Skip Navigation LinksHome > June 2014 - Volume 58 - Issue 6 > Update to the Management of Pediatric Acute Pancreatitis: H...
Journal of Pediatric Gastroenterology & Nutrition:
doi: 10.1097/MPG.0000000000000360
Invited Review

Update to the Management of Pediatric Acute Pancreatitis: Highlighting Areas in Need of Research

Abu-El-Haija, Maisam; Lin, Tom K.; Palermo, Joseph

Free Access
Continued Medical Education
Article Outline
Collapse Box

Author Information

Division of Pediatric Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, OH.

Address correspondence and reprint requests to Maisam Abu-El-Haija, MD, Division of Gastroenterology, Cincinnati Children's Hospital Medical Center, 3333 Burnet Ave, MLC 2010, Cincinnati, OH 45229 (e-mail:

Received 4 December, 2013

Accepted 28 February, 2014

This article has been developed as a Journal CME Activity by NASPGHAN. Visit to view instructions, documentation, and the complete necessary steps to receive CME credit for reading this article.

The authors report no conflict of interest.

Collapse Box


ABSTRACT: Acute pancreatitis is an emerging problem in pediatrics, with an incidence that is rising in the last 2 decades. Data regarding the optimal management and physician practice patterns are lacking. We present a literature review and updates on the management of pediatric pancreatitis. Prospective multicenter studies defining optimal management of pediatric pancreatitis are needed to guide care and improve outcomes for this patient population.

Pancreatitis is an insult to the pancreas that leads to the presence of acute inflammatory cells, edema, and necrosis that may result in organ damage or fibrosis (1). In the majority of patients this inflammation is self-limited and reversible, leading to a 1-time acute pancreatitis (AP) episode. In some patients, AP progresses to acute recurrent pancreatitis (ARP) or chronic pancreatitis (CP) (2). Patients with CP experience pain and possible pancreatic exocrine and/or endocrine insufficiency (3).

In the last 2 decades, an increased incidence of AP has been observed in the pediatric population (4). Although the cause is unclear, it may be explained by a heightened awareness of AP in children (5). Despite this more frequent presentation, data are lacking on the best diagnostic and management approaches to pediatric AP. The present management is extrapolated from adult studies and guidelines (6), in which the etiology is distinct. Biliary etiologies and alcohol play significant roles in adult AP (7,8), whereas pediatric cases are associated with different etiologies including biliary, metabolic, hereditary, and anatomic anomalies (2,4,9). Moreover, the natural history of progression from AP to ARP and CP is unknown. Only recently have consensus definitions for AP, ARP, and CP in pediatrics been published by the International Study Group of Pediatric Pancreatitis: In Search for a Cure (INSPPIRE) (10). The overall lack of well-designed prospective studies represents a major obstacle to developing diagnostic and therapeutic guidelines for pediatric AP. In this void, it is likely that management of pediatric AP varies widely among practitioners, and offers an opportunity for standardization of care to improve outcomes for these patients.

In the present article we provide a framework to review the management of uncomplicated AP in pediatrics and identify areas for clinical research so that evidence-based guidelines for management of pediatric AP can eventually be developed.

Back to Top | Article Outline


According to the Atlanta criteria and INSPPIRE definitions (10–13), a diagnosis of AP is achieved by meeting 2 of the following 3 elements: clinical symptoms, including abdominal pain, nausea, vomiting, or back pain; serum levels of pancreatic amylase and/or lipase ≥3 times the upper limit of normal; radiographic evidence of AP including pancreatic edema on ultrasound (US) or computed tomography (CT).

A detailed history to inquire about possible etiologies of AP should be obtained to allow appropriate management. Information obtained should include trauma history, gallstones, medications, viral infections, and other possible etiologies of AP (2).

Back to Top | Article Outline
Laboratory Testing

During an AP episode, pancreatic enzymes are released from the acinar cells into the circulation (14). When AP is suspected, serum and/or urinary pancreatic enzymes are evaluated. The most common tests are serum lipase and amylase. In 1 study, measurements of serum lipase had a sensitivity and specificity of 96.6% and 99.4%, respectively, whereas serum amylase had a sensitivity and specificity of 78.6% and 99.1%, respectively (15). Serum amylase has a shorter half-life and rises earlier than serum lipase, generally within hours of pancreatic injury (16). Based on its longer half-life, serum lipase is believed to be more useful in delayed presentations of AP, when the amylase levels may have already normalized. Thus, it is not uncommon to have normal serum amylase in AP, a phenomenon seen in approximately 20% of patients (17). Moreover, amylase may be normal in patients with AP and hyperlipidemia (18). In addition, findings of serum hyperamylasemia and hyperlipidemia are not limited to pancreatitis and can be reflective of other disorders including renal disease, intestinal inflammation, appendicitis, salivary gland disorders, or gynecological disease (19,20). Although other pancreatic enzymes have been described as markers of inflammation including carboxyl ester lipase, isoamylase, and phospholipase-A2 to diagnose pancreatitis (21), these enzymes have not been validated for common usage.

Other laboratories to be obtained during an attack are ones that would help identify the different etiologies or assess the severity of pancreatitis. These include calcium, triglycerides, transaminases, bilirubin, white blood cell count, urea nitrogen, and serum albumin (22). Directed therapy is important in patients when the etiology is clearly known, such as lowering the triglyceride level in hypertriglyceridemic pancreatitis (23).

Back to Top | Article Outline
Imaging Studies

Despite the present availability of advanced imaging modalities, abdominal US remains the first imaging study to be ordered in most patients with AP, including pediatric AP (9,24). US can be used to help confirm the clinical diagnosis of AP, and to assist in identifying underlying etiologies such as biliary pancreatitis. It is important to recognize the limitations of ultrasonography, specifically its lower sensitivity of approximately 70% in visualizing the pancreas in patients with AP compared with a sensitivity of >90% for CT scans (25,26). Abdominal CT is the second most common imaging modality used to diagnose and identify etiologies of pancreatitis (9,24). CT may be most helpful in patients with severe and complicated AP because it allows better visualization of masses, necrosis, and hemorrhage (27,28).

Although magnetic resonance cholangiopancreatography (MRCP) is seldom required for first attack of AP, it constitutes a valuable tool in the evaluation of pancreaticobiliary abnormalities. It has the advantages of not requiring ionizing radiation or the administration of iodinated contrast, and it provides high-quality multiplanar images of the pancreatic and biliary ductal systems. MRCP is useful in detecting intrahepatic and pancreatic ductal abnormalities, common bile duct abnormalities, choledocholithiasis, strictures, pancreas divisum, long common channel, and pancreatic and biliary tumors (29,30). Hence, MRCP has supplanted endoscopic retrograde cholangiopancreatography (ERCP) for diagnostic evaluation of the pancreaticobiliary system in many instances and has become the imaging study of choice to assess for ductal abnormalities. The use of MRCP during an episode of AP remains controversial because edema can obscure visualization of the ductal system (31). Intravenous secretin, a synthetic human hormone, increases the pressure of the sphincter of Oddi, leading to distention of the pancreatic ducts. It also has a role in detecting pancreatic divisum that may be missed in about one fourth of patients if an MRCP is performed without secretin (32). Literature on the use of secretin in MRCP is sparse in pediatrics. Although a few pediatric studies have shown improved visualization of the pancreatic duct by using secretin in MRCP (33,34), a recent study showed a small but significant increase in pancreatic and intrahepatic duct diameters, importantly, without a significant difference in overall image quality or duct visibility after the administration of secretin (35). In addition, MRCP with secretin may be used to assess duodenal filling and pancreatic duct compliance, as possible markers of abnormal exocrine pancreatic function—an area that needs further research in pediatrics (36).

Endoscopic US is yet another imaging study that may be considered in AP when there is no underlying cause identified by alternative modalities. The advantage of endoscopic US is the ability to obtain biopsies under direct visualization from lesions when indicated (37).

The authors recommend an US as the first-choice imaging modality and would reserve ordering of CT and/or MRCP for patients with complicated and severe pancreatitis.

Back to Top | Article Outline
Pain Management

Abdominal pain is the most common presenting symptom of AP. Pain management requires a careful balance between adequate control and oversedation. There are no data on optimal pain management in pediatric AP, and studies in adults have not identified a single superior medication. Morphine or related opioids were used in 94% of children with AP according to the INSPPIRE physicians’ questionnaire (10). Despite concerns that morphine may cause sphincter of Oddi spasm and thus exacerbate AP, there are limited and conflicting data that the effect of morphine is significantly different from that of other opioids (38). Meperidine is used in adults but has the limitations of a shorter duration than morphine and the risk of neurotoxic metabolites with repeated dosing. Direct comparison of meperidine and morphine in AP is lacking.

More specialized pain management with celiac (39) and thoracic epidural analgesia (40) has been used effectively for AP pain in adults. The procedures do have associated risks (41), and their safety and efficacy have not been reported in pediatric AP. For patients requiring long-term use of narcotics, constipation is a well-recognized adverse effect. Recent studies in adults have found that μ-opioid antagonists methylnaltrexone (42) and alvimopan (43) improve opioid-induced dysmotility but have not been used routinely in pediatrics.

Narcotic-sparing medications including indomethacin have shown promise in pain management in AP (44). Newer medications including intravenous acetaminophen and ketorolac have also shown promise in reducing narcotic use following surgery in pediatric patients (45), and clinical trials of these narcotic-sparing medications in pediatric AP are warranted.

Back to Top | Article Outline
Intravenous Fluid Management

Supportive care in the management of uncomplicated AP, irrespective of etiology, continues to be the mainstay of therapy. Fluid resuscitation is an integral part of this care as evidenced by recently published guidelines (12,46). Unanswered questions remain as to the optimal components, timing, rate, and volume of fluid administration. The adult literature on the approach to optimal fluid resuscitation is limited, whereas comparative available pediatric data are grossly deficient. Most commonly, crystalloid solutions are the fluid of choice for intravenous fluid resuscitation (47). Recently, a randomized controlled trial on the use of lactated Ringer's solution versus normal saline in adult patients with AP found a reduction in the systemic inflammatory response syndrome presumably secondary to the greater pH-buffering capacity in lactated Ringer's solution (48). In line with efforts to favorably alter the course of AP, there is now supportive evidence for early, aggressive fluid resuscitation (47,49). “Early resuscitation” has been defined as receiving greater than one-third of the total 72-hour intravenous fluid volume within the first 24 hours of presenting to the emergency department (47). These findings emphasize the importance of first responders for patients with AP, starting with the emergency department providers, to implement early fluid management strategies, which may significantly affect the morbidity and/or mortality of patients with AP.

A small number of studies have concluded that aggressive fluid therapy may be associated with negative outcomes (50,51). In this context, it is worth mentioning that these studies had limitations of including only patients with severe pancreatitis (52), and in 1 the fluid therapy was predominantly given during the second 24-hour period (51). Despite these results, the intuitive value of fluid resuscitation based on objective measurements instead of a 1-size-fits-all approach seems logical and prospective studies are needed to define optimal fluid management in pediatric AP.

Back to Top | Article Outline

Nutrition has an important role in the management of AP through maintenance of the gut barrier function, inhibiting bacterial translocation and lowering the systemic inflammatory response (53,54). There are no published studies on the optimal timing of nutritional intervention and mode of nutrition in pediatric pancreatitis. The data from adults are convincing that the earlier the nutrition is implemented, typically within 24 to 72 hours, the more favorable the outcomes and the lower the risk of progression into a multisystemic disease (55,56). According to recent meta-analyses, enteral nutrition was superior to total parenteral nutrition with a lower incidence of infection and multiorgan failure, resulting in lower mortality rates and a shorter hospital stay (57). To date, studies have shown that early enteral feeding via oral, nasogastric, or nasojejunal routes is safe and well tolerated in moderate and severe AP (58). A full general oral diet was tolerated in mild AP in adult patients and was not associated with abdominal pain relapse (59). In addition, there were no differences in outcomes between polymeric and elemental formulas and no evidence that immunoenhanced nutrients or probiotics are helpful in the management of AP (56). Optimal nutritional therapy in pediatrics should be further studied so that it can be uniformly applied.

Back to Top | Article Outline
Pharmacological Therapies

During the 350 years since Tulp first described AP (60), multiple attempts at medical therapies have failed to alter the course of the disease (61). More important, the latest meta-analyses have all concluded that initiation of antibiotics at presentation does not improve outcomes in adult AP and thus prophylactic antibiotic use is not recommended (62). A query of identified a number of studies under way targeting the inflammatory response (dexamethasone, activated protein C, ulinastatin), pancreatic perfusion (pentoxifylline, localized low-molecular-weight heparin infusion, epidural anesthesia), and enteral supplements (glutamine, fish oil emulsions) in patients with AP. All clinical trials must overcome the fact that when targeting patients with predicted severe outcome early in the clinical course, it is likely that the inflammatory cascade has been triggered for a significant and variable period of time before treatment resulting in a heterogeneous population in which “early intervention” is a misnomer.

Back to Top | Article Outline

Endoscopic therapy, specifically ERCP, should have a limited role in the management of AP. With the advancement in imaging modalities, ERCP is now used primarily as an interventional therapeutic tool in the care of both adults and children. In the setting of AP, ERCP is most helpful for gallstone pancreatitis in alleviating obstructive stones or sludge (63). According to the American Gastroenterology Association recommendations, urgent ERCP (within 24 hours) should be performed in gallstone pancreatitis with cholangitis, and early ERCP (within 72 hours) should be performed in patients who present with a high suspicion of a persistent common bile duct stone (64).

Gallstone pancreatitis usually needs to be managed by cholecystectomy or an ERCP before cholecystectomy (65,66). Data are lacking on the best management and timing of cholecystectomy for gallstone pancreatitis in pediatrics.

Pancreatic trauma is perhaps 1 unique diagnostic application of ERCP and has been used to define pancreatic ductal injury (67,68). In this setting, therapeutic intervention of pancreatic duct stenting to help resolve a peripancreatic fluid collection has also been safely and effectively applied (69).

Back to Top | Article Outline
Prognosis of Severity

There is no validated scoring system to predict severity in pediatric AP. Ranson criteria (70), the modified Glasgow scale (71), and the Apache II index (72) have been used to predict severity of adult AP, but all have limitations when applied to pediatrics (73,74). Newer, simplified scoring systems applied at time of admission have shown promise in adult AP (75,76). The first reported pediatric-specific severity score compared favorably with Ranson criteria and modified Glasgow scale with a higher sensitivity (67% vs 33% and 25%, respectively) but lower specificity (81% vs 93% and 90%, respectively) (77). This score requires 48 hours to complete, and it has not been validated in larger prospective studies. There are limited data on the use of CT scan for severity scoring in adults and pediatrics (78,79).

A single retrospective study in pediatric patients found elevated lipase >7 times upper limit of normal within the first 24 hours had an 85% sensitivity and 54% specificity for predicting severe AP (80).

A recent editorial that included a summary of the progress in AP scoring in pediatrics called for the need to develop a solid criteria to define severe pancreatitis and to form a scoring system that will predict the severe disease at presentation (81). Early identification of pediatric patients at risk for severe AP will continue to be a challenge without a prospectively validated scoring system for this population.

Back to Top | Article Outline
Further Testing, Genetic Mutation Analysis

The most common genes involved in pancreatitis are cationic trypsinogen (PRSS1) (82,83), the serine protease inhibitor Kazal type 1 (SPINK1) (84,85), the cystic fibrosis transmembrane regulator (CFTR) (86,87), chymotrypsin C (CTRC) (88,89), and calcium-sensing receptor (CASR) genes (90). Because of the fact that the majority of patients with AP do not have subsequent attacks in the future, assessing for genetic mutations should be reserved for patients with ARP or CP history.

Back to Top | Article Outline


Pediatric AP is diagnosed with increasing frequency, yet because of the lack of pediatric guidelines, management remains greatly variable. The present adult data support the use of intravenous fluids, early enteral nutrition, and pain management as the mainstays of therapy for uncomplicated AP but have not been validated in pediatrics. Well-designed prospective studies are needed in all areas of management of pediatric AP including the following:

1. Determine the optimal imaging modality for diagnosis of pediatric AP and validate advanced imaging techniques to assess pancreatic function in pediatrics.

2. Evaluate the use of narcotic-sparing medications in pediatric AP and the effect of standardized pain management on narcotic use, length of stay, tolerance of feeds, and complications.

3. Assess the safety and efficacy of weight-based rehydration strategies to identify the ideal intravenous fluid composition and rate of administration during initial management of pediatric AP.

4. Identify the optimal route and timing for introduction of enteral nutrition in pediatric AP.

5. Define the indications for and timing of surgical intervention for gallstone pancreatitis.

6. Prognostic scores: we need studies that could identify early markers for disease severity in pediatric AP. We need a robust and practical prognostic scoring system for pediatric AP.

Finally, the present review highlights the urgent need for prospective multicenter studies delineating optimal management of pediatric AP to develop evidence-based guidelines, improve patient outcomes, and hopefully alter the progression to ARP and CP.

Back to Top | Article Outline

The authors are thankful to Daniel J. Podberesky, MD, for reviewing the imaging section.

Back to Top | Article Outline


1. Sarles H. Definitions and classifications of pancreatitis. Pancreas 1991; 6:470–474.

2. Bai HX, Lowe ME, Husain SZ. What have we learned about acute pancreatitis in children? J Pediatr Gastroenterol Nutr 2011; 52:262–270.

3. Drewes AM. Understanding and treatment of chronic pancreatitis. World J Gastroenterol 2013; 19:7219–7221.

4. Lopez MJ. The changing incidence of acute pancreatitis in children: a single-institution perspective. J Pediatr 2002; 140:622–624.

5. Morinville VD, Barmada MM, Lowe ME. Increasing incidence of acute pancreatitis at an American pediatric tertiary care center: is greater awareness among physicians responsible? Pancreas 2010; 39:5–8.

6. Working Group IAP/APA Acute Pancreatitis GuidelinesIAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology 2013; 13 (4 suppl 2):e1–e15.

7. Yadav D, Whitcomb DC. The role of alcohol and smoking in pancreatitis. Nat Rev Gastroenterol Hepatol 2010; 7:131–145.

8. Wang GJ, Gao CF, Wei D, et al. Acute pancreatitis: etiology and common pathogenesis. World J Gastroenterol 2009; 15:1427–1430.

9. Park AJ, Latif SU, Ahmad MU, et al. A comparison of presentation and management trends in acute pancreatitis between infants/toddlers and older children. J Pediatr Gastroenterol Nutr 2010; 51:167–170.

10. Morinville VD, Husain SZ, Bai H, et al. Definitions of pediatric pancreatitis and survey of present clinical practices. J Pediatr Gastroenterol Nutr 2012; 55:261–265.

11. Bradley EL 3rd. A clinically based classification system for acute pancreatitis. Summary of the International Symposium on Acute Pancreatitis, Atlanta, Ga, September 11 through 13, 1992. Arch Surg 1993; 128:586–590.

12. Banks PA, Freeman ML. Practice Parameters Committee of the American College of GastroenterologyPractice guidelines in acute pancreatitis. Am J Gastroenterol 2006; 101:2379–2400.

13. Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013; 62:102–111.

14. Matull WR, Pereira SP, O’Donohue JW. Biochemical markers of acute pancreatitis. J Clin Pathol 2006; 59:340–344.

15. Gomez D, Addison A, De Rosa A, et al. Retrospective study of patients with acute pancreatitis: is serum amylase still required? BMJ Open 2012; 2:

16. Winslet M, Hall C, London NJ, et al. Relation of diagnostic serum amylase levels to aetiology and severity of acute pancreatitis. Gut 1992; 33:982–986.

17. Clavien PA, Robert J, Meyer P, et al. Acute pancreatitis and normoamylasemia. Not an uncommon combination. Ann Surg 1989; 210:614–620.

18. Okerberg K, Lee M. Spuriously normal amylase levels in a patient with acute pancreatitis secondary to hypertriglyceridemia. J Am Board Fam Pract 1999; 12:68–70.

19. Swensson EE, Maull KI. Clinical significance of elevated serum and urine amylase levels in patients with appendicitis. Am J Surg 1981; 142:667–670.

20. Frank B, Gottlieb K. Amylase normal, lipase elevated: is it pancreatitis? A case series and review of the literature. Am J Gastroenterol 1999; 94:463–469.

21. Sternby B, O’Brien JF, Zinsmeister AR, et al. What is the best biochemical test to diagnose acute pancreatitis? A prospective clinical study. Mayo Clin Proc 1996; 71:1138–1144.

22. Park A, Latif SU, Shah AU, et al. Changing referral trends of acute pancreatitis in children: a 12-year single-center analysis. J Pediatr Gastroenterol Nutr 2009; 49:316–322.

23. Scherer J, Singh VP, Pitchumoni CS, et al. Issues in hypertriglyceridemic pancreatitis: an update. J Clin Gastroenterol 2014; 48:195–203.

24. Kandula L, Lowe ME. Etiology and outcome of acute pancreatitis in infants and toddlers. J Pediatr 2008; 152:106–110.110.e1.

25. McKay AJ, Imrie CW, O’Neill J, et al. Is an early ultrasound scan of value in acute pancreatitis? Br J Surg 1982; 69:369–372.

26. Silverstein W, Isikoff MB, Hill MC, et al. Diagnostic imaging of acute pancreatitis: prospective study using CT and sonography. AJR Am J Roentgenol 1981; 137:497–502.

27. Freeny PC. Incremental dynamic bolus computed tomography of acute pancreatitis. Int J Pancreatol 1993; 13:147–158.

28. Raizner A, Phatak UP, Baker K, et al. Acute necrotizing pancreatitis in children. J Pediatr 2013; 162:788–792.

29. Maccioni F, Martinelli M, Al Ansari N, et al. Magnetic resonance cholangiography: past, present and future: a review. Eur Rev Med Pharmacol Sci 2010; 14:721–725.

30. Tirkes T, Menias CO, Sandrasegaran K. MR imaging techniques for pancreas. Radiol Clin North Am 2012; 50:379–393.

31. Gulati K, Catalano OA, Sahani DV. Review: advances in magnetic resonance cholangiopancreatography: from morphology to functional imaging. Indian J Radiol Imaging 2007; 17:247–253.

32. Mosler P, Akisik F, Sandrasegaran K, et al. Accuracy of magnetic resonance cholangiopancreatography in the diagnosis of pancreas divisum. Dig Dis Sci 2012; 57:170–174.

33. Arcement CM, Meza MP, Arumanla S, et al. MRCP in the evaluation of pancreaticobiliary disease in children. Pediatr Radiol 2001; 31:92–97.

34. Manfredi R, Lucidi V, Gui B, et al. Idiopathic chronic pancreatitis in children: MR cholangiopancreatography after secretin administration. Radiology 2002; 224:675–682.

35. Trout AT, Podberesky DJ, Serai SD, et al. Does secretin add value in pediatric magnetic resonance cholangiopancreatography? Pediatr Radiol 2013; 43:479–486.

36. Balci NC, Smith A, Momtahen AJ, et al. MRI and S-MRCP findings in patients with suspected chronic pancreatitis: correlation with endoscopic pancreatic function testing (ePFT). J Magn Reson Imaging 2010; 31:601–606.

37. Fujii LL, Chari ST, El-Youssef M, et al. Pediatric pancreatic EUS-guided trucut biopsy for evaluation of autoimmune pancreatitis. Gastrointest Endosc 2013; 77:824–828.

38. Thompson DR. Narcotic analgesic effects on the sphincter of Oddi: a review of the data and therapeutic implications in treating pancreatitis. Am J Gastroenterol 2001; 96:1266–1272.

39. Rykowski JJ, Hilgier M. Continuous celiac plexus block in acute pancreatitis. Reg Anesth 1995; 20:528–532.

40. Bernhardt A, Kortgen A, Niesel H, et al. Using epidural anesthesia in patients with acute pancreatitis—prospective study of 121 patients. Anaesthesiol Reanim 2002; 27:16–22.

41. Rainov NG, Heidecke V, Burkert WL. Spinal epidural hematoma. Report of a case and review of the literature. Neurosurg Rev 1995; 18:53–60.

42. Licup N, Baumrucker SJ. Methylnaltrexone: treatment for opioid-induced constipation. Am J Hosp Palliat Care 2011; 28:59–61.

43. Buchler MW, Seiler CM, Monson JR, et al. Clinical trial: alvimopan for the management of post-operative ileus after abdominal surgery: results of an international randomized, double-blind, multicentre, placebo-controlled clinical study. Aliment Pharmacol Ther 2008; 28:312–325.

44. Ebbehoj N, Friis J, Svendsen LB, et al. Indomethacin treatment of acute pancreatitis. A controlled double-blind trial. Scand J Gastroenterol 1985; 20:798–800.

45. Hong JY, Won Han S, Kim WO, et al. Fentanyl sparing effects of combined ketorolac and acetaminophen for outpatient inguinal hernia repair in children. J Urol 2010; 183:1551–1555.

46. Forsmark CE, Baillie J. AGA Institute technical review on acute pancreatitis. Gastroenterology 2007; 132:2022–2044.

47. Warndorf MG, Kurtzman JT, Bartel MJ, et al. Early fluid resuscitation reduces morbidity among patients with acute pancreatitis. Clin Gastroenterol Hepatol 2011; 9:705–709.

48. Wu BU, Hwang JQ, Gardner TH, et al. Lactated Ringer's solution reduces systemic inflammation compared with saline in patients with acute pancreatitis. Clin Gastroenterol Hepatol 2011; 9:710.e1–717.e1.

49. Gardner TB, Vege SS, Chari ST, et al. Faster rate of initial fluid resuscitation in severe acute pancreatitis diminishes in-hospital mortality. Pancreatology 2009; 9:770–776.

50. Eckerwall G, Olin H, Andersson B, et al. Fluid resuscitation and nutritional support during severe acute pancreatitis in the past: what have we learned and how can we do better? Clin Nutr 2006; 25:497–504.

51. Mao EQ, Fei J, Peng YB, et al. Rapid hemodilution is associated with increased sepsis and mortality among patients with severe acute pancreatitis. Chin Med J (Engl) 2010; 123:1639–1644.

52. Fisher JM, Gardner TB. The “golden hours” of management in acute pancreatitis. Am J Gastroenterol 2012; 107:1146–1150.

53. Eckerwall GE, Tingstedt BB, Bergenzaun PE, et al. Immediate oral feeding in patients with mild acute pancreatitis is safe and may accelerate recovery—a randomized clinical study. Clin Nutr 2007; 26:758–763.

54. Kumar S, Gariepy CE. Nutrition and acute pancreatitis: review of the literature and pediatric perspectives. Curr Gastroenterol Rep 2013; 15:338.

55. Olah A, Pardavi G, Belagyi T, et al. Early nasojejunal feeding in acute pancreatitis is associated with a lower complication rate. Nutrition 2002; 18:259–262.

56. Olah A, Romics L Jr. Evidence-based use of enteral nutrition in acute pancreatitis. Langenbecks Arch Surg 2010; 395:309–316.

57. Yi F, Ge L, Zhao J, et al. Meta-analysis: total parenteral nutrition versus total enteral nutrition in predicted severe acute pancreatitis. Intern Med 2012; 51:523–530.

58. Eatock FC, Chong P, Menezes N, et al. A randomized study of early nasogastric versus nasojejunal feeding in severe acute pancreatitis. Am J Gastroenterol 2005; 100:432–439.

59. Moraes JM, Felga GE, Chebli LA, et al. A full solid diet as the initial meal in mild acute pancreatitis is safe and result in a shorter length of hospitalization: results from a prospective, randomized, controlled, double-blind clinical trial. J Clin Gastroenterol 2010; 44:517–522.

60. Tulp N. Observationum Medicarum Editio nova et aucta [Medical Observations. New and Enlarged Edition), 2nd ed. Amsterdam; 1652 [Book 4].

61. Lankisch PG, Lerch MM. Pharmacological prevention and treatment of acute pancreatitis: where are we now? Dig Dis 2006; 24:148–159.

62. Wittau M, Mayer B, Scheele J, et al. Systematic review and meta-analysis of antibiotic prophylaxis in severe acute pancreatitis. Scand J Gastroenterol 2011; 46:261–270.

63. Nowak A, Marek TA, Nowakowska-Dulawa E, et al. Biliary pancreatitis needs endoscopic retrograde cholangiopancreatography with endoscopic sphincterotomy for cure. Endoscopy 1998; 30:A256–A259.

64. American Gastroenterological Association Institute on “Management of Acute Pancreatits” Clinical Practice and Economics Committee. AGA Institute Governing BoardAGA Institute medical position statement on acute pancreatitis. Gastroenterology 2007; 132:2019–2021.

65. de C Ferreira LE, Baron TH. Acute biliary conditions. Best Pract Res Clin Gastroenterol 2013; 27:745–756.

66. Gurusamy KS, Nagendran M, Davidson BR. Early versus delayed laparoscopic cholecystectomy for acute gallstone pancreatitis. Cochrane Database Syst Rev 2013; 9:CD010326.

67. Rescorla FJ, Plumley DA, Sherman S, et al. The efficacy of early ERCP in pediatric pancreatic trauma. J Pediatr Surg 1995; 30:336–340.

68. Houben CH, Ade-Ajayi N, Patel S, et al. Traumatic pancreatic duct injury in children: minimally invasive approach to management. J Pediatr Surg 2007; 42:629–635.

69. Canty TG Sr, Weinman D. Treatment of pancreatic duct disruption in children by an endoscopically placed stent. J Pediatr Surg 2001; 36:345–348.

70. Ranson JH. Acute pancreatitis. Curr Probl Surg 1979; 16:1–84.

71. Blamey SL, Imrie CW, O’Neill J, et al. Prognostic factors in acute pancreatitis. Gut 1984; 25:1340–1346.

72. Larvin M, McMahon MJ. APACHE-II score for assessment and monitoring of acute pancreatitis. Lancet 1989; 2:201–205.

73. Lautz TB, Chin AC, Radhakrishnan J. Acute pancreatitis in children: spectrum of disease and predictors of severity. J Pediatr Surg 2011; 46:1144–1149.

74. Suzuki M, Fujii T, Takahiro K, et al. Scoring system for the severity of acute pancreatitis in children. Pancreas 2008; 37:222–223.

75. Papachristou GI, Muddana V, Yadav D, et al. Comparison of BISAP, Ranson's, APACHE-II, and CTSI scores in predicting organ failure, complications, and mortality in acute pancreatitis. Am J Gastroenterol 2010; 105:435–441.

76. Oskarsson V, Mehrabi M, Orsini N, et al. Validation of the harmless acute pancreatitis score in predicting nonsevere course of acute pancreatitis. Pancreatology 2011; 11:464–468.

77. DeBanto JR, Goday PS, Pedroso MR, et al. Acute pancreatitis in children. Am J Gastroenterol 2002; 97:1726–1731.

78. Balthazar EJ, Ranson JH, Naidich DP, et al. Acute pancreatitis: prognostic value of CT. Radiology 1985; 156:767–772.

79. Lautz TB, Turkel G, Radhakrishnan J, et al. Utility of the computed tomography severity index (Balthazar score) in children with acute pancreatitis. J Pediatr Surg 2012; 47:1185–1191.

80. Coffey MJ, Nightingale S, Ooi CY. Serum lipase as an early predictor of severity in pediatric acute pancreatitis. J Pediatr Gastroenterol Nutr 2013; 56:602–608.

81. Uc A. Predicting the severity of pediatric acute pancreatitis: are we there yet? J Pediatr Gastroenterol Nutr 2013; 56:584–585.

82. Whitcomb DC, Gorry MC, Preston RA, et al. Hereditary pancreatitis is caused by a mutation in the cationic trypsinogen gene. Nat Genet 1996; 14:141–145.

83. Whitcomb DC, Preston RA, Aston CE, et al. A gene for hereditary pancreatitis maps to chromosome 7q35. Gastroenterology 1996; 110:1975–1980.

84. Pfutzer RH, Barmada MM, Brunskill AP, et al. SPINK1/PSTI polymorphisms act as disease modifiers in familial and idiopathic chronic pancreatitis. Gastroenterology 2000; 119:615–623.

85. Witt H, Luck W, Hennies HC, et al. Mutations in the gene encoding the serine protease inhibitor, Kazal type 1 are associated with chronic pancreatitis. Nat Genet 2000; 25:213–216.

86. Cohn JA, Friedman KJ, Noone PG, et al. Relation between mutations of the cystic fibrosis gene and idiopathic pancreatitis. N Engl J Med 1998; 339:653–658.

87. Sharer N, Schwarz M, Malone G, et al. Mutations of the cystic fibrosis gene in patients with chronic pancreatitis. N Engl J Med 1998; 339:645–652.

88. Rosendahl J, Witt H, Szmola R, et al. Chymotrypsin C (CTRC) variants that diminish activity or secretion are associated with chronic pancreatitis. Nat Genet 2008; 40:78–82.

89. Masson E, Chen JM, Scotet V, et al. Association of rare chymotrypsinogen C (CTRC) gene variations in patients with idiopathic chronic pancreatitis. Hum Genet 2008; 123:83–91.

90. Felderbauer P, Klein W, Bulut K, et al. Mutations in the calcium-sensing receptor: a new genetic risk factor for chronic pancreatitis? Scand J Gastroenterol 2006; 41:343–348.


acute pancreatitis; acute recurrent pancreatitis; chronic pancreatitis; pediatric

© 2014 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology,


Article Tools


Article Level Metrics

Search for Similar Articles
You may search for similar articles that contain these same keywords or you may modify the keyword list to augment your search.

Connect With Us