Introduction Chronic pancreatitis is an inflammatory disorder of the pan- creas that leads to changes in the structure of the gland, ulti- mately resulting in impairment of its endocrine and exocrine functions [1]. As opposed to acute pancreatitis, where injury to the gland is transient, the morphologic and functional changes associated with chronic pancreatitis are irreversible [1–3]. Because of variations in presentation, the true preva- lence of chronic pancreatitis has been difficult to study, although most estimates range from 0.04 to 5% [1]. The vari- ous causes of chronic pancreatitis are discussed in detail in Chapters 39–43. While the gold standard for the diagnosis of chronic pancre- atitis is histologic, such an invasive approach is not feasible for most patients. As such, the diagnosis of chronic pancreatitis is typically made by other tests of pancreatic structure and func- tion [4]. Endoscopic retrograde cholangiopancreatography (ERCP), magnetic resonance cholangiopancreatography (MRCP), and endoscopic ultrasound (EUS) are three imaging modalities which, over the past decade, have rapidly changed both the diagnostic and the therapeutic approach to chronic pancreatitis. This chapter discusses the role of each of these modalities in the diagnosis of chronic pancreatitis. Diagnosis In patients with advanced disease, the diagnosis of chronic pancreatitis can be made by virtually any available test, obvi- ating the need for invasive testing [4,5]. Although a history of alcohol abuse and longstanding epigastric pain coupled with the finding of pancreatic calcifications on plain abdominal radiography is pathognomonic of chronic pancreatitis, this occurs in only 30% of cases [1]. The presentation of chronic pancreatitis can be highly variable, with differing pain pat- terns and duration; up to 20% of patients may present with so-called “painless pancreatitis.” Indeed, some patients may be minimally symptomatic or “presymptomatic” despite advanced degrees of pancreatic fibrosis [6]; these patients may often have normal laboratory and imaging studies. In this group of individuals with so-called “early” chronic pancreati- tis, the diagnosis may be particularly challenging [7]. Endoscopic retrograde cholangiopancreatography Historically, ERCP has been thought to be the most specific and sensitive imaging technique for the diagnosis of chronic pancreatitis [8–10]. In most studies, the sensitivity and speci- ficity of ERCP for the diagnosis of chronic pancreatitis have ranged from 70 to 90% and 80 to 100%, respectively [5,11–16] (Table 49.1). Ductal abnormalities detected using ERCP can be classified from normal to severe depending on the appearance of the main pancreatic duct, the number of abnormal ductal side branches identified, and the presence or absence of additional features such as evidence of ductal obstruction, severe dilation, or irregularity. Together, these cri- teria comprise the Cambridge classification of pancreato- graphic findings in chronic pancreatitis [17] (Table 49.2). Alternating strictures with ductal dilations, also known as the “chain-of-lakes” appearance, are pathognomonic for chronic pancreatitis. Other common findings include a dif- fusely dilated pancreatic duct and the presence of visible side branches (Fig. 49.1). The sensitivity and specificity of ERCP for the diagnosis of chronic pancreatitis are greatest when obvi- ous, advanced ductal abnormalities such as these are present. The sensitivity and specificity decrease as the ductal changes 477 Endoscopic retrograde cholangiopancreatography, magnetic resonance cholangiopancreatography, and endoscopic ultrasound in chronic pancreatitis Andrew S. Ross and Irving Waxman 49 9781405146647_4_049.qxd 1/30/08 11:46 AM Page 477 The Pancreas: An Integrated Textbook of Basic Science, Medicine, and Surgery, Second Edition Edited by H. G. Beger, A. L. Warshaw, M. W. Büchler, R. A. Kozarek, M. M. Lerch, J. P. Neoptolemos, K. Shiratori, D. C. Whitcomb, and B. M. Rau © 2008 Blackwell Publishing Limited, ISBN: 978-1-405-14664-7 become more subtle [11,18]. This is likely due to the fact that subtle ductal abnormalities can be caused by diseases other than chronic pancreatitis. In addition, less dramatic pancre- atographic changes are open to a certain degree of subjectivity, resulting in a high degree of interobserver variation in inter- pretation [4,11]. Several additional factors may work to negatively impact the accuracy of ERCP in the diagnosis of chronic pancreatitis. The quality of the study may have a significant effect on diag- nostic accuracy. A good-quality ERCP is defined as filling of the pancreatic duct to the second generation of side branches in the absence of a movement artifact [4,11,19]. Some have suggested that up to one-third of all studies do not meet these criteria [4]. In addition, many of the pancreatographic find- ings associated with chronic pancreatitis are nonspecific. Normal aging, pancreatic carcinoma, acute pancreatitis, and pancreatic stent placement may produce changes similar to those found in chronic pancreatitis [4,11,20,21]. As always, all radiographic findings should be interpreted within the con- text of the clinical history. ERCP has traditionally been used to establish the diagnosis of chronic pancreatitis in symptomatic patients with normal abdominal radiographs and the absence of steatorrhea. In most patients, abnormalities on ERCP correlate with func- tional pancreatic impairment. Ductal abnormalities detected using ERCP may or may not correlate with the degree of func- tional pancreatic impairment. Bozkurt et al. [16] prospectively compared ERCP findings and pancreatic function in 48 patients with an established diagnosis of chronic pancreatitis. Pancreatic insufficiency was found in none of the patients with a normal pancreatogram, whereas almost all of those with markedly abnormal studies (Cambridge class III) were found to have abnormal functional pancreatic testing. However, some patients, especially those with early chronic pancreatitis, have a normal pancreatogram [17]. In such cases, where clinical suspicion remains high despite a normal ERCP, additional diagnostic testing is warranted. Aside from the diagnosis of chronic pancreatitis, ERCP has been used to pro- vide a “road-map” of the pancreatic duct in patients with severe disease or complications requiring surgery. The use of therapeutic ERCP in chronic pancreatitis is discussed in Chapter 53. Despite its wide availability and high sensitivity for the diag- nosis of chronic pancreatitis, ERCP is an invasive procedure with a significant associated complication rate [22]. Short-term complications including perforation, hemorrhage, infection, cardiopulmonary problems, and pancreatitis have been reported to occur in 5–10% of all patients undergoing the pro- cedure, regardless of whether endoscopic sphincterotomy was performed [22,23]. In addition, ERCP carries a 0.1–0.5% mor- tality risk [11]. The risk of complications associated with ERCP is closely related to operator skill and experience [22]. Given these risks, the use of other imaging modalities (such as CHAPTER 49 478 Figure 49.1 Pancreatogram revealing a diffusely dilated main pancreatic duct with multiple visible side branches. These findings are consistent with severe chronic pancreatitis. Table 49.1 Sensitivity and specificity of endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic ultrasound (EUS) for the diagnosis of chronic pancreatitis. Imaging Sensitivity Specificity technology (%) (%) ERCP 70–90 80–100 EUS 79–87 72–91 Table 49.2 Cambridge classification of pancreatographic findings of chronic pancreatitis. (From ref. 10 with permission.) Terminology Main pancreatic duct Duct side branches Additional features Normal Normal None None Equivocal Normal Ͻ3 None Class I Normal Ն3 None Class II Abnormal Ն3 None Class III Abnormal Ն3 One or more of large cavity, filling defects, severe dilation, or irregularity 9781405146647_4_049.qxd 1/30/08 11:46 AM Page 478 EUS and MRCP) to establish the diagnosis of chronic pancre- atitis has greatly increased, thus relegating ERCP to a more therapeutic role [24]. Endoscopic ultrasound Although ERCP has high sensitivity for the diagnosis of chronic pancreatitis, it is limited because it is only able to visu- alize the pancreatic duct; pancreatic parenchymal changes cannot be appreciated. As discussed previously, the diagnostic sensitivity of ERCP for chronic pancreatitis is therefore great- est when ductal changes consistent with severe advanced chronic pancreatitis are present [7,11]. EUS was developed in the 1980s as an imaging modality designed to perform high- resolution imaging of the entire pancreas [25–27]. The use of high-frequency transducers allows the user to detect subtle parenchymal changes and minor ductal abnormalities in patients with chronic pancreatitis [28,29]. In addition, the use of EUS overcomes the major obstacles to pancreatic imaging by transabdominal ultrasound, namely intestinal bowel gas and fat [30]. EUS of the normal pancreas reveals a homogeneous echo- texture that is more echogenic than the liver. The main pan- creatic duct diameter is approximately 2.4 mm in the head, 1.8 mm in the body, and 1.2 mm in the tail. Side branches are visible using EUS; however, they are narrow, with the greatest diameter (0.8 mm) occurring in the head of the gland [30,31]. The diagnosis of chronic pancreatitis by EUS is based on the presence of up to nine abnormalities of the pancreatic duct and parenchyma [29] (Table 49.3). Ductal abnormalities include increased wall echogenicity, irregular caliber or dila- tion of the main pancreatic duct, dilation of side branches, and the presence of calculi (Fig. 49.2). Parenchymal changes include focal areas of reduced echogenicity, hyperechoic foci, the presence of cysts, and lobular morphology (Fig. 49.3). Studies vary with regard to the number of abnormalities required to make the diagnosis of chronic pancreatitis by EUS, ERCP, MRCP AND EUS IN CHRONIC PANCREATITIS 479 Table 49.3 Endoscopic ultrasound features of chronic pancreatitis. (From Ref. 32 with permission.) Parenchymal Focal areas of reduced echogenicity Hyperechoic foci (Ͼ3 mm diameter) Gland size, cysts Accentuation of lobular pattern (hypoechoic areas surrounded by hyperechoic septae) Ductal Increased duct wall echogenicity Irregular caliber of main pancreatic duct Dilation of main pancreatic duct (Ͼ3 mm in head, Ͼ2mm in body, Ͼ1 mm in tail) Dilation of side branches Calculi Figure 49.2 Endoscopic ultrasound (EUS) image revealing a dilated pancreatic duct with increased echogenicity of the duct wall. These ductal changes are commonly seen when EUS is performed in patients with chronic pancreatitis. Figure 49.3 Endoscopic ultrasound (EUS) image revealing a heterogeneous pancreas with hyperechoic foci. These findings are consistent with the parenchymal changes often identified during EUS performed in patients with chronic pancreatitis. 9781405146647_4_049.qxd 1/30/08 11:46 AM Page 479 although almost all require a minimum of three [7,29,32–36]. Minimal standard terminology for the description of endosonographic changes consistent with chronic pancreatitis has been developed [37] (Table 49.4). The sensitivity and specificity of EUS for the diagnosis of chronic pancreatitis (see Table 49.1) remains the subject of much controversy. By definition, the sensitivity and specificity of any diagnostic test are determined by comparison with the “gold standard” test for the condition of interest. A reliable gold standard for the diagnosis of chronic pancreatitis has not been universally agreed [7]. The ideal gold standard for the diagnosis of chronic pancreatitis would be pancreatic histol- ogy, but this is clearly not feasible due to the high risk associ- ated with pancreatic biopsy. In many studies, ERCP is chosen as the diagnostic gold standard, although this technique is not without its problems [7]. Chronic pancreatitis can exist in the setting of a normal pancreatogram [4,17], a high degree of interobserver variability exists in the interpretation of pancre- atograms [4,38], and the ERCP changes of chronic pancreati- tis are nonspecific [4,7,38,39]. Because of the lack of an approved gold standard diagnostic test, EUS has been compared with several different modalities in order to better understand its sensitivity and specificity for the diagnosis of chronic pancreatitis. Multiple studies have compared EUS with ERCP [7,28,29,32–36] for the diagnosis of chronic pancreatitis. In three studies [29,32,35], both stan- dard EUS criteria and the Cambridge classification for ERCP were used and the results can therefore be compared with each other directly [30]. If three endosonographic criteria are used as a cutoff for the diagnosis of chronic pancreatitis, EUS and ERCP agree in approximately 80% of cases [7,30]. Agreement is highest in cases of severe advanced chronic pancreatitis. However, in the majority of cases where the two tests disagree, EUS demonstrated abnormalities when ERCP was normal. The major question that has arisen is whether EUS is more sensitive than ERCP or whether endosonographers are simply overdiagnosing chronic pancreatitis [7,30]. The overall sensi- tivity and specificity of EUS using ERCP as the gold standard are 87% and 75%, respectively [29,32,35]. The sensitivity and specificity of EUS compared with ERCP vary with respect to the number of endosonographic criteria required to make the diagnosis of chronic pancreatitis [30]. When pancreatic function testing is used as the comparison gold standard for the diagnosis of chronic pancreatitis, EUS has a sensitivity of 79% and specificity of 72% [29,32]. Agreement was seen between the two tests in 75% of cases; however, simi- lar to the case with ERCP, of the 25% of cases where there was disagreement, 71% had abnormal EUS in the setting of normal pancreatic function testing [30], again raising the issue as to whether EUS is “overdiagnosing” chronic pancreatitis. One small study compared pancreatic histopathology with EUS for the diagnosis of chronic pancreatitis [40]. Histopathology was obtained by pancreatectomy or pancreatic biopsy in 34 patients, all of whom had undergone prior EUS. Using a threshold of three endosonographic criteria for the diag- nosis of chronic pancreatitis, the sensitivity and specificity of EUS were 87% and 64%, respectively. As the number of criteria was increased, the sensitivity and specificity moved in opposite directions. When six or more endosonographic criteria were required to diagnose chronic pancreatitis, the sensitivity and specificity were 43% and 91%, respectively. The results of this study suggested that the use of four or more endosonographic criteria (sensitivity 78%, specificity 73%) was ideal for the diag- nosis of chronic pancreatitis [30]. While pancreatic biopsy to obtain histopathology is highly invasive and associated with sig- nificant operative risk, the use of EUS-guided fine-needle aspira- tion (FNA) is less so. Although limited to cytology, the addition of FNA has expanded the utility and diagnostic accuracy of EUS for a variety of conditions. A single study [41] found that adding FNA to EUS increased the negative predictive value of EUS to CHAPTER 49 480 Table 49.4 Minimal standard terminology (MST) definitions for endoscopic ultrasound (EUS) findings in chronic pancreatitis. (From ref. 37.) EUS criteria for chronic pancreatitis MST definition Hyperechoic foci Small distinct reflectors Hyperechoic strand Small string-like hyperechoic structures Lobular out gland margin No MST definition Lobularity Containing lobules: rounded homogeneous areas separated by strands of another echogenicity Cyst Abnormal anechoic round or oval structure Stone Hyperechoic lesion with acoustic shadowing within a duct or gallbladder Calcification Hyperechoic lesion with acoustic shadow within a parenchymal organ or a mass Ductal dilation No MST definition Side-branch dilation No MST definition Duct irregularity Coarse, uneven outline of the duct Hyperechoic duct margins No MST definition Atrophy No MST definition Nonhomogeneous echo pattern No MST definition 9781405146647_4_049.qxd 1/30/08 11:46 AM Page 480 100% and the specificity to 64% when compared with ERCP as the diagnostic gold standard. Although no standardized histo- logic or cytologic criteria exist for the diagnosis of chronic pan- creatitis by FNA, a scoring system was used which graded each specimen with regard to the presence of an inflammatory cellular infiltrate. The results of this study suggest that FNA is most help- ful for excluding chronic pancreatitis when mild or patchy parenchymal abnormalities with unclear significance are identi- fied on EUS. FNA was generally well tolerated; mild acute pan- creatitis occurred in 2 of 27 patients studied. Given the ability to visualize both the pancreatic parenchyma and duct, in addition to its excellent sensitivity and low associ- ated procedural risk, the use of EUS for the diagnosis of chronic pancreatitis has increased over the past decade. As such, the use of minimal standard terminology to describe endosonographic findings and the appropriate number of endosonographic abnormalities required to make the diagnosis of chronic pancre- atitis are of critical importance. The accuracy of any diagnostic test is related to the reproducibility of its results [7]. When 11 experienced endosonographers who were blinded to the clinical history independently evaluated previously taped examinations for the presence of EUS criteria of chronic pancreatitis, diagnos- tic agreement was reached at a rate comparable with other endoscopic or radiographic tests [42]. Agreement was highest for ductal dilatation and lobularity. As with any diagnostic test, the clinical history is key to interpreting the results of EUS in the diagnosis of chronic pancreatitis. Magnetic resonance cholangio- pancreatography While ERCP has been associated with an incidence of acute pancreatitis in up to 10% of individuals who undergo this procedure [32], MRCP is able to provide high-quality imaging of the pancreatic and biliary ducts in a noninvasive manner [43]. Wallner et al. [44] first described MRCP in 1991. At that time, the study was time-consuming with questionable image quality. Over the past 15 years, however, the acquisition time for single images has gone from 5 min to 2 s, allowing more widespread use of this technology. In most centers, the imple- mentation of high-quality MRCP into clinical practice has replaced diagnostic ERCP [24]. Takehara et al. [45] first compared MRCP, specifically mag- netic resonance pancreatography, with ERCP for the diagnosis of chronic pancreatitis. High-quality images of the pancreatic duct in the head, body, and tail of the gland were obtained in 70%, 64%, and 53%, respectively, of patients, all of whom had been previously diagnosed with chronic pancreatitis based on ERCP. Agreement between the two tests was observed in 83–92% of cases of ductal dilatation, 70–92% of cases of ductal narrowing, and 92–100% of cases with ductal filling defects. This study also found low interobserver variation for most findings, although MRCP did tend to overestimate the extent of pancreatic ductal stenosis [43,45]. Other studies have yielded similar findings [46]. Secretin is a hormone secreted by the gastrointestinal tract that leads to rapid secretion of a bicarbonate-rich fluid from the exocrine pancreas [43,47]. As a result, the volume of fluid in the pancreatic duct increases. The administration of intra- venous secretin to improve imaging of the pancreatic duct was first described in combination with transabdominal ultra- sonography for the diagnosis of chronic pancreatitis [48,49]. Because of the tendency of MRCP to overestimate pancreatic ductal stenosis, Takehara et al. [50] studied the use of secretin stimulation during the acquisition of images in order to improve signal intensity and imaging of the pancreatic duct in patients suspected of having pancreatic disease. The investiga- tors found that the use of secretin improved evaluation of the main pancreatic duct and its side branches compared with imaging not using secretin stimulation (Fig. 49.4). These results have been replicated by other groups [47,51]. Since this initial study, several investigations have focussed specifically on secretin-enhanced MRCP for the diagnosis of chronic pancreatitis [52,53]. Manfredi et al. [52] studied this modality in 31 patients with chronic pancreatitis. The use of secretin increased the percentage of visible pancreatic duct segments from 91 to 100% and side branches from 71 to 100%. Although the improved ductal visualization with secretin was not statistically significant, the authors noted that improved visualization of the ductal side branches may allow earlier diagnosis of chronic pancreatitis, thus reducing the ERCP, MRCP AND EUS IN CHRONIC PANCREATITIS 481 Figure 49.4 Secretin-stimulated magnetic resonance cholangiopancreatography revealing a markedly dilated main pancreatic duct with multiple visible side branches. These findings are consistent with severe chronic pancreatitis. 9781405146647_4_049.qxd 1/30/08 11:46 AM Page 481 false-negative rate and improving the specificity of MRCP for this diagnosis. Standardized criteria for the diagnosis of chronic pancreatitis by MRCP have yet to be developed. Aside from improving delineation of the pancreatic ductal morphology, secretin-enhanced MRCP may have value in the measurement of pancreatic exocrine function. Matos et al. [47] performed MRCP in 10 volunteers and 13 patients with sus- pected pancreatic disease. Pancreatograms were obtained prior to and then at 30-s intervals following the administration of secretin. The volume of filling within the duodenum was used as a quantitative measure of pancreatic function. The results were compared with ERCP and secretin stimulation testing. The study found that the mean duodenal filling score was sig- nificantly lower in patients with known reduced exocrine func- tion compared with that in volunteers, thus providing the first evidence that secretin-stimulated MRCP has the potential to detect impaired pancreatic exocrine function. These results have been confirmed by other investigators [52,54–56]. Direct comparisons of MRCP with EUS for the diagnosis of chronic pancreatitis have yet to be performed. In comparison with EUS and ERCP, MRCP is certainly the least invasive. Secretin-stimulated MRCP has the additional advantage of evaluating pancreatic function, an attribute not shared by EUS or ERCP. Although not yet studied, this feature may enhance the specificity of MRCP for the diagnosis of chronic pancreati- tis. ERCP does not provide detailed images of the pancreatic parenchyma; this is a potential disadvantage compared with EUS, which has the ability to detect both ductal and parenchy- mal abnormalities. Magnetic resonance imaging (MRI) of the pancreas is possible at the same time as MRCP, although this adds cost and time to the examination. The MRI findings asso- ciated with chronic pancreatitis [57] are beyond the scope of this chapter. Due to its minimally invasive nature and high cor- relation with ERCP findings, MRCP is often ordered as the first test for the diagnosis of chronic pancreatitis in cases where advanced imaging modalities are required [52]. Diagnostic approach The use of advanced imaging modalities such as ERCP, MRCP, and EUS for the diagnosis of chronic pancreatitis is not required in the majority of cases. Indeed, in many cases of chronic alcoholic pancreatitis, the clinical history alone can be sufficient to make the diagnosis [11]. However, in some cases, especially early chronic pancreatitis, advanced imaging is required. Of these three modalities, EUS likely has the greatest ability to diagnose early disease. Although it is an invasive diagnostic test, the complication rate associated with EUS is less than that of ERCP and it has the ability to detect both mor- phologic and ductal abnormalities. While MRCP is clearly the least invasive, it is an expensive test with results that may be center-dependent. In addition, the ability to visualize the pan- creatic duct alone may decrease its diagnostic sensitivity for early disease. Finally, it is the least studied of the three modali- ties discussed in this chapter. While it is often considered the gold standard, the high rate of procedure-related complications associated with ERCP has limited its use in chronic pancreatitis to the performance of therapeutic interventions. References 1. Steer ML, Waxman I, Freedman S. Chronic pancreatitis. N Engl J Med. 1995;332:1482–90. 2. Singer MV, Gyr K, Sarles H. Revised classification of pancreatitis. Report of the Second International Symposium on the Classification of Pancreatitis in Marseille, France, March 28–30, 1984. Gastroenterology 1985;89:683–5. 3. Sarner M, Cotton PB. Classification of pancreatitis. Gut 1984;25:756–9. 4. Forsmark CE, Toskes PP. What does an abnormal pancreatogram mean? Gastrointest Endosc Clin North Am 1995;5:105–23. 5. Niederau C, Grendell JH. Diagnosis of chronic pancreatitis. Gastroenterology 1985;88:1973–95. 6. Pitchumoni CS, Glasser M, Saran RM, Panchacharam P, Thelmo W. Pancreatic fibrosis in chronic alcoholics and nonalcoholics without clinical pancreatitis. Am J Gastroenterol 1984;79:382–8. 7. Forsmark CE. The diagnosis of chronic pancreatitis. Gastrointest Endosc 2000;52:293–8. 8. Axon AT. Endoscopic retrograde cholangiopancreatography in chronic pancreatitis. Cambridge classification. Radiol Clin North Am 1989;27:39–50. 9. Novis BH, Narunsky L, Bank S. Endoscopic retrograde cholan- giopancreatography in the evaluation of pancreatic disease. S Afr Med J 1976;50:1501–5. 10. Bolan PJ, Fink AS. Endoscopic retrograde cholangiopancreatog- raphy in chronic pancreatitis. World J Surg 2003;27:1183–91. 11. Forsmark CE. Chronic pancreatitis. In: Feldman M, Friedman L, Sleisenger M, eds. Gastrointestinal and Liver Disease. Philadelphia: WB Saunders, 2002: 953. 12. Girdwood AH, Hatfield AR, Bornman PC, Denyer ME, Kottler RE, Marks IN. Structure and function in noncalcific pancreatitis. Dig Dis Sci 1984;29:721–6. 13. Malfertheiner P, Buchler M, Stanescu A, Ditschuneit H. Exocrine pancreatic function in correlation to ductal and parenchymal mor- phology in chronic pancreatitis. Hepatogastroenterology 1986; 33:110–14. 14. Lankisch PG, Seidensticker F, Otto J et al. Secretin–pancreozymin test (SPT) and endoscopic retrograde cholangiopancreatography (ERCP): both are necessary for diagnosing or excluding chronic pancreatitis. Pancreas 1996;12:149–52. 15. Braganza JM, Hunt LP, Warwick F. Relationship between pancre- atic exocrine function and ductal morphology in chronic pancre- atitis. Gastroenterology 1982;82:1341–7. 16. Bozkurt T, Braun U, Leferink S, Gilly G, Lux G. Comparison of pancreatic morphology and exocrine functional impairment in patients with chronic pancreatitis. Gut 1994;35:1132–6. 17. Axon AT, Classen M, Cotton PB, Cremer M, Freeny PC, Lees WR. Pancreatography in chronic pancreatitis: international defi- nitions. Gut 1984;25:1107–12. 18. Lehman GA. Role of ERCP and other endoscopic modalities in chronic pancreatitis. Gastrointest Endosc 2002;56(6 suppl):S237–S240. 19. Johanson JF, Cooper G, Eisen GM et al. Quality assessment of ERCP. Endoscopic retrograde cholangiopacreatography. Gastrointest Endosc 2002;56:165–9. CHAPTER 49 482 9781405146647_4_049.qxd 1/30/08 11:46 AM Page 482 20. Anand BS, Vij JC, Mac HS, Chowdhury V, Kumar A. Effect of aging on the pancreatic ducts: a study based on endoscopic retro- grade pancreatography. Gastrointest Endosc 1989;35:210–13. 21. Sherman S, Hawes RH, Savides TJ et al. Stent-induced pancreatic ductal and parenchymal changes: correlation of endoscopic ultra- sound with ERCP. Gastrointest Endosc 1996;44:276–82. 22. Freeman ML. Adverse outcomes of endoscopic retrograde cholangiopancreatography. Rev Gastroenterol Disord 2002; 2:147–68. 23. Masci E, Toti G, Mariani A et al. Complications of diagnostic and therapeutic ERCP: a prospective multicenter study. Am J Gastroenterol 2001;96:417–23. 24. Anon. NIH state-of-the-science statement on endoscopic retro- grade cholangiopancreatography (ERCP) for diagnosis and ther- apy. NIH Consens State Sci Statements 2002;19:1–26. 25. Dimagno EP, Regan PT, Clain JE, James EM, Buxton JL. Human endoscopic ultrasonography. Gastroenterology 1982;83:824–9. 26. DiMagno EP, Buxton JL, Regan PT et al. Ultrasonic endoscope. Lancet 1980;i:629–31. 27. Hisanaga K, Hisanaga A, Nagata K, Ichie Y. High speed rotating scanner for transgastric sonography. Am J Roentgenol 1980; 135:627–9. 28. Kahl S, Glasbrenner B, Leodolter A, Pross M, Schulz HU, Malfertheiner P. EUS in the diagnosis of early chronic pancreati- tis: a prospective follow-up study. Gastrointest Endosc 2002; 55:507–11. 29. Wiersema MJ, Hawes RH, Lehman GA, Kochman ML, Sherman S, Kopecky KK. Prospective evaluation of endoscopic ultrasonog- raphy and endoscopic retrograde cholangiopancreatography in patients with chronic abdominal pain of suspected pancreatic ori- gin. Endoscopy 1993;25:555–64. 30. Raimondo M, Wallace MB. Diagnosis of early chronic pancreati- tis by endoscopic ultrasound. Are we there yet? JOP 2004;5:1–7. 31. Wiersema MJ, Wiersema LM. Endosonography of the pancreas: normal variation versus changes of early chronic pancreatitis. Gastrointest Endosc Clin North Am 1995;5:487–96. 32. Catalano MF, Lahoti S, Geenen JE, Hogan WJ. Prospective eval- uation of endoscopic ultrasonography, endoscopic retrograde pancreatography, and secretin test in the diagnosis of chronic pancreatitis. Gastrointest Endosc 1998;48:11–17. 33. Nattermann C, Goldschmidt AJ, Dancygier H. Endosonography in chronic pancreatitis: a comparison between endoscopic retro- grade pancreatography and endoscopic ultrasonography. Endoscopy 1993;25:565–70. 34. Buscail L, Escourrou J, Moreau J et al. Endoscopic ultrasonogra- phy in chronic pancreatitis: a comparative prospective study with conventional ultrasonography, computed tomography, and ERCP. Pancreas 1995;10:251–7. 35. Sahai AV, Zimmerman M, Aabakken L et al. Prospective assess- ment of the ability of endoscopic ultrasound to diagnose, exclude, or establish the severity of chronic pancreatitis found by endoscopic retrograde cholangiopancreatography. Gastrointest Endosc 1998;48:18–25. 36. Hastier P, Buckley MJ, Francois E et al. A prospective study of pancreatic disease in patients with alcoholic cirrhosis: compara- tive diagnostic value of ERCP and EUS and long-term signifi- cance of isolated parenchymal abnormalities. Gastrointest Endosc 1999;49:705–9. 37. Aabakken L. Standardized terminology in endoscopic ultra- sound. Eur J Ultrasound 1999;10:179–83. 38. Schmitz-Moormann P, Himmelmann GW, Brandes JW et al. Comparative radiological and morphological study of human pancreas. Pancreatitis like changes in postmortem ductograms and their morphological pattern. Possible implication for ERCP. Gut 1985;26:406–14. 39. Hayakawa K, Tanaka F, Torizuka T et al. Bronchial artery embolization for hemoptysis: immediate and long-term results. Cardiovasc Intervent Radiol 1992;15:154–8; discussion 8–9. 40. Zimmerman M, Mishra G, Lewin D et al. Comparison of EUS findings with histopathology in chronic pancreatitis [Abstract]. Gastrointest Endosc 1997;45:AB185. 41. Hollerbach S, Klamann A, Topalidis T, Schmiegel WH. Endoscopic ultrasonography (EUS) and fine-needle aspiration (FNA) cytology for diagnosis of chronic pancreatitis. Endoscopy 2001;33:824–31. 42. Wallace MB, Hawes RH, Durkalski V et al. The reliability of EUS for the diagnosis of chronic pancreatitis: interobserver agreement among experienced endosonographers. Gastrointest Endosc 2001;53:294–9. 43. Merkle EM, Baillie J. Exocrine pancreatic function: evaluation with MR imaging before and after secretin stimulation. Am J Gastroenterol 2006;101:137–8. 44. Wallner BK, Schumacher KA, Weidenmaier W, Friedrich JM. Dilated biliary tract: evaluation with MR cholangiography with a T2-weighted contrast-enhanced fast sequence. Radiology 1991;181:805–8. 45. Takehara Y, Ichijo K, Tooyama N et al. Breath-hold MR cholan- giopancreatography with a long-echo-train fast spin-echo sequence and a surface coil in chronic pancreatitis. Radiology 1994;192:73–8. 46. Barish MA, Yucel EK, Soto JA, Chuttani R, Ferrucci JT. MR cholangiopancreatography: efficacy of three-dimensional turbo spin-echo technique. Am J Roentgenol 1995;165:295–300. 47. Matos C, Metens T, Deviere J et al. Pancreatic duct: morphologic and functional evaluation with dynamic MR pancreatography after secretin stimulation. Radiology 1997;203:435–41. 48. Bolondi L, Gaiani S, Gullo L, Labo G. Secretin administration induces a dilatation of main pancreatic duct. Dig Dis Sci 1984;29:802–8. 49. Glaser J, Hogemann B, Krummenerl T et al. Sonographic imaging of the pancreatic duct. New diagnostic possibilities using secretin stimulation. Dig Dis Sci 1987;32:1075–81. 50. Takehara Y, Ichijo K, Tooyama N et al. [Enhanced delineation of the pancreatic duct in MR cholangiopancreatography (MRCP) with a combined use of secretin.] Nippon Igaku Hoshasen Gakkai Zasshi 1995;55:255–6. 51. Nicaise N, Pellet O, Metens T et al. Magnetic resonance cholan- giopancreatography: interest of IV secretin administration in the evaluation of pancreatic ducts. Eur Radiol 1998;8:16–22. 52. Manfredi R, Costamagna G, Brizi MG et al. Severe chronic pan- creatitis versus suspected pancreatic disease: dynamic MR cholangiopancreatography after secretin stimulation. Radiology 2000;214:849–55. 53. Manfredi R, Costamagna G, Vecchioli A, Colagrande C, Spina S, Marano P. [Dynamic pancreatography with magnetic resonance after functional stimulus with secretin in chronic pancreatitis.] Radiol Med (Torino) 1998;96:226–31. 54. Cappeliez O, Delhaye M, Deviere J et al. Chronic pancreatitis: evaluation of pancreatic exocrine function with MR pancreatog- raphy after secretin stimulation. Radiology 2000;215:358–64. 55. Heverhagen JT, Battmann A, Kirsch M et al. Magnetic resonance hydrometry: non-invasive quantification of the exocrine pancre- atic function. ROFO 2002;174:291–6. 56. Punwani S, Gillams AR, Lees WR. Non-invasive quantification of pancreatic exocrine function using secretin-stimulated MRCP. Eur Radiol 2003;13:273–6. 57. Miller FH, Keppke AL, Wadhwa A, Ly JN, Dalal K, Kamler VA. MRI of pancreatitis and its complications: part 2, chronic pancre- atitis. Am J Roentgenol 2004;183:1645–52. ERCP, MRCP AND EUS IN CHRONIC PANCREATITIS 483 9781405146647_4_049.qxd 1/30/08 11:46 AM Page 483 484 Introduction In the minority of patients (i.e., 5.8–20%), chronic pancreatitis takes a primarily painless course [1–7]. Exocrine and endocrine insufficiency are the dominating symptoms. For the majority of patients, however, pain is the decisive symptom, causing much discomfort in their daily lives. Some studies have correlated the course of pain in chronic pancreatitis with the duration of the disease, progressing exocrine and endocrine pancreatic insuffi- ciency, and morphologic changes such as pancreatic calcifica- tion and duct abnormalities. Furthermore, the course of pain has been studied following alcohol abstinence and after surgery in some groups. Pain decrease and duration of chronic pancreatitis Whether progressive parenchymal destruction of the pancreas leads to pain decrease has been repeatedly debated [8,9]. Ammann’s group has claimed that pain decreases with increas- ing duration of the disease [3,10,11]. In one long-term study, 85% of 145 patients with chronic pancreatitis felt no more pain after 4.5 years (median) from onset of the disease [3]. In another series, in which the interval between the onset of alcohol- induced chronic pancreatitis and pain relief was compared in surgically and nonsurgically treated patient groups, the curves were virtually parallel: pain relief was obtained in about 50% within 6 years and in more than 80% within 10 years from the onset of illness [12]. The reports from Zürich are at variance with the studies from Japan and Germany. Miyake et al. [6] found that only 48.2% of patients with chronic pancreatitis became free of pain within 5 years, but 66–73% became free of pain after more than 5 years. This showed that every third or fourth patient still suffered from relapsing pain attacks even after a long observation period. Our group reported that the incidence of relapsing pain attacks decreased during the observation period, but more than half of the patients (53%) still suffered from relapsing pain attacks after more than 10 years of observation [7]. At present, the course of pain in alcoholic and idiopathic chronic pancreatitis remains unclarified. Layer et al. [13] investigated a group of patients with idiopathic chronic pancreatitis who had never consumed alcoholic beverages dur- ing their lifetime. They found that patients with early-onset pancreatitis (under 35 years of age) have a long course of severe pain from the start of their illness, whereas patients with late- onset pancreatitis (over 35 years) have a mild and often painless course. Both forms differ from alcoholic pancreatitis in having an equal gender distribution and a much slower rate of calcifi- cation. In contrast, our group has found that the course of pain is the same in alcohol- and nonalcohol-induced chronic pancre- atitis [14]. Even when we divided the nonalcoholic group into teetotallers and patients with little alcohol consumption, and separately compared their course of pain with alcoholics, there were no differences concerning pain relief among the three groups [15]. Further studies are required. Pain decrease and progressing exocrine and endocrine pancreatic insufficiency The Swiss group have repeatedly observed pain decrease when exocrine and endocrine pancreatic function declines [8–11]. Similarly, Girdwood et al. [16] have reported from South Africa that pain decreases when exocrine pancreatic function deteriorates. Conversely, groups from Denmark and Germany have reported the opposite. Thorsgaard Pedersen et al. [17] from Copenhagen found no correlation between pain and exocrine pancreatic function. Our group in Göttingen [7] have used the secretin–pancreozymin test and fecal fat analysis to evaluate exocrine pancreatic insufficiency, whereas the Swiss group had used only indirect pancreatic function tests, i.e., chymotrypsin measurements, to evaluate exocrine pancreatic insufficiency [3]. We used a clear-cut grading of the severity of exocrine pan- creatic insufficiency: mild impairment was defined as reduced enzyme output, moderate impairment as a decreased bicarbon- ate concentration along with reduced enzyme output but nor- mal fecal fat excretion, and severe impairment was equated with an abnormal secretin–pancreozymin test plus steatorrhea. At the end of the observation period, 141 (45%) of 311 patients with painful chronic pancreatitis had severe exocrine pancreatic insufficiency. The majority of them (81/144, 57%) still suffered from pain attacks. Additionally, we studied the course of pain in correlation with endocrine pancreatic insufficiency. Endocrine pancreatic insuffi- ciency was classified as absent, moderate (diabetes mellitus Natural course of chronic pancreatitis Paul Georg Lankisch 50 9781405146647_4_050.qxd 1/30/08 11:46 AM Page 484 The Pancreas: An Integrated Textbook of Basic Science, Medicine, and Surgery, Second Edition Edited by H. G. Beger, A. L. Warshaw, M. W. Büchler, R. A. Kozarek, M. M. Lerch, J. P. Neoptolemos, K. Shiratori, D. C. Whitcomb, and B. M. Rau © 2008 Blackwell Publishing Limited, ISBN: 978-1-405-14664-7 treated only by diet with or without oral medication), and severe (requiring insulin). At the end of the observation period, 117 (38%) patients were classified as having severe endocrine pan- creatic insufficiency. The majority of them (69/117, 59%) still suffered from pain attacks [7,18]. Thus, according to our results, the progression of exocrine and endocrine pancreatic insufficiency has limited, if any, influence on the course of pain in chronic pancreatitis. Pain decrease and development of morphologic changes in the pancreas (pancreatic calcifications and/or duct abnormalities) The Swiss group [3,10] showed an increased incidence of pan- creatic calcifications, which in turn was associated with pain decrease. However, in a later survey the same group reported regression of pancreatic calcifications in a long-term study of patients with chronic pancreatitis [19]. Thus, the prognostic role of pancreatic calcifications in determining the course of pain is unclear. Furthermore, the Swiss results are at variance with two other studies. Malfertheiner et al. [20] found that 89% of patients had pain despite pancreatic calcifications observed on computed tomography, of whom 39% had very intense pain. In our study, freedom from pain was significantly higher in the calcification group compared with the noncalcification group. However, the majority of patients with pancreatic calcifica- tions (56%) still had relapsing pain attacks [7]. The correlation between pain and pancreatic duct changes or pressure in the duct system is also not clear. Ebbehøj et al. [21,22] measured pancreatic tissue fluid pressure percuta- neously or intraoperatively and found a significant correlation with pain in patients with chronic pancreatitis but not with the results of endoscopic retrograde cholangiopancreatography (ERCP), i.e., regional pressure tended to be highest in the region of the pancreas with the largest but not the smallest duct diam- eter. Jensen et al. [23] found no correlation between pancreatic duct changes and pain. Warshaw et al. [24] found that 2 of 10 patients, 1 year after lateral pancreaticojejunostomy, had no pain relief despite a patent anastomosis detected by ERCP. Two investigations have confirmed the nonparallelism between pancreatic duct changes and pain relief. Malfertheiner et al. [20] found severe pain in only 62% of patients who had advanced pancreatic duct changes demonstrated by ERCP. We found no significant correlation between pancreatic duct abnormalities detected by ERCP and pain in 88 patients with chronic pancre- atitis [7]. Severe pancreatic duct abnormalities, as defined by the Cambridge classification [25], were present in 42 patients, but only 16 (31%) of these became free of pain. Despite a normal pancreatic duct in 14 patients, 10 (71%) suffered from persisting pain [7]. Thus, morphologic changes such as pancreatic calcifications or pancreatic duct abnormalities are not necessarily helpful in determining the prognosis of chronic pancreatitis or predict- ing the course of pain. Recently it has been shown that smok- ing has an effect on the natural course of the disease since it increases the risk of pancreatic calcification in late-onset but not early-onset idiopathic chronic pancreatitis [26]. Pain decrease and alcohol abuse Since alcoholism is the leading etiologic factor in chronic pan- creatitis, several studies have investigated whether alcohol abstinence influences pain or progression of the disease. Sarles and Sahel [27] reported that 50% of their patients with chronic pancreatitis experienced pain relief when alcohol abuse was discontinued, whereas Trapnell [28] reported a fig- ure of 75%. Two other investigations have confirmed that abstinence can be helpful. Miyake et al. [6] demonstrated pain relief in 60% of their patients who discontinued or reduced alcohol intake, whereas spontaneous pain relief was seen in only 26% of the group who continued drinking. In another study, 66 (31%) of 214 patients with alcoholic chronic pancreatitis were motivated to stop drinking [7]. Pain relief was obtained in only 52% of these patients, whereas spontaneous relief in alcoholics was seen in 37%. Thus, alcohol abstinence in every second patient with chronic pancreatitis will probably lead to some improve- ment of pain, but why exactly abstinence helps in some cases but not others remains to be investigated. Pain decrease and interventional procedures Interventional procedures for pain treatment in chronic pancre- atitis include fragmentation of stones by extracorporeal shock- wave lithotripsy (ESWL), endoscopic stone extraction, and bridging of pancreatic strictures by stent applications. Reports of the effect of these procedures on pain are controversial and con- trolled studies are lacking. A large Japanese study of 555 patients who underwent ESWL for pancreatic stones reported a success rate of 92.4% (fragmentation of stones) and a complete stone clearance rate after ESWL alone or in combination with inter- ventional endoscopy of 72.6%. Symptom relief was achieved in 91.1% of the patients. Complications developed in 6.3% of the patients, including acute pancreatitis in 5.4%. A total of 504 patients were followed up for a mean of 44.3 months, during which 122 (22%) suffered stone recurrence (mean time to recur- rence, 25.1 months); 22 (4.1%) required surgery [29]. In another series from Japan, a total of 117 patients with pancreatic stones underwent ESWL and endoscopic treatment. Immediate pain relief was achieved in 97% and complete removal of stones in 56%. During long-term follow-up over 3 years, 70% of the patients continued to be asymptomatic [30]. These results are at variance with a smaller German study in 80 patients with chronic pancreatitis, in whom ESWL was always followed by a further NATURAL COURSE OF CHRONIC PANCREATITIS 485 9781405146647_4_050.qxd 1/30/08 11:46 AM Page 485 CHAPTER 50 486 endoscopic procedure. Treatment success was defined as com- plete clearance of the main pancreatic duct or partial clearance that allowed implantation of a pancreatic stent. Successful treat- ment was more frequent in patients with solitary stones. The mean duration of follow-up was 40 (range 24–92) months. Pain relief and necessity for further analgesia was independent of ESWL results [31] (Table 50.1). Thus, in this study pancreatic drainage by ESWL and endoscopy had almost no effect on pain in chronic pancreatitis in the long term [32]. The effect of pancreatic stents on pain in chronic pancreatitis is even more controversial. Patients undergoing pancreatic duct stent placement for disrupted ducts, isolated strictures, pancreas divisum, and hypertensive pancreatic sphincters showed subse- quent ductal changes consistent with chronic pancreatitis in 36%, even though 72% of these patients had a normal initial pancreatogram [33]. Furthermore, patients with preoperative endoscopic pancreatic stenting had frequent postoperative com- plications, mostly septic, and a prolonged hospital stay [34]. A surgical review of the pitfalls and liminations of stenting in chronic pancreatitis reported that the indications for surgery in patients with a pancreatic stent were severe abdominal pain in 100%, relapsing pain attacks in 77%, and necrotizing pan- creatitis in 14%. Before being selected for surgery, 4.5 ERCPs and 3.7 stent exchanges were performed per patient. Thus, from the surgical point of view, endoscopic pancreatic duct stenting in chronic pancreatitis seems not to be indicated because of a low success rate and a substantial risk of complications [35]. The latter results are in sharp contrast to a long-term out- come study of pancreatic stenting in severe chronic pancreati- tis in 100 patients from Belgium. The majority (70%) of patients who responded to pancreatic stenting remained pain- free after definitive stent removal. However, a significantly higher restenting rate was observed in patients with chronic pancreatitis and pancreas divisum [36]. Obviously, the results are also different in special subgroups. Endoscopic stenting of biliary strictures in chronic pancreatitis provided an excellent short-term but only moderate long-term result in another study from Germany. Patients without calcifications of the pancreatic head benefit from biliary stenting. However, patients with calcifications had a 17-fold increased risk of fail- ure during the course of a 12-month follow-up [37]. Of special interest is a recent prospective randomized trial that compared endoscopic with surgical treatment of chronic pancreatitis. Endoscopic treatment included pancreatic sphinc- terotomy in all and additional stenting of the pancreatic duct in 33 (52%) patients. Mean duration of stent treatment was 16 (range 12–27) months, and stents were exchanged six times (range 4–9). Surgical treatment included pancreatic resection in 61 (80%) and drainage procedures in 15 (20%) patients. Although the short-term effects were similar, the results after 5 years of follow-up showed a comparatively low rate of patients with complete absence of abdominal pain. However, the results for surgery were significantly better than for endotherapy (Table 50.2) [38]. The study has been criticized for the random- ization, which was agreed to by only 51.4% of the patients. For the time being, reports of treatment of chronic pancre- atitis using ERCP by removal or destruction of stones, place- ment of stents, and dilation of strictures suggest that both immediate and long-term pain relief are possible. No con- trolled studies support the generalizability of this finding or the merit of this approach compared with other management strategies. Studies of this area would be of value [39]. Pain decrease and surgery During the course of the disease, every second to fourth patient needs surgical treatment because of pain and/or organ compli- cations, such as pancreatic pseudocysts [3,7]. The choice of surgical procedure depends on the special circumstances of each patient. However, it is unclear to what extent surgical treatment influences the course of pain since the different stud- ies cannot be compared for the following reasons. • The definition of freedom from pain was often vague, and pain symptoms were usually not measured. Measurement on an analog scale is recommended [18]. • Not all patients received the same surgical treatment for the same indication. Several authors do not recommend perform- ing an indicated resection in alcoholics because of the difficult postoperative treatment of diabetes mellitus in these patients [40,41]. • Although continued alcohol abuse distinctly worsens the effect of surgical treatment [42–44], it is still difficult to deter- mine whether postoperative deterioration results from chronic pancreatitis or continued alcohol abuse, or from the surgical treatment. Table 50.1 Long-term effect on pain in 80 patients with chronic pancreatitis treated with extracorporeal shock wave lithotripsy. (From ref. 31 with permission.) Successful Unsuccessful treatment treatment (N ϭ 43) (N ϭ 37) P value Considerable or complete pain relief 34 (79%) 27 (73%) 0.75 No further analgesia necessary 27 (63%) 16 (43%) 0.23 Table 50.2 Five years follow-up of abdominal pain in a prospective randomized trial comparing endoscopic with surgical treatment for chronic pancreatitis. (From ref. 38 with permission.) Abdominal Endotherapy Surgery pain (N ϭ 64) (N ϭ 76) P value Complete absence 14.3% 36.9% 0.002 Partial relief 50.8% 49.3% NS No success 34.9% 13.8% NS NS, not significant. 9781405146647_4_050.qxd 1/30/08 11:46 AM Page 486 [...]... thrombosis, and to evaluate the remaining pancreas and bile duct ERCP is also used to define whether the pseudocyst is in communication with the main pancreatic duct and whether pancreatic duct obstruction exists If the diagnosis of pseudocyst is not secure based on the patient’s history and evolution of the imaging studies, EUS allows further characterization of the pseudocyst and also allows aspiration of. .. reintegration, compliance, and may mitigate the further course of the disease and decrease the complication rate Abstinence from smoking may retard the progress of arteriosclerosis, may reduce the progression of pancreatic fibrosis, and prevent complications of smoking such as lung cancer Therapy of pain is based on its supposed pathogenesis, which is multifactorial Therapy of pain should be based on the cause... 50 18 Lankisch PG, Andrén-Sandberg Å Standards for the diagnosis of chronic pancreatitis and for the evaluation of treatment Int J Pancreatol 1993;14:205–12 19 Ammann RW, Muench R, Otto R, Buehler H, Freiburghaus AU, Siegenthaler W Evolution and regression of pancreatic calcification in chronic pancreatitis A prospective long-term study of 107 patients Gastroenterology 1988;95:1018–28 20 Malfertheiner... Ultimately, treatment should be based on defining the natural history of the pseudocyst and by understanding the relationship of the pseudocyst to the surrounding organs and the pancreatic ductal system References 1 Buscher HC, Jansen JB, van Dongen R, Bleichrodt RP, van Goor H Long-term results of bilateral thoracoscopic splanchnicectomy in patients with chronic pancreatitis Br J Surg 2002;89:158–62 2 Elechi... fluid collections and acute pseudocysts On the other hand, the natural history of chronic pseudocysts more clearly demonstrates that resolution rarely occurs Aranha et al [7] reported 93 patients with pseudocysts who were followed by serial ultrasound to define natural history Overall, only 28% of pseudocysts resolved The Pancreas: An Integrated Textbook of Basic Science, Medicine, and Surgery, Second... with the main pancreatic duct and whether any downstream pancreatic duct obstruction exists If communication does not exist or if a distal pancreatic duct stricture is present, resolution of the pseudocyst may not occur and this may guide the surgeon in determining the optimal treatment strategy If the diagnosis of pseudocyst is not secured based on the patient’s history and CT scan, EUS allows further... Duodenum-preserving resection of the head of the pancreas in chronic pancreatitis with inflammatory mass in the head World J Surg 1990;14:83–7 67 Adams DB, Ford MC, Anderson MC Outcome after lateral pancreaticojejunostomy for chronic pancreatitis Ann Surg 1994;219:481–9 68 Frey CF, Amikura K Local resection of the head of the pancreas combined with longitudinal pancreaticojejunostomy in the management of patients with... 90%, and 92%, respectively Morbidity ranged from 9 to 36% and included bleeding from the surgical anastamosis, infection of the pseudocyst, erosion of the pseudocyst wall, and rupture of pseudoaneurysms Several studies have also compared surgical with percutaneous drainage of pancreatic pseudocysts In a study by Morton et al [29], a national comparison of these two techniques was investigated by analyzing... known chronic pancreatitis and pancreatic duct changes of chronic pancreatitis Finally, Bourliere and Sarles [9] reviewed 106 consecutive patients with pseudocysts of the pancreas associated with pancreatitis Of these, 77 patients presented with chronic pancreatitis but only 9% resolved spontaneously, the majority of pseudocysts being less than 3 cm in size Pseudocysts that resolve spontaneously may... Surgical management of complications associated with percutaneous and/ or endoscopic management of pseudocyst of the pancreas Ann Surg 2005;241:948–60 22 Lewandrowski KB, Southern JF, Pins MR, Compton CC, Warshaw AL Cyst fluid analysis in the differential diagnosis of pancreatic cysts A comparison of pseudocysts, serous cystadenomas, mucinous cystic neoplasms, and mucinous cystadenocarcinoma Ann Surg 1993;217:41–7 . of 79% and specificity of 72% [29 , 32] . Agreement was seen between the two tests in 75% of cases; however, simi- lar to the case with ERCP, of the 25 % of. High-quality images of the pancreatic duct in the head, body, and tail of the gland were obtained in 70%, 64%, and 53%, respectively, of patients, all of whom had