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CLINICIAN'S CORNER
A 21-Year-Old Man With Chronic Pancreatitis
Mark P. Callery, MD;
Steven D. Freedman, MD, PhD
JAMA. 2008;299(13):1588-1594.
ABSTRACT
Chronic pancreatitis is a disease for which the diagnosis may be difficult to ascertain and the treatments are limited. Using the case of a 21-year-old man who has had recurrent episodes of epigastric pain since age 10 years and was ultimately diagnosed as having idiopathic pancreatitis complicated by pancreatic duct stones, we discuss the evaluation and treatment of chronic pancreatitis. Diagnosis is based on thorough history taking, physical examination, and carefully selected imaging studies. Etiologies may be structural or nonstructural; genes predisposing to chronic pancreatitis have been identified. An evidence-based approach to treatment is limited by a paucity of randomized controlled trials. We address the patient's concerns regarding chronic pancreatitis, including what he should expect over the next several years, whether endoscopic or surgical therapies should be considered, and whether there are any cures.
INTRODUCTION
DR SHIP: Mr C is a 21-year-old man with chronic pancreatitis. He is a junior in college and is studying sports management. He is active, playing on a golf team and coaching basketball. He lives at home with his parents and brother in rural Massachusetts. He has managed care insurance.
Mr C was initially diagnosed as having pancreatitis at age 10 years. He has been evaluated for multiple etiologies without any diagnosis; he has been told that it is idiopathic. For the first 4 years after diagnosis, he was hospitalized for flares about once a year. During high school, attacks requiring hospitalization occurred about twice a year, predictably in the fall and the spring. Each time he would be hospitalized for 5 to 10 days and placed on bowel rest, and he sometimes underwent testing and therapeutic intervention with endoscopic retrograde cholangiopancreatography (ERCP) or stent placement. He experiences "minor attacks," which involve abdominal pain that he can manage at home with bowel rest and oral medication, about 3 to 4 times a year. Five months ago, he underwent an ERCP with pancreatic sphincterotomy and stent placement. Multiple pancreatic stones were found. He did well until 4 months later, when he had another flare of pain requiring hospitalization. He then had another ERCP with removal of stones and the stent. He has been stable since that time.
The only other intervention he has tried is alteration of his diet. He reduced the fat in his diet to 25 g/d for a period of months without noticing a difference in the pattern of his attacks. Currently, his only dietary modification is total avoidance of alcohol.
Aside from his pancreatitis, he is healthy. His bowel habits are normal. His illness has not interfered with his schoolwork or athletics, except for the time hospitalization has taken from these activities. He does not feel limited in his life. His only medication is pancreatic enzymes, which he takes before meals and snacks. He has been unable to tell if these have made a measurable difference in the frequency or intensity of his flares. He does not take any pain medication regularly. He does not smoke. There is no family history of pancreatitis or cystic fibrosis.
On physical examination, he was a thin, well-appearing man, with a temperature of 36.5°C, blood pressure of 106/88 mm Hg, and heart rate of 65/min. His abdomen was soft, nontender, and nondistended, without rebound or guarding.
His laboratory test results were normal, including complete blood cell count, electrolytes, and kidney and liver function. His amylase and lipase levels were normal. His most recent ERCP showed dilation and irregularity of the pancreatic duct. There was a short segment of ductal stricture in the mid body of the pancreas. Multiple filling defects were seen. Several small stones and sludge were reportedly extracted from the pancreatic duct.
MR C: HIS VIEW
When I was 10 years old, I was diagnosed for the first time with pancreatitis, and it really came out of nowhere. I woke up in the morning with severe pain in my sternum area and really didn't know what was going on. So we went to the doctors, went through all the procedures; they checked my appendix, my gallbladder, liver. Come to find out it was pancreatitis. From there, I had about 1 or 2 attacks per year, all through high school, ranging from 5 to 10 days in the hospital because of elevated enzyme levels. I had a lot of tests done—CT [computed tomography] scans, ERCPs, MRIs [magnetic resonance imaging], all that stuff, and really, they haven't come to a conclusion as to the reason why I get pancreatitis.
The first thing they tried was just controlling my diet and keeping the fat levels low. Especially when I got out of the hospital, after an attack, they would try to keep it to 25 g of fat per day. That hasn't really seemed to help. Four years ago, they put me on Creon [pancrelipase] pills, where I would have to take 4 pills for every meal before I ate, and 2 with a snack, just so it would take the workload off my pancreas a little bit. It's tough to say whether or not that works.
I’m usually fine. It's always on my mind, but it's nothing to call a doctor about. Today, most days, no problems. Maybe once or twice per month, I have small little pains, nothing really to worry about, no more than somebody will get a headache, but in the pancreas area.
The biggest way this pancreatitis problem has affected my life is just trying to stay ahead of schedule, whether it be school or basketball. Especially in high school, when it was happening once or twice a year and I’d be out of school for a week or two, to stay up with my work or get ahead of my work, or just work that much harder in what I was doing outside of school. So when it did come along, I wouldn't fall as far behind as I would be if I was just going along at a normal rate.
During the last ERCP, they went in and they saw my ducts, and they talked about one of my pancreatic ducts being larger than it should be. They mentioned surgery to keep my ducts in line where they're not abnormally large. I guess that would be the next step outside of ERCPs.
Down the road, will we have to take more drastic procedures and maybe intensify the level of surgery or procedures? With the condition that my pancreas is in right now, the damage and everything, what will be the effect on the rest of my life from that? And if possible, are there any predictions on whether it can ever be cured completely? What's the outlook?
AT THE CROSSROADS: QUESTIONS FOR DRS CALLERY AND FREEDMAN
How is the diagnosis of chronic pancreatitis made? What is the natural history of untreated chronic pancreatitis and does treatment make a difference? What are the options for and risks and benefits of medical treatment? What are the surgical treatment options, risks, and benefits, both short- and long-term? What are the indications for surgical vs medical treatment? What do you recommend for Mr C?
DR FREEDMAN: Mr C highlights a number of the critical questions that plague individuals with recurrent abdominal pain, who may or may not have chronic pancreatitis. In addition, Mr C's management illustrates the lack of knowledge in understanding the natural history and evidence-based medical approach to the treatment of chronic pancreatitis.
Initial Evaluation and Management
Chronic pancreatitis is a disease for which the diagnosis may be difficult to ascertain and the treatments are limited. As with Mr C, the most common presentation is chronic or recurrent abdominal pain that frequently occurs in the epigastrium but may localize to the right or left upper quadrants.1 Patients may experience pain radiating through to the back, and nausea is common. Ultimately, the diagnosis of chronic pancreatitis is based on clinical assessment. Obtaining a thorough history and review of the primary laboratory data and, especially, carefully selected imaging studies is critical. Many patients undergo repeated imaging and endoscopic studies that are of little clinical or therapeutic benefit. Although increases in amylase and lipase may be diagnostic in acute pancreatitis, they are not predictive of chronic pancreatitis, in which values may range from normal to up to 3 times the upper limit of normal. The diagnosis can be made based on any of the following1: (1) pathognomonic calcifications of the pancreas on plain films or axial imaging; (2) characteristic abnormal pancreatogram based on ERCP or magnetic resonance cholangiopancreatography demonstrating beading of the pancreatic duct or ductal stones,2 as Mr C has; (3) endoscopic ultrasound demonstrating changes in the pancreatic duct, including hyperechoic walls, stones, and ductal dilation, or in the parenchyma, consisting of hyperechoic foci and strands, calcifications, and lobularity consistent with chronic pancreatitis3; (4) abnormal secretin pancreatic function testing with a peak bicarbonate concentration of less than 75 mEq/L4-5; or (5) tissue histology confirming chronic pancreatitis.
Etiology
The etiologies of chronic/recurrent acute pancreatitis can be categorized according to structural and nonstructural causes. Structural causes include pancreatic duct obstruction due to stones, strictures, ampullary or periampullary mechanical or functional stenosis (eg, sphincter of Oddi dysfunction), or neoplasms such as adenocarcinoma or intraductal papillary mucinous tumors.1 Nonstructural causes include metabolic disorders (eg, hypercalcemia,6 hypertriglyceridemia7), infections, and toxins (eg, alcohol), drugs, and genetic mutations. It has been debated whether recurrent acute pancreatitis, defined as discrete painful acute episodes of pancreatitis followed by asymptomatic intervals, can lead to chronic pancreatitis. This concept is supported by the fact that a subset of individuals, especially in the setting of hereditary pancreatitis and hypertriglyceridemia,7 progress from recurrent acute episodes to chronic pain.
Thirty percent of patients with acute pancreatitis have no identifiable cause, and of these, 3% to 27% experience recurrent episodes.8-9 In these studies, the median age was 55 years, with a median follow-up of 44 months. Microlithiasis and biliary sludge were frequent causes, with cholecystectomy being curative. These biliary juice abnormalities can explain recurrent acute pancreatitis but do not play a role in chronic pancreatitis.
Two genes have been implicated in the pathogenesis of recurrent acute and chronic pancreatitis. The first is the PRSS-1 (protease serine 1 [trypsinogen]) gene, responsible for hereditary pancreatitis.10-12 The most common mutation results in a substitution of histidine for arginine at position 117 in cationic trypsinogen, producing a form that is no longer spontaneously degraded within the pancreatic acinar cell. Patients typically present in their teens with recurrent acute pancreatitis and progress to a chronic course. Mr C could have a mutation in this gene, although there is no family history to support this. The other gene is the cystic fibrosis transmembrane conductance regulator (CFTR) gene.13-15 This is strongly associated with idiopathic recurrent acute and chronic pancreatitis as well as pancreatitis in the setting of pancreas divisum.16 A limited CFTR gene screen was negative in Mr C, but this screens for the most common mutations leading to classic cystic fibrosis and not the mutations associated with non–cystic fibrosis pancreatitis. Sweat chloride testing examines if there is a functional defect in CFTR and may be more helpful in defining an underlying CFTR abnormality.16 Mutations in the trypsin inhibitor (SPINK-1) gene have also been linked as a modifier gene in chronic pancreatitis, with 1 study demonstrating that 25% of patients with chronic pancreatitis have 1 or 2 alleles compared with 2% of the general population.17 However, patients homozygous for SPINK-1 mutations can be asymptomatic; hence, screening for this gene is not beneficial at this time.
Autoimmune pancreatitis often presents in patients who are older than 50 years with persistent upper abdominal pain, variable jaundice, and fullness in the head of the pancreas18; in these patients, the differential diagnosis must include neoplasm. The diagnosis of autoimmune pancreatitis can be inferred by the finding of elevated IgG4 levels, seen in up to 47% of individuals, or abnormal autoimmune markers in the serum, including rheumatoid factor, carbonic anhydrase II, lactoferrin, and antinuclear antibodies.18 Magnetic resonance imaging can show the characteristic hypointense rim on T2 weighting. Histology demonstrates lymphoplasmacytic infiltrates.
Evaluation
Evaluation of pancreatitis involves answering 3 important questions: (1) When should intervention begin? (2) Which tests should be obtained before assuming pancreatitis is idiopathic? and (3) When should intervention stop? In my experience, many patients undergo excessive testing and procedures that have no evidence to support them and are ineffective. However, after a detailed patient and family history is taken, some type of cross-sectional imaging is indicated. The specific type is institution-dependent but generally would include either a dedicated CT or MRI/magnetic resonance cholangiopancreatography of the pancreas. No data suggest that one mode is better than the other. If no abnormalities are found, further testing may be warranted, including an ERCP or secretin pancreatic function test. Endoscopic ultrasound requires an experienced operator and, even then, uncommonly identifies the diagnosis alone unless multiple features are present.3, 19-20 Endoscopic tests may be valuable when neoplasms such as adenocarcinoma or, especially, intraductal papillary mucinous neoplasm are in the differential diagnosis. An ERCP has the advantage of allowing therapeutic procedures to be performed, as in this case.
Mr C had initially undergone a CT scan, which showed multiple stones within his pancreatic duct, with mild dilatation proximally. No clear etiology for his chronic pancreatitis was identified. A finding of pancreatic duct stones and dilatation of the pancreatic duct suggested partial obstruction of the duct as a contributing factor to his symptoms and appropriately prompted an ERCP for confirmation of the findings and as a therapeutic mode.
Screening for gene mutations has not been fully defined. In patients presenting in their teens, the PRSS-1 (hereditary pancreatitis) gene should be evaluated, especially if there is a family history of pancreatitis.12 Sweat testing for evidence of CFTR mutations should be considered in patients younger than 40 years. It is abnormal in 10% of patients with idiopathic pancreatitis.15 The role of CFTR gene sequencing remains to be determined.
Serum triglycerides and calcium should also be analyzed. Other blood tests, including for serum amylase and lipase, are generally unhelpful.1 If a patient has chronic diarrhea, stool studies for fecal elastase levels of less than 200 µg/g can confirm pancreatic steatorrhea.21
Natural History
In studies of the natural history of pancreatitis, both idiopathic and alcohol-related, patients were divided into early onset idiopathic chronic pancreatitis, as defined by age younger than 35 years, vs late onset of disease, wherein symptoms occur after age 35 years.22-24 Early onset disease is characterized by pancreatic insufficiency and diabetes mellitus developing over a 15- to 20-year period, whereas exocrine and endocrine insufficiency is less often associated with late-onset disease. Pain is a common feature of early onset disease and is typically more severe than in late-onset disease. Despite Mr C's early onset of disease, he is at low risk of developing diabetes and pancreatic exocrine insufficiency, given his intermittent attacks that have responded to endoscopic therapy. Assuming he is adherent to a low-fat diet and avoids alcohol, he likely will continue to have pain-free periods with recurrent episodes of pain over time because of formation of more pancreatic duct stones. Whether he will eventually proceed to chronic pain cannot be determined at this time.
Medical Therapy
Therapy is aimed at the principal symptom of pancreatitis—pain. Although there are no randomized trials, the following recommendations are based on physician practice. Since pain is triggered by eating, and particularly by fatty foods, low-fat diets (<20 g/d) are advised. Mr C notes that a low-fat diet has made no difference in his pain. Patients should meet with a dietitian since a balanced diet with appropriate vitamins and antioxidants may be helpful. In patients with refractory pain and inability to tolerate oral intake, total parenteral nutrition for several weeks or longer may be needed both for nutrition as well as to "rest the pancreas," although there is no direct evidence to support that the latter results in symptom improvement. Whether enteral tube feedings into the jejunum are more advantageous is unknown. One study examining the role of oral feeding of a liquid supplement containing medium-chain triglycerides, dipeptides and tripeptides, and antioxidants demonstrated an improvement in pain scores in patients with idiopathic chronic pancreatitis.25
Pancreatic enzyme supplementation is used both for the treatment of pancreatic steatorrhea and for pain. For the former, there are multiple preparations, including slow-release forms. However, for the treatment of pain, only nonenteric-coated formulations are potentially effective. The theory is that high doses of trypsin in these pancreatic enzyme supplements will degrade cholecystokinin-releasing factor and prevent cholecystokinin-stimulated pancreatic secretion.26 The fact that high doses of trypsin, which must be sustained in the duodenum, are needed to inhibit secretion explains the necessity for nonenteric-coated formulations and the variable response in patients. However, this treatment is controversial, with studies showing mixed results.26-30 Generally, supplementation has been more effective in women without dilated pancreatic ducts,27, 29-30 although the reason for this is unknown.
In patients whose pain is not relieved, narcotic analgesics and antiemetics may be needed. Other approaches include nerve ablation procedures such as celiac neurolysis (either percutaneous or endoscopic31-33) or thoracoscopic splanchnicectomy.34-35 Response in both of these procedures is quite limited and frequently of short duration.
Endoscopic Therapy
In patients such as Mr C with chronic pancreatitis associated with pancreatic duct strictures, papillary stenosis, and presence of pancreatic duct stones (as shown in the Figure from another patient with similar findings), endoscopic studies have demonstrated that removal of the obstruction results in short-term symptomatic improvement.36-39 In Mr C, endoscopic therapy with sphincterotomy, stone extraction, and transient stenting appears to have had some therapeutic benefit. However, this approach is not always effective on a long-term basis; stones and multiple duct strictures may be a reflection of the underlying pancreatic parenchymal inflammatory disease. To date, no randomized, blinded, sham-controlled clinical trials have tested the role of therapeutic endoscopic interventions, and long-term pancreatic duct stenting can lead to complications such as stricture formation.40-41 In patients with sphincter of Oddi dysfunction, a highly controversial topic, the response to sphincterotomy ranges from 15% to 86% depending on the investigator.42 This therapy appears most effective in patients with type 1 sphincter of Oddi dysfunction, in which pancreatic pain, pancreatic duct dilatation and delayed drainage, abnormal liver function blood test results, and elevated amylase and/or lipase are present. However, in some patients, sphincter of Oddi dysfunction may be secondary to chronic inflammation and not the primary initiating event.
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Figure. ERCP-Generated Image of the Bile and Pancreatic Ducts of a Patient Similar to Mr C
The bile duct appears normal. The pancreatic duct is significantly dilated (approximately 13 mm), irregular, and contains multiple filling defects (arrowheads) consistent with stones. ERCP indicates endoscopic retrograde cholangiopancreatography.
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Finally, although surgical procedures as discussed below may be warranted under certain conditions, up to 40% of patients undergoing total pancreatectomy will continue to have the same pain.43 The refractory nature of this condition to medical and surgical procedures prompted us to hypothesize that one mechanism leading to pain in these patients is cortical dysfunction of the region in the brain regulating visceral sensation, suggesting that symptoms are sustained by a pancreas-independent, neural-based mechanism. In support of this hypothesis, our group has shown in a double-blind, sham-controlled pilot trial of repetitive transcranial magnetic stimulation (rTMS) to suppress cortical excitation that a single session of low-frequency rTMS applied to the right secondary somatosensory area decreased pain and medication use in patients with idiopathic chronic pancreatitis.43 A larger, National Institutes of Health–funded study with longer-duration rTMS is ongoing.
Indications for Surgical Treatment
DR CALLERY: The principal role of surgery in chronic pancreatitis is palliative.42 Long-term functional improvements and enhanced quality of life are possible. By far, the most common indication for surgery is disabling chronic pain that has failed to respond to medical and endoscopic therapies, along with a clear anatomic correctable abnormality.1, 43
When the fibrosis and inflammation of chronic pancreatitis affect neighboring structures, surgery ultimately becomes necessary. This includes biliary obstruction and duodenal obstruction, which are often associated with pancreatic head–predominant disease. Pancreatic resection procedures are usually indicated in such cases. Less common but important indications for surgery relate to disruptions of the pancreatic duct. These include pseudocysts, fistulas, and pancreatic ascites.44 The surgical approaches to these consequences of advanced disease are continually being refined,45 and the best outcomes will correlate with surgeon experience.
Which Operation and Why
The choice of surgical procedure is one of the most active debates among pancreatic surgeons worldwide. No randomized trials are available to inform the debate. A surgeon's objective must be to preserve functional pancreatic tissue while addressing the anatomical abnormalities found.46 Often, the choice of operation is dictated entirely by a patient's anatomy. In the simplest classification, chronic pancreatitis can be considered as large-duct disease, small-duct disease, or head-predominant disease. The surgical correlates are drainage procedures, parenchymal resections, and various approaches to pancreatic head resection, respectively.
In patients with large-duct chronic pancreatitis characterized by a dilated (>7 mm) main pancreatic duct, drainage procedures such as the Puestow procedure or lateral pancreaticojejunostomy47 are used. Operative mortality is low (<1%) and up to 70% of properly selected patients will have enduring pain relief.47 The major problem with these drainage procedures is recurrence of symptoms after 1 year. In the case of Mr C, his response to endoscopic management mitigates against surgical intervention. However, if he has recurrent symptoms that cannot be relieved with endoscopic stone removal, a Puestow procedure would likely be of benefit, assuming his pancreatic duct is larger than 7 mm.
Because surgical drainage of nondilated ducts is ineffective, resection procedures are used for small-duct disease.48 The question is always how much of the diseased pancreas to remove. Focal duct strictures and/or cysts in the body and tail causing "segmental" pancreatitis can be managed by distal pancreatectomy. For diffuse small-duct disease, partial and even total pancreatectomy have rendered variable results. Pain does improve, but extended parenchymal resections deepen endocrine/exocrine insufficiency, prompting some to add rescue autologous islet transplantation.49
The indications for and techniques of pancreatic head resection are particularly controversial. Head-predominant disease is common, and the head is argued by some experts in the field to be the "pacemaker" of chronic pancreatitis pain. Pancreaticoduodenectomy (Whipple procedure) remains the preferred approach50 and standard for comparison.51-53
Looking Ahead
From a pancreatic surgeon's perspective, Mr C is atypical. He represents those who feel well, are active, and are productive between acute attacks. All of the operations I have described are major endeavors and predicated on certain anatomical variants of chronic pancreatitis. Mr C's pancreatic duct is not yet sufficiently dilated to warrant a ductal drainage procedure, especially since his main problem is episodic flares. An aggressive parenchymal resection would offer uncertain benefit as well, we believe, but would assuredly reduce his endocrine and exocrine functional reserve at a young age. In time, his anatomy may better declare itself as his chronic pancreatitis persists.
With regard to medical therapy, there are very few evidence-based approaches to guide decisions. However, current research is focusing on other genetic factors that may predispose to the development of chronic pancreatitis or be predictive of severity. In addition, the pathways that are involved in visceral pain are beginning to be elucidated both in animal models54 and in humans43 with chronic pancreatitis.
QUESTIONS AND DISCUSSION
QUESTION: Dr Freedman and Dr Callery, what you would each recommend for Mr C?
DR FREEDMAN: First, I would obtain a detailed, careful history, including whether there is a trigger event, such as dehydration, dietary changes, or other precipitating factors. Given his flares up to 4 times per year, it is important to have patients call as soon as possible to try to abort a severe bout. In this case, I would assess by cross-sectional imaging to see if stones or strictures have reformed and led to the attack. If so, this may be amenable to therapeutic endoscopic intervention. It is not clear that giving Mr C pancreatic enzymes will be effective.
DR CALLERY: I would recommend that Mr C not have surgery at this time and stage in his life. He has acute periodic exacerbations of chronic pancreatitis. I would suggest that he be plugged in fully with a multidisciplinary team who deal with this each day and think about these things together.
QUESTION: This young man asked what the future will hold for him after 12 years of these symptoms? What would you tell him?
DR FREEDMAN: I’d tell him that his pain should eventually resolve, although we cannot predict when this will occur. Although this has been studied in patients with idiopathic and alcohol-induced chronic pancreatitis, the time to loss of pain is highly variable and generally occurs within 10 to 15 years in alcoholism and much later in those with idiopathic pancreatitis.23-24 I would check for mutations in pancreatitis genes, as that could predict a lack of efficacy with endoscopic or surgical procedures. Mutations in the PRSS-1 gene would predict an increased risk of pancreatic cancer.55
DR CALLERY: If you had the chance to hear his entire interview, it would really strike you how poised, intelligent, and well-versed Mr C is. I think the best thing to do for this young man right now is to help him really understand his disease. He's an excellent student, he's an excellent athlete, and he has a very close-knit family. He has the support that he needs. And if you listen to his history, he talks more about his problems occurring in high school than currently. I think he is getting better. Hopefully, he's getting to the point where his pain will ultimately resolve. He's down to 1, at most 2, major flares per year. Pancreatic operations are difficult and can have significant complications, and therefore I would not advise surgery at present.
QUESTION: Have the majority of patients already had a cholecystectomy by the time they come to see you? When you see patients with pancreatitis, is there a downside to doing a cholecystectomy to rule out that as a contributing factor early on?
DR FREEDMAN: In chronic pancreatitis, there is never a reason to take out the gallbladder. There is no literature to support cholecystectomy for chronic pancreatitis, and I’ve never seen anyone get better from it. Recurrent and acute pancreatitis is a different story, though. If a patient is in his 50s or older, is having recurrent, acute pancreatitis, and is otherwise perfectly well in between episodes, then a cholecystectomy is suggested.8-9 If a patient is younger, ie, 20s or 30s, with recurrent acute pancreatitis, there is no clear data that cholecystectomy will be effective.
QUESTION: This patient is somewhat atypical in that he's not taking long-term pain medications. My understanding is that most patients with chronic pancreatitis are taking high doses of narcotics to manage pain. Are there any things that internists can do before patients reach you in terms of treatment, diagnosis, or approach to minimize patients' dependence on pain medications with this chronic disease?
DR FREEDMAN: As physicians, our mission is to treat pain. One of the problems is that chronic pancreatitis has a bad stigma associated with it, especially since there is an association with alcohol abuse. Unfortunately, patients are questioned whether they are closet alcoholics or narcotic addicts. I do talk to patients at length about the issue of narcotics and the potential for narcotic addiction. I first try other alternatives, including high doses of pancreatic enzymes, low doses of amitriptyline, or other agents at bedtime to help them with sleep as well as decrease visceral pain. If they're having significant pain, then narcotics may be necessary. As to whether they will become addicted to narcotics, it is unlikely if used judiciously and clearly for the purpose of pain control.
DR CALLERY: If I was referred a patient with chronic pancreatitis such as Mr C, the decision not to operate on him doesn't mean that my care of him is over. I will continue to see this patient regularly as part of a multidisciplinary approach. And the patient is part of that team. Only over that long period are we going to grasp whether the patient is progressing from "do nothing" to increase medical therapy to an actual operative phase.
AUTHOR INFORMATION
Corresponding Author: Steven D. Freedman, MD, PhD, Beth Israel Deaconess Medical Center, Dana 501, 330 Brookline Ave, Boston, MA 02215 (sfreedma{at}bidmc.harvard.edu).
Financial Disclosures: None reported.
Funding/Support: This Clinical Crossroads was made possible in part by a grant from the Jacqueline and Martin J. Shaevel Charitable Trust.
Role of the Sponsor: The funding organization did not participate in the collection, analysis, and interpretation of the data or in the preparation, review, or approval of the article.
Additional Contributions: We thank the patient for sharing his story and for providing permission to publish it. We thank Erin E. Hartman, MS, and Richard A. Parker, MD, Harvard Medical School and Beth Israel Deaconess Medical Center, for their thoughtful editing of this article. Ms Hartman received compensation for her contributions; Dr Parker was not paid.
This conference took place at the Surgical Grand Rounds held at Beth Israel Deaconess Medical Center, Boston, Massachusetts, on June 1, 2005.
Clinical Crossroads at Beth Israel Deaconess Medical Center is produced and edited by Risa B. Burns, MD, Eileen E. Reynolds, MD, and Amy N. Ship, MD. Tom Delbanco, MD, is series editor.
Author Affiliations: Dr Callery is Associate Professor of Surgery, Harvard Medical School, and Chief, Division of General Surgery, Beth Israel Deaconess Medical Center, and Dr Freedman is Associate Professor of Medicine, Harvard Medical School, Medical Director, Clinical Research Affairs, and Director, Pancreas Center, Beth Israel Deaconess Medical Center, Boston, Massachusetts.
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