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2 Diagnosis andMedical Management ofAcute Pancreatitis
42. de Madaria E, Banks PA, Moya-Hoyo N, Wu BU, Rey-Riveiro M, Acevedo-Piedra NG, etal. Early factors associated with uid sequestration and outcomes of patients with acute pancre­atitis. Clin Gastroenterol Hepatol. 2014;12(6):997–1002.
43. Jang JW, Kim MH, Oh D, Cho DH, Song TJ, Park DH, etal. Factors and outcomes associated with pancreatic duct disruption in patients with acute necrotizing pancreatitis. Pancreatology. 2016;16(6):958–65.
44. Crockett SD, Wani S, Gardner TB, Falck-Ytter Y, Barkun AN, American Gastroenterological Association Institute Clinical Guidelines Committee. American Gastroenterological Association Institute Guideline on Initial Management of Acute Pancreatitis. Gastroenterology. 2018;154(4):1096–101.
45. Singh VK, Bollen TL, Wu BU, Repas K, Maurer R, Yu S, etal. An assessment of the severity of interstitial pancreatitis. Clin Gastroenterol Hepatol. 2011;9(12):1098–103.
46. Sinha A, Quesada-Vázquez N, Faghih M, Afghani E, Zaheer A, Khashab MA, et al. Early predictors of uid sequestration in acute pancreatitis: a validation study. Pancreas. 2016;45(2):306–10.
47. Kiriyama S, Gabata T, Takada T, Hirata K, Yoshida M, Mayumi T, etal. New diagnostic crite­ria of acute pancreatitis. J Hepatobiliary Pancreat Sci. 2010;17(1):24–36.
48. Ismail OZ, Bhayana V.Lipase or amylase for the diagnosis of acute pancreatitis? Clin Biochem. 2017;50(18):1275–80.
49. Weiss FU, Hesselbarth N, Párniczky A, Mosztbacher D, Lämmerhirt F, Ruffert C, et al. Common variants in the CLDN2-MORC4 and PRSS1-PRSS2 loci confer susceptibility to acute pancreatitis. Pancreatology. 2018;18(5):477–81.
50. Garg R, Rustagi T.Management of Hypertriglyceridemia Induced Acute Pancreatitis. Biomed Res Int. 2018;2018:4721357.
51. Vipperla K, Somerville C, Furlan A, Koutroumpakis E, Saul M, Chennat J, etal. Clinical pro­le and natural course in a large cohort of patients with hypertriglyceridemia and pancreatitis. J Clin Gastroenterol. 2017;51(1):77–85.
52. Türkvatan A, Erden A, Türkoğlu MA, Seçil M, Yener Ö. Imaging of acute pancreatitis and its complications. Part 1: acute pancreatitis. Diagn Interv Imaging. 2015;96(2):151–60.
53. Kondo S, Isayama H, Akahane M, Toda N, Sasahira N, Nakai Y, etal. Detection of com­mon bile duct stones: comparison between endoscopic ultrasonography, magnetic reso­nance cholangiography, and helical-computed-tomographic cholangiography. Eur J Radiol. 2005;54(2):271–5.
54. Wan J, Ouyang Y, Yu C, Yang X, Xia L, Lu N. Comparison of EUS with MRCP in idio­pathic acute pancreatitis: a systematic review and meta-analysis. Gastrointest Endosc. 2018;87(5):1180–1188.e9.
55. De Lisi S, Leandro G, Buscarini E. Endoscopic ultrasonography versus endoscopic retro­grade cholangiopancreatography in acute biliary pancreatitis: a systematic review. Eur J Gastroenterol Hepatol. 2011;23(5):367–74.
56. Makary MA, Duncan MD, Harmon JW, Freeswick PD, Bender JS, Bohlman M, etal. The role of magnetic resonance cholangiography in the management of patients with gallstone pancre­atitis. Ann Surg. 2005;241(1):119–24.
57. Ardengh JC, Malheiros CA, Rahal F, Pereira V, Ganc AJ.Microlithiasis of the gallbladder: role of endoscopic ultrasonography in patients with idiopathic acute pancreatitis. Rev Assoc Med Bras (1992). 2010;56(1):27–31.
58. Papachristou GI, Muddana V, Yadav D, O’Connell M, Sanders MK, Slivka A, 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(2):435–41. quiz 442
59. Ranson JH, Pasternack BS.Statistical methods for quantifying the severity of clinical acute pancreatitis. J Surg Res. 1977;22(2):79–91.
60. Di MY, Liu H, Yang ZY, Bonis PAL, Tang JL, Lau J.Prediction models of mortality in acute pancreatitis in adults: a systematic review. Ann Intern Med. 2016;165(7):482–90.
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61. Singh VK, Wu BU, Bollen TL, Repas K, Maurer R, Johannes RS, etal. A prospective evalua­tion of the bedside index for severity in acute pancreatitis score in assessing mortality and inter­mediate markers of severity in acute pancreatitis. Am J Gastroenterol. 2009;104(4):966–71.
62. Forsmark CE, Yadav D. Predicting the prognosis of acute pancreatitis. Ann Intern Med. 2016;165(7):523–4.
63. Koutroumpakis E, Wu BU, Bakker OJ, Dudekula A, Singh VK, Besselink MG, etal. Admission hematocrit and rise in blood urea nitrogen at 24 h outperform other laboratory markers in pre­dicting persistent organ failure and pancreatic necrosis in acute pancreatitis: a post hoc analy­sis of three large prospective databases. Am J Gastroenterol. 2015;110(12):1707–16.
64. Umapathy C, Raina A, Saligram S, Tang G, Papachristou GI, Rabinovitz M, et al. Natural history after acute necrotizing pancreatitis: a large US tertiary care experience. J Gastrointest Surg. 2016;20(11):1844–53.
65. Zavyalov T, Khotsyna Y, Tenner S.The role of antibiotics in the management of patients with acute necrotizing pancreatitis. Curr Infect Dis Rep. 2010;12(1):13–8.
66. Banks PA, Bollen TL, Dervenis C, Gooszen HG, Johnson CD, Sarr MG, etal. Classication of acute pancreatitis—2012: revision of the Atlanta classication and denitions by international consensus. Gut. 2013;62(1):102–11.
67. Buxbaum JL, Quezada M, Da B, Jani N, Lane C, Mwengela D, et al. Early aggressive hydration hastens clinical improvement in mild acute pancreatitis. Am J Gastroenterol. 2017;112(5):797–803.
68. Gardner TB, Vege SS, Pearson RK, Chari ST.Fluid resuscitation in acute pancreatitis. Clin Gastroenterol Hepatol. 2008;6(10):1070–6.
69. Gardner TB, Vege SS, Chari ST, Petersen BT, Topazian MD, Clain JE, etal. Faster rate of initial uid resuscitation in severe acute pancreatitis diminishes in-hospital mortality. Pancreatology. 2009;9(6):770–6.
70. Singh VK, Gardner TB, Papachristou GI, Rey-Riveiro M, Faghih M, Koutroumpakis E, etal. An international multicenter study of early intravenous uid administration and outcome in acute pancreatitis. United European Gastroenterol J. 2017;5(4):491–8.
71. Villatoro E, Mulla M, Larvin M.Antibiotic therapy for prophylaxis against infection of pan­creatic necrosis in acute pancreatitis. Cochrane Database Syst Rev. 2010;2010(5):CD002941.
72. Adler DG, Chari ST, Dahl TJ, Farnell MB, Pearson RK.Conservative management of infected necrosis complicating severe acute pancreatitis. Am J Gastroenterol. 2003;98(1):98–103.
73. Runzi M, Niebel W, Goebell H, Gerken G, Layer P.Severe acute pancreatitis: nonsurgical treatment of infected necroses. Pancreas. 2005;30(3):195–9.
74. Bakker OJ, van Brunschot S, van Santvoort HC, Besselink MG, Bollen TL, Boermeester MA, etal. Early versus on-demand nasoenteric tube feeding in acute pancreatitis. N Engl J Med. 2014;371(21):1983–93.
75. Coté GA.Early enteral feeding does not improve outcomes in patients with predicted severe acute pancreatitis. Gastroenterology. 2015;148(7):1476–8.
76. Vaughn VM, Shuster D, Rogers MAM, Mann J, Conte ML, Saint S, et al. Early versus delayed feeding in patients with acute pancreatitis: a systematic review. Ann Intern Med. 2017;166(12):883–92.
77. Bevan MG, Asrani VM, Bharmal S, Wu LM, Windsor JA, Petrov MS.Incidence and predictors of oral feeding intolerance in acute pancreatitis: a systematic review, meta-analysis, and meta­regression. Clin Nutr. 2017;36(3):722–9.
78. Bakker OJ, van Brunschot S, Farre A, Johnson CD, Kalfarentzos F, Louie BE, etal. Timing of enteral nutrition in acute pancreatitis: meta-analysis of individuals using a single-arm of randomised trials. Pancreatology. 2014;14(5):340–6.
79. Jin M, Zhang H, Lu B, Li Y, Wu D, Qian J, etal. The optimal timing of enteral nutrition and its effect on the prognosis of acute pancreatitis: a propensity score matched cohort study. Pancreatology. 2017;17(5):651–7.
80. Petrov MS, van Santvoort HC, Besselink MGH, van der Heijden GJMG, Windsor JA, Gooszen HG. Enteral nutrition and the risk of mortality and infectious complications in
C. T. Huerta et al.
2 Diagnosis andMedical Management ofAcute Pancreatitis
patients with severe acute pancreatitis: a meta-analysis of randomized trials. Arch Surg. 2008;143(11):1111–7.
81. Afghani E, Pandol SJ, Shimosegawa T, Sutton R, Wu BU, Vege SS, et al. Acute pancreatitis- progress and challenges: a report on an international symposium. Pancreas. 2015;44(8):1195–210.
82. Vege SS, DiMagno MJ, Forsmark CE, Martel M, Barkun AN.Initial medical treatment of acute pancreatitis: American Gastroenterological Association Institute Technical Review. Gastroenterology. 2018;154(4):1103–39.
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Chapter 3
Acute Pancreatitis: Non-surgical Therapies Including Gallstone Management
AnneNagelhout, MartijnW.J.Stommel, StefanA.W.Bouwense, MarcG.Besselink, andfor the Dutch Pancreatitis Study Group

Introduction

Acute pancreatitis has an increasing incidence worldwide and is one of the most common gastrointestinal disorders requiring acute hospitalization [1, 2]. The cur­rent incidence in the Western World is 34 per 100.000 person-years [3]. The clinical course and severity of acute pancreatitis varies a lot, ranging from a mild course with transient abdominal discomfort till a severe course with multiorgan failure and high mortality.
Approximately 80% of the patients present with mild acute pancreatitis, which is self-limiting, usually within 1week [4, 5]. The other 20% of patients develop mod­erate to severe acute pancreatitis, with (multiple) organ failure and often (infected)
A. Nagelhout (*) Department of Surgery, Radboudumc, Nijmegen, The Netherlands
Department of Research and Development, St. Antonius Hospital, Nieuwegein, The Netherlands e-mail: a.nagelhout@antoniusziekenhuis.nl
M. W. J. Stommel Department of Surgery, Radboudumc, Nijmegen, The Netherlands e-mail: martijn.stommel@radboudumc.nl
S. A. W. Bouwense Department of Surgery, Maastricht University Medical Centre+, Maastricht, The Netherlands e-mail: stefan.bouwense@mumc.nl
M. G. Besselink Department of Surgery, Amsterdam UMC, Location University of Amsterdam, Amsterdam, The Netherlands
Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam, The Netherlands e-mail: m.g.besselink@amsterdamumc.nl
Switzerland AG 2025 E. P. Ceppa et al. (eds.), The SAGES Manual of Evolving Techniques in Pancreatic Surgery, https://doi.org/10.1007/978-3-031-78409-5_3
39© The Author(s), under exclusive license to Springer Nature
40
necrosis of the pancreatic or peripancreatic tissue [46]. In these patients, the mor­tality rate is high (10–30%) in contrast to low mortality in mild pancreatitis (less than 1%) [5, 7, 8]. The treatment of pancreatitis patients is predominantly aimed at supporting the vital organ systems and providing comfort and nutrition when needed.
This chapter provides an overview of the non-surgical therapy of acute pancre­atitis. First, initial therapies (i.e., uid resuscitation, pain management, nutrition, and the role of antibiotics) will be discussed, followed by the specic treatment for biliary pancreatitis, including the role of endoscopic retrograde cholangiopancrea­tography (ERCP), magnetic resonance cholangiopancreatography (MRCP), and endoscopic ultrasound (EUS), the timing of cholecystectomy. The prevention of disease recurrence and recommendations for future research will also be discussed.
A. Nagelhout et al.
Early andLate Phase ofAcute Pancreatitis
In case of mild pancreatitis, the disease is limited to the early phase. A mild sys­temic inammatory reaction may take place and patients usually improve spontane­ously after a few days. However, in case of a more severe inammatory response, two overlapping phases of acute pancreatitis can be recognized: the early and the late phase. Due to excessive local pancreatic cell injury, the early phase is character­ized by activation of large cytokine cascades which can cause the systemic inam­matory response syndrome (SIRS) [4]. As a result of persistent SIRS, the risk of infections and development of organ failure arises [4, 9]. (Multi)organ failure, including cardiovascular, respiratory, or renal failure, can develop early in acute pancreatitis and is the main reason for early mortality in patients with severe acute pancreatitis [4, 9, 10]. The late phase of acute pancreatitis is characterized by per­sistence of systemic signs of inammation, generally caused by compensatory anti­inammatory response syndrome (CARS) [5]. During this phase, patients are again susceptible to infections like pneumonia, sepsis, or secondary infection of (peri) pancreatic necrosis [5, 7].

Initial Treatment

The initial treatment of acute pancreatitis in the early phase consists of supportive measures and preventing/treating (multi)organ failure which comprises uid resus­citation, pain management, and proper nutrition. For management of the disease, a multidisciplinary team (including a surgeon, gastroenterologist, radiologist, and dietitian) in hospitals is recommended.
3 Acute Pancreatitis: Non-surgical Therapies Including Gallstone Management
41
Reducing Severity of Acute Pancreatitis
Until this date, the cornerstone of treatment in patients with severe acute pancreati­tis is supportive care. Several studies have been conducted in the early phase of acute pancreatitis in order to prevent severe disease progression and reduce compli­cations [1114]. Unfortunately, these studies showed no improvement in clinical outcomes and the right treatment in the early phase of acute pancreatitis for reduc­tion of organ failure and mortality is still lacking. An option for treatment may be modication of the immune response in the early phase of predicted severe acute pancreatitis through the administration of early intravenous omega-3 fatty acids in patients. Omega-3 fatty acids replace arachidonic acids (omega-6) in the inamma­tory mediator production cascade [15]. In addition, omega-3 fatty acids provide increased production of resolvins which improve normalization of inammatory tissue [16]. These actions of omega-3 fatty acids could potentially lead to an effec­tive response of the immune system. A meta-analysis [17] was performed to inves­tigate the safety and efcacy of omega-3in patients with acute pancreatitis and sepsis. The meta-analysis demonstrated a lower incidence of mortality after omega-3 fatty acids infusion. Furthermore, a recent single-center randomized controlled trial [18] demonstrated decreased CRP levels and decreased onset of new organ failure in patients with predicted severe pancreatitis after administration of omega-3 fatty acids. To provide solid evidence on the true potential of omega-3 fatty acids, the PLANCTON multicenter randomized trial is currently in progress in the Netherlands in patients with predicted severe acute pancreatitis.
Fluid Resuscitation
Adequate uid resuscitation is required during the rst few days of acute pancreati­tis to correct for possible intravascular hypovolemia, which is caused by local and systemic immune responses. Infusion with Ringer’s lactate is recommended as it reduces the risk of developing SIRS when compared to normal saline infusion [1,
1922]. In fact, such immune responses induce cell apoptosis and increase vascular
permeability, resulting in extravasation of uid in the third space, and could lead to hypoperfusion, (multiple) organ failure, and ultimately death [2, 23, 24]. On the other hand, aggressive and undirected uid infusion contributes to higher morbidity and even higher mortality as was shown by two randomized trials [25, 26]. Therefore, careful monitoring of the vital signs during uid resuscitation is necessary [1, 25,
26]. The preferred approach according to the current IAP/APA treatment guideline
for acute pancreatitis focuses on resuscitation until certain goals are reached (heart rate less than 120 per minute, mean arterial pressure between 65 and 85mmHg, and urinary output more than 0.5 till 1.0mL/kg/h) [1].
The recent Waterfall trial [27] compared aggressive versus moderate uid resus­citation in patients with acute pancreatitis. Aggressive uid resuscitation consisted
42
of 20 mL/kg Ringer’s lactate over 2 h, followed by 3 mL/kg/h. Patients in the moderate- resuscitation group received 1.5 mL/kg/h and only a bolus of 10 mL/ kg/2 h in patients with hypovolemia. This trial demonstrated that patients with aggressive uid resuscitation had a higher risk of uid overload compared to moder­ate resuscitation (20.5 vs. 6.3%). These ndings underline the importance of care­fully monitoring vital signs and achieving the resuscitation goals to prevent both hypovolemia and hypervolemia.
A. Nagelhout et al.
Pain Management
Severe, persistent upper abdominal pain is the predominant symptom in patients with acute pancreatitis, which remains dominant during the rst few days of hospi­tal admission. Therefore, adequate pain treatment according to the World Health Organization (WHO) analgesic ladder is required [28]. The use of opioids could reduce the number of patients that need supplementary analgesia [29]. One study suggested that epidural anesthesia prevents early tissue damage and improves the perfusion of the pancreas [30]. More recent, a multicenter retrospective study sug­gested that the use of epidural anesthesia was associated with reduced 30-day mor­tality in patients with severe acute pancreatitis compared to patients without epidural anesthesia (2 vs. 17%) [31]. Nevertheless, more prospective studies are needed on the use of epidural anesthesia before it can be recommended in the standard sup­portive care for acute pancreatitis.
Nutrition
Gut barrier dysfunction is present in most patients with acute pancreatitis [32]. Therefore, optimal enteral nutritional support is important to maintain the intestinal barrier integrity, but it also prevents bacterial overgrowth and decreases SIRS. [32,
33] According to the multicenter randomized PYTHON trial [11], early enteral tube
feeding within 24h after admission does not decrease rates of infection (25 vs. 26%) or mortality (11 vs. 7%) in comparison to on-demand feeding in patients with predicted severe acute pancreatitis. Oral feeding on-demand is recommended and can be started as early as a patient request. Enteral tube feeding should only be con­sidered if an oral diet is not tolerated after 72 h form the time of presentation. Enteral feeding is strongly preferred over parenteral feeding because of the lower risks of complications such as (multi)organ failure, central venous catheter infec­tions, and mortality [34, 35].
3 Acute Pancreatitis: Non-surgical Therapies Including Gallstone Management
43
Preventing Infectious Complications
In acute pancreatitis, both early infections, especially bacteremia, and secondary infection of (peri)pancreatic necrosis in a later phase, may increase mortality [9]. Disruption of the normal gut barrier, which results in translocation of microorgan­isms, is believed to be the major cause of secondary infection of (peri)pancreatic necrosis [32, 36, 37]. Multiple studies have shown that prophylactic administration of antibiotics does not reduce the risk of infected (peri)pancreatic necrosis [3841]. Moreover, the use of prophylactic antibiotics is associated with an increased inci­dence of fungal and multidrug-resistant bacterial infections [42, 43]. Administration of antibiotics in acute pancreatitis are therefore only advised as treatment for proven or clinically suspected infected necrosis [1, 44]. Another believed potential prophy­lactic strategy for the prevention of (secondary) infections by protecting the gut barrier was the use of probiotics. The multicenter randomized PROPATRIA trial [12] found a higher rate of mortality in patients with predicted severe acute pancre­atitis who received probiotics compared to a placebo group. Therefore, the admin­istration of probiotics for the treatment of acute pancreatitis is not recommended.
Nevertheless, the perfect strategy for protecting the gut barrier and eventually preventing infectious complications remains challenging. A possible strategy may be the use of the short-chain fatty acid “butyrate” which is produced by different types of bacteria in the gut. Butyrate has an anti-inammatory and antimicrobial effect in the gut that improves the gut integrity and the mucosal immune system [45]. A recent study showed the positive effect of oral supplementation of butyrate in a mouse model of biliary necrotizing pancreatitis on the gut barrier [46]. Another possible benecial effect on preventing bacterial translocation may be modulating the gut’s microora. The gut microbiome is believed to play a role in the develop­ment of sepsis and (multi)organ failure [47]. Future research should be conducted to investigate both possible strategies.
Management ofBiliary Pancreatitis
Currently, the most frequent cause of acute pancreatitis in the Western world is gallstones (45%) [48]. Gallstones can induce acute biliary pancreatitis as a result of (transient) obstruction of the bile and pancreatic duct. Cholangitis, organ failure, and further potentially fatal consequences can occur in patients with biliary pancre­atitis [4, 49, 50].
44
A. Nagelhout et al.
Role ofERCP
According to current guidelines, ERCP is not recommended for mild biliary pancre­atitis without cholangitis or predicted severe biliary pancreatitis without cholangitis and no presence of common bile duct obstruction [1, 51]. Urgent ERCP (within 24h of admission) might be favorable in patients with persistent cholestasis and is cur­rently only indicated in patients with biliary pancreatitis and concurrent acute chol­angitis [1, 52, 53]. It was hypothesized that ERCP combined with papillotomy might also reduce the severity of biliary pancreatitis by reducing pressure in the common bile duct [54]. The multicenter randomized APEC trial [55] demonstrated that routine urgent ERCP with biliary papillotomy did not lower rates of mortality or major complications in patients with predicted severe acute biliary pancreatitis when compared to conservative treatment (38 vs. 44%). It therefore appears that only patients with acute biliary pancreatitis and concurrent cholangitis benet from ERCP, especially in the rst 24h of admission.
Role ofEUS andMRCP
Similar to ERCP, EUS and MRCP are not advised in patients with mild biliary pan­creatitis without signs of common bile duct obstruction [1]. In case of uncertainty regarding common bile duct obstruction in the absence of cholangitis, an EUS (or MRCP) could detect gallstones in the common bile duct. A negative MRCP, how­ever, does not reliably (sensitivity of 88%) rule out the presence of small stones (less than 5mm) in the common bile duct, which are known to cause acute biliary pan­creatitis [56, 57]. If stones are visualized on EUS, an elective ERCP with papillot­omy and stone extraction may be indicated to prevent new episodes of biliary pancreatitis [58]. However, an ERCP with papillotomy does not prevent gallbladder stones-related conditions such as cholecystitis and biliary colic [1, 59]. For that reason, cholecystectomy after ERCP and papillotomy is recommended [1].
Timing ofCholecystectomy
In case of mild biliary pancreatitis, same-admission cholecystectomy is advised [1]. This advice emerged out of the multicenter randomized PONCHO trial [60], which demonstrated that same-admission cholecystectomy safely reduces the risk of recurrent gallstone-related complications and mortality when compared with a delayed elective cholecystectomy (5 vs. 17%). In patients with necrotizing biliary pancreatitis, cholecystectomy is advised if necrotic peripancreatic collections have resolved or persist after 6weeks [1, 61]. Before cholecystectomy, assessment of the presence and location of peripancreatic collections should be performed [62].
3 Acute Pancreatitis: Non-surgical Therapies Including Gallstone Management
45
Whether or not cholecystectomy can be performed safely obviously depends on the clinical condition of the patient, but also on the location of the persistent peripancre­atic collections, which should be avoided in the surgical eld of the cholecystectomy.
Prevention ofRecurrence
Besides gallstones, alcohol and smoking are common risk factors for recurrence of acute pancreatitis [63]. Recurrence could be reduced by alcohol abstinence after the rst episode of the acute alcoholic pancreatitis [6466]. However, quitting exces­sive use of alcohol is widely known to be difcult. A single-center randomized trial from Finland reported that standardized follow-up with repeated intervention against alcohol consumption lowers the recurrence rate of acute alcoholic pancreati­tis after 2years compared to single standardized intervention alone during the initial hospitalization (8 vs. 21%) [66]. Currently, the multicenter randomized PANDA trial in the Netherlands is assessing the effect of an optimally timed personalized multidisciplinary alcohol cessation program on the recurrence rate in patients with acute alcoholic pancreatitis.
Approximately 20% of the etiology of acute pancreatitis in patients remains idio­pathic [67, 68]. In these patients, it is advised to repeat the transabdominal ultra­sound after discharge, as the accuracy of a second transabdominal ultrasound is higher than the rst one [1, 69]. In 2015, a multicenter randomized trial from Finland reported that patients with idiopathic pancreatitis should undergo laparoscopic cho­lecystectomy [70]. However, in this study EUS was not used. The current advice is, in case of a negative repeat transabdominal ultrasound, to perform EUS to detect occult microlithiasis, as well as neoplasms and chronic pancreatitis [1, 71, 72]. If both transabdominal and EUS are negative, some experts advise (secretin-enhanced) MRCP to search for rare anatomical anomalies [1]. In case of recurrent attacks of idiopathic pancreatitis, genetic counseling should be considered [1]. The role of laparoscopic cholecystectomy in patients with “EUS-negative” idiopathic pancre­atitis is currently unclear and being studied in the multicenter randomized PICUS-2 trial.

References

1. IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology. 2013;13(4):e1–15.
2. Boxhoorn L, Voermans RP, Bouwense SA, Bruno MJ, Verdonk RC, Boermeester MA, etal. Acute pancreatitis. Lancet. 2020;396(10252):726–34.
3. Xiao AY, Tan MLY, Wu LM, Asrani VM, Windsor JA, Yadav D, etal. Global incidence and mortality of pancreatic diseases: a systematic review, meta-analysis, and meta-regression of population-based cohort studies. Lancet Gastroenterol Hepatol. 2016;1(1):45–55.