14 15 Petrov MS, Shanbhag S, Chakraborty M, et al. Organ failure and infection of pancreatic necrosis as determinants of mortality in patients with acute pancreatitis. Gastroenterology 2010; 139(3):813–820.
15 16 Bradley EL. 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(5):586–590.
16 17 Freeny PC, Hauptmann E, Althaus SJ, et al. Percutaneous CT‐guided catheter drainage of infected acute necrotizing pancreatitis: techniques and results. AJR Am J Roentgenol 1998; 170(4):969–975.
17 18 Bello B, Matthews JB. Minimally invasive treatment of pancreatic necrosis. World J Gastroenterol 2012; 18(46):6829–6835.
18 19 Van Baal MC, Van Santvoort HC, Bollen TL, et al. Systematic review of percutaneous catheter drainage as primary treatment for necrotizing pancreatitis. Br J Surg 2011; 98(1):18–27.
19 20 van Grinsven J, van Dijk SM, Dijkgraaf MG, et al. Postponed or immediate drainage of infected necrotizing pancreatitis (POINTER trial): study protocol for a randomized controlled trial. Trials 2019; 20(1):239.
20 21 Poves I, Burdío F, Dorcaratto D, Grande L. Minimally invasive techniques in the treatment of acute biliary pancreatitis. Central Eur J Med 2013; 60(Suppl 7):13–19.
21 22 Carter CR, McKay CJ, Imrie CW. Percutaneous necrosectomy and sinus tract endoscopy in the management of infected pancreatic necrosis: an initial experience. Ann Surg 2000; 232(2):175–180.
22 23 Goenka MK, Goenka U, Mujoo MY et al. Pancreatic necrosectomy through sinus tract endoscopy. Clin Endosc 2018; 51(3):279–284.
23 24 Bakker OJ, van Santvoort HC, van Brunschot S, et al. Endoscopic transgastric vs surgical necrosectomy for infected necrotizing pancreatitis: a randomized trial. JAMA 2012; 307(10):1053–1061.
24 25 Baron TH, Thaggard WG, Morgan DE, Stanley RJ. Endoscopic therapy for organized pancreatic necrosis. Gastroenterology 1996; 111(3):755–764.
25 26 Escourrou J, Shehab H, Buscail L, et al. Peroral transgastric/transduodenal necrosectomy. Ann Surg 2008; 248(6):1074–1080.
26 27 van Brunschot S, van Grinsven J, van Santvoort HC, et al. Endoscopic or surgical step‐up approach for infected necrotising pancreatitis: a multicentre randomised trial. Lancet 2018; 391(10115):51–58.
27 28 Gambiez LP, Denimal FA, Porte HL, et al. Retroperitoneal approach and endoscopic management of peripancreatic necrosis collections. Arch Surg 1998; 133(1):66–72.
28 29 Horvath KD, Kao LS, Wherry KL, et al. A technique for laparoscopic‐assisted percutaneous drainage of infected pancreatic necrosis and pancreatic abscess. Surg Endosc 2001; 15(10):1221–1225.
29 30 Morató O, Poves I, Ilzarbe L, et al. Minimally invasive surgery in the era of step‐up approach for treatment of severe acute pancreatitis. Int J Surg 2018; 51:164–169.
30 31 Eickhoff RM, Steinbusch J, Seppelt P, et al. Videoassistiertes retroperitoneales DébridementVideo‐assisted retroperitoneal debridement. Der Chir 2017; 88(9):785–791.
31 32 Wani SV, Patankar RV, Mathur SK. Minimally invasive approach to pancreatic necrosectomy. J Laparoendosc Adv Surg Tech A 2011; 21(2):131–136.
32 33 Parekh D. Laparoscopic‐assisted pancreatic necrosectomy. Arch Surg 2006; 141(9):895.
33 34 Castellanos G, Piñero A, Parrilla P. Is there a place for laparoscopic surgery in the management of acute pancreatitis? In: Domínguez Muñoz JE (ed.) Clinical Pancreatology for Practising Gastroenterologists and Surgeons. Oxford: Blackwell Publishing, 2005:156–165.
34 35 Worhunsky DJ, Qadan M, Dua MM, et al. Laparoscopic transgastric necrosectomy for the management of pancreatic necrosis. J Am Coll Surg 2014; 219(4):735–743.
Note
1 † Deceased September 2019.
16 Endoscopic Necrosectomy in Clinical Practice : Indications, Technical Issues, and Optimal Timing
Jodie A. Barkin1 and Andres Gelrud2
1 Department of Medicine, Division of Gastroenterology, Leonard M. Miller School of Medicine, University of Miami, Miami, FL, USA
2 GastroHealth and Miami Cancer Institute, Miami, FL, USA
Introduction
Acute pancreatitis (AP) is the third leading cause of gastroenterology‐related hospitalizations in the United States, accounting for approximately 280 000 admissions annually and more than US$2 billion in annual healthcare costs [1,2]. Despite advances in treatment algorithms over time, AP has an associated mortality rate of approximately 5%, with further increases to greater than 15% in those with severe AP in the presence of multiorgan failure [3]. Interstitial edematous pancreatitis accounts for the majority of AP cases; under 10% of AP patients develop necrotizing pancreatitis with the presence of pancreatic and/or peripancreatic tissue necrosis. While necrosis may be seen on imaging at presentation or early in the disease course, necrosis may slowly evolve over a number of days after the onset of symptoms, and lack of necrosis initially does not preclude its development thereafter [4,5]. If a concern exists for worsening clinical status days to weeks after prior imaging, consideration for repeat imaging to evaluate for complications including the presence of fluid and/or necrotic collections is advisable. The 2012 Revised Atlanta Classification guides the characterization of these local complications based on the presence or absence of tissue debris in the collection and on a time course after development to allow maturation of the collection with a well‐defined wall [6]. There are four types of local collections associated with AP, including acute fluid collection (AFC), pancreatic pseudocyst (PP), acute necrotic collection (ANC), and walled‐off necrosis (WON). AFCs develop early (under four weeks post AP episode) in interstitial edematous AP, contain only fluid without solid debris, classically appear homogeneous on cross‐sectional contrast‐enhanced imaging, and likely lack a well‐defined wall or capsule. AFCs persisting beyond four weeks post AP are reclassified as PPs containing just fluid without solid debris and, importantly, having the presence of a clearly demarcated capsule. In contrast, collections in which solid debris is seen are classified as ANCs or WON depending on time course post AP and presence or absence of a clearly defined wall. ANCs develop within four weeks of necrotizing AP, contain both fluid and solid debris internally, and lack a clear wall. Once a wall has formed, again usually after four weeks, these are reclassified as WON. Superimposed infection may occur in approximately 40–70% of patients with necrotizing AP, with an associated drastic increase in mortality, from 15% in those with sterile necrosis to roughly 40% in those with infected necrosis [7]. Oftentimes, differentiation of AFC from ANC may be challenging early on as both may appear homogeneous with fluid consistency on imaging. Delaying subsequent follow‐up imaging for one to two weeks if clinical status is stable is advisable to maximize the informative value of subsequent scans in differentiating AFC from ANC.
Most AFCs and ANCs will spontaneously resolve, with only a proportion persisting beyond four weeks and going on to develop a clearly defined capsule to become PP or WON. Interestingly, most ANCs will spontaneously resolve over time, and even in those who develop WON, approximately half will spontaneously resolve without intervention in a six‐month period [8]. The critical juncture is to decide which patients with PP or WON require intervention, as intervention in AFC and ANC should be delayed until clear maturation of the wall is seen. The primary criterion for need to intervene is the presence of symptoms. Asymptomatic patients should be conservatively managed and observed regardless of collection size, while those who are symptomatic should be evaluated for potential intervention. Historically, open surgical intervention was the primary option especially for patients with large WON; however, patients often had prolonged