acute pancreatitis, chronic pancreatitis has an unknown etiology in a significant number of cases (30%).29,30
PATHOPHYSIOLOGY
Chronic pancreatitis is an inflammatory process that occurs over a long period of time. The inflammation damages the enzyme-producing cells in the pancreas and can also disrupt or destroy the endocrine function of the pancreas by causing diffuse scarring and fibrosis.30,31 Ethanol abuse may cause precipitation of pancreatic enzymes in the ducts of the pancreas leading to chronic inflammation and damage. Ethanol may also be directly toxic to pancreatic cells.32 Counterintuitively, the amount of ethanol consumed does not correlate with the incidence or progression of chronic pancreatitis.33 A patient who “binge drinks” by consuming large amounts of ethanol over short periods of time is as likely to develop chronic pancreatitis as someone who chronically consumes socially acceptable amounts of alcohol. Patients who die from the first diagnosed episode of chronic pancreatitis may have had undiagnosed chronic pancreatitis for some time.34
Long-term sequelae of chronic pancreatitis include dietary malabsorption, impaired glucose tolerance, cholangitis, and potential addiction to opioid analgesics. As patients lose exocrine function of the pancreas, they have decreased ability to absorb lipids and protein ingested with normal dietary intake. Weight loss from nutritional malabsorption is a common symptom of chronic pancreatitis not often seen in acute pancreatitis. Fatty- or protein-containing stools are also common; carbohydrate absorption is usually unaffected. Even though patients with chronic pancreatitis have decreased ability to absorb lipid from the GI tract, there does not appear to be an increased incidence of fat-soluble vitamin deficiency in these patients.36
CLINICAL PRESENTATION AND DIAGNOSIS
Differentiating an episode of acute from chronic pancreatitis may be difficult because the clinical presentations can be similar. The diagnosis of chronic pancreatitis is made by looking for the effects of chronic pancreatic inflammation and scarring on the pancreas and the patient as a whole. CT or ERCP will allow visualization of chronic calcified lesions in the pancreas when present.39
TREATMENT
Desired Outcomes
The goals of pharmacotherapy for chronic pancreatitis are: (a) prevention and resolution of chronic abdominal pain and (b) correction of dietary malabsorption with exogenous pancreatic enzymes.
Nonpharmacologic Therapy
Lifestyle modifications are an important part of the therapy for chronic pancreatitis. Patients who completely avoid ethanol after an attack of ethanol-induced pancreatitis are: significantly less likely to have a recurrence than patients who ingest even casual amounts of ethanol. Avoidance of ethanol and fatty meals can decrease the pain of chronic pancreatitis.
Clinical Presentation and Diagnosis of Chronic Pancreatitis
General
• The presentation of chronic pancreatitis can be similar to that of acute pancreatitis.
Symptoms
• Pain is the most common chief complaint. Pain can be dull or sharp, and it may be localized to the area around the stomach or can radiate to the back. The pain is not relieved by antacids and can be provoked by ethanol ingestion or a fatty meal.35
• Weight loss can result from chronic fat and protein malabsorption.
Signs
• Patients often present with chronic fat-containing diarrhea due to dietary lipid malabsorption.
• GI bleeding can result from erosion of intestinal blood vessels by pancreatic enzymes or as a result of thrombosis.
• Chronic obstruction of the common bile duct by the inflamed pancreas can cause icterus, cholangitis, and biliary cirrhosis.37
Laboratory Tests
• Glucose intolerance may occur because of chronic destruction of the endocrine function of the pancreas.38
• Serum amylase and lipase levels are not usually elevated in chronic pancreatitis.
• The serum bilirubin or alkaline phosphatase may be elevated due to inflammation near the common bile duct.
Many surgical procedures have been employed to reduce the inflammation or remove the strictures that cause pain in chronic pancreatitis. However, most procedures, including nerve blocks, have not been proven effective in clinical trials and carry a high risk of morbidity and mortality.40
Pharmacologic Therapy
Analgesics
Pain management is an important component of therapy and is similar to that of acute pancreatitis. Nonopioid analgesics (e.g., tramadol) are preferred, but the severe and persistent nature of the pain often requires opioid therapy. Patients can require chronic doses of opioid analgesics, with a resulting risk of addiction. Pain can also be managed by removing the stimulus of exacerbation if identified.32,41
Pancreatic Enzymes
The goal of pancreatic enzyme supplementation is to deliver exogenous enzyme to the duodenum without causing further GI side effects from the medication, risking noncompliance due to the large number of dosage units required, or causing undue medication expense.42
Supplementation with pancreatic enzymes may reduce the pain and fatty diarrhea associated with chronic pancreatitis (Table 23–3). Best results are achieved in patients who have mild nonalcoholic pancreatic disease. Common pancreatic enzyme supplements contain lipase, amylase, and protease in varying proportions. Thus, the dose can be tailored to the patient’s requirement for exogenous enzyme supplementation and response to therapy.
Nonenteric-coated pancreatic enzyme supplements require high doses to compensate for loss of enzyme due to destruction by the low pH of the stomach. This effect can be minimized by administering a histamine2-receptor antagonist or proton pump inhibitor (PPI). Nonenteric-coated pancreatic enzyme supplements may have an advantage in minimizing pain early in the disease state through regulation of proteases in the duodenum.
Table 23–3 Frequently Used Pancreatic Enzyme Preparations
Nonenteric-coated pancreatic enzyme supplements can be used for initial therapy. The relative dose of amylase, lipase, and protease maybe increased until control of pain and fatty diarrhea are achieved or the patient experiences intolerable side effects. If pain and diarrhea control are achieved, the patient can be transitioned to an enteric-coated supplement to maximize compliance. A reasonable example starting regimen is Viokase-8, six tablets with each meal and at bedtime, given with famotidine 20 mg at bedtime.
Patient Encounter 2
The same patient described in the first encounter is now 34 years old (she delivered a healthy baby boy without complications). She presents to the clinic with RUQ pain radiating to her back. She is also jaundiced and nauseated.
PMH: Gravida 2 para 2, cholelithiasis
SH: Consumes one to two alcoholic beverages per evening; no tobacco
Meds: Multivitamin one tablet daily; pantoprazole 40 mg orally once daily; maalox 15 mL orally four times daily as needed for heartburn/stomach upset; acetaminophen 325 mg orally every 6 hours as needed for pain/headache
ROS: Positive for sharp RUQ abdominal pain radiating to the back, nausea, and recent unintentional weight loss; negative for chest pain or shortness of breath, fatty diarrhea present for months
PE:
VS: BP 130/86 mm Hg, p 80 bpm, RR 16 per minute, T 37.0°C (98.6°F), wt 80 kg (176 lb), ht 5’5” (165 cm).
CV: Regular rate and rhythm, no murmurs noted
Abd: Distended, (+) rebound tenderness, (+) bowel sounds, marked hepatosplenomegaly
Labs: Amylase 100 units/L (1.67 μKat/L), lipase 100 units/L (1.67 μKat/L)
CT Scan: Diffuse pancreatic scarring and calcifications
Formulate a care plan for this patient.
Why are the serum amylase and lipase normal?
What lifestyle modifications can this patient make to minimize impact from her disease state?
Is this patient taking any medication(s) that could exacerbate pancreatitis? If so, what alternatives can you offer?
What medications may help alleviate the fatty diarrhea the patient is experiencing?
How would you monitor the effectiveness of your recommendations?
Most pancreatic enzyme supplements are enteric coated to release enzymes in the alkaline environment of the intestine; this minimizes enzyme destruction in the stomach. Enteric-coated pancreatic enzyme supplements require fewer daily dosage units, but delivery of the drug to the site of action and effectiveness may be delayed by gastric emptying time.43
Pancreatic enzyme supplements should be taken immediately prior to meals to aid in the digestion and absorption of food. Alternately, patients can supplement their diet with medium-chain triglycerides (MCTs) or ingest foods rich in MCTs since they do not require pancreatic enzymes for absorption. An appropriate regimen incorporates the successful doses of each enzyme (amylase, lipase, and protease) from the starting Nonenteric-coated regimen. As with the previous example, a patient stabilized on Viokase-8, six tablets with each meal, can be transitioned to Pancrease MT-16 three tablets with meals. The famotidine can then be discontinued.
OUTCOME EVALUATION
• Monitor for adequate pain control and the need for escalation or de-escalation of analgesia.
Patient Care and Monitoring
1. Determine whether ethanol is a contributing causative factor. If so, reinforce counseling on the need for abstinence and provide appropriate resources to maintain abstinence (e.g., professional counseling, alcoholics anonymous).
2. Obtain a thorough history of prescription, nonprescription, and dietary supplement use to identify products that may exacerbate chronic pancreatitis.
3. Refer the patient for nutritional counseling if there is decreased caloric intake and weight loss. Compare actual body weight to ideal body weight.
4. Make a plan for analgesia, in conjunction with a pain management service if possible, to control and prevent pain. Recommend an analgesic with ease of dosing and minimal side effects, realizing that patients with chronic pancreatitis may require large doses of opioids.
5. Optimize pancreatic enzyme supplementation, starting first with a nonenteric-coated enzyme supplement and a histamine2-receptor antagonist. When pain and diarrhea are stabilized, consider switching to an enteric-coated enzyme supplement for ease of dosing.
6. Develop a plan for reassessing pancreatic enzyme supplementation and analgesia on an outpatient basis.
7. Assess improvement in quality of life measures such as physical, psychological, and social functioning and well-being.
• If pain relief is achieved by avoiding ethanol or fatty meals, encourage continuation of these practices.
• When dietary malabsorption exists, monitor patients for weight gain or loss, activity level, and ability to perform activities of daily living.
• Ask patients to monitor the frequency and consistency of stool output as an indicator of malabsorption.
• Educate patients that compliance with and proper use of dietary pancreatic enzyme supplementation is key to improved outcomes.32,35,41~43
Abbreviations Introduced in This Chapter
Self-assessment questions and answers are available at http://www.mhpharmacotherapy.com/pp.html.
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