cystic neoplasms of the pancreas from these lesions, as cystic neoplasms can be malignant or have

malignant potential. Cystic lesions of the pancreas are being diagnosed with increasing frequency due to

the routine use of CT and MRI scans. Cystic neoplams of the pancreas can usually be differentiated from

pseudocysts and walled-off necrosis by the lack of evidence for antecedent pancreatitis or pancreatic

trauma, or by the appearance on imaging studies. Pseudocysts are typically round, unilocular, and have

a dense wall. In contrast, walled-off necrosis is typically heterogeneous with liquid and nonliquid

density, with varying degrees of loculations, and is encapsulated by a well-defined wall. FNA, either by

an image-guided percutaneous approach or an EUS-guided approach, can be used in cases where it is

difficult to differentiate between pseudocysts or walled-off necrosis and cystic neoplasms. Pseudocysts

and walled-off necrosis usually contain fluid with high amylase concentrations. In contrast, most

neoplastic cysts do not communicate with the pancreatic duct and contain fluid with low amylase

concentrations. These criteria, however, lack absolute predictive power.

Figure 53-5. Computed tomography scan of pancreatic pseudocyst.

Figure 53-6. Computed tomography scan of walled-off necrosis. Arrows indicate the presence of solid material within the

collection.

14 The management of pseudocysts and walled-off necrosis continues to evolve. In the past, surgical

drainage of pseudocysts was recommended for all pseudocysts (even if asymptomatic) that persisted

beyond a 6-week period of observation. This recommendation was based on a widely quoted report

which suggested that pseudocysts that persist more than 6 weeks rarely resolve spontaneously and are

associated with high complication rates.47 However, subsequent reports suggest that the natural history

of asymptomatic pseudocysts follows a more benign course, with most pseudocysts less than 6 cm in

diameter resolving spontaneously without complications.48,49 Even large, persistent collections may

never cause symptoms or complications. Current well-accepted indications for intervention in the

absence of infection include the presence of symptoms attributable to the collection such as intractable

pain or obstruction of the stomach, duodenum, or bile duct.9,10,35,50

15 There are multiple treatment options available for the treatment of pancreatic pseudocysts and

sterile walled-off necrosis, including percutaneous aspiration, percutaneous drainage, and internal

drainage (performed transabdominally or endoscopically). The optimal indications for these procedures

1379

are not conclusively determined. Percutaneous aspiration alone is associated with high recurrence rates.

Patients with chronic pancreatitis or pancreatic ductal abnormalities, particularly severe strictures or

discontinuity of the pancreatic duct, have a high rate of failure with percutaneous drainage of

pseudocysts. Percutaneous drainage alone should be avoided in these circumstances but may have a high

rate of success in patients with normal ducts.51 Endoscopic cystgastrostomy is an option for patients in

whom the pseudocyst or walled-off necrosis is intimately adherent to the stomach or duodenum. This

procedure is accomplished by transmural puncture of the pseudocyst, balloon dilation of the tract, and

placement of a stent connecting the pseudocyst to the stomach. A small, single-center randomized

controlled trial of surgical cystgastrostomy versus endoscopic cystgastrostomy (along with ERCP and

stenting of pancreatic duct leaks or strictures) for pseudocysts showed equal efficacy along with

decreased hospital stay and cost for the endoscopic arm.52 The treatment of symptomatic sterile walledoff necrosis can also be accomplished endoscopically (see description of DEN above). Due to the

presence of necrotic debris within these collections, in contrast to pseudocyts, the need for multiple

stents and/or multiple procedures, often with mechanical débridement, should be expected when

walled-off necrosis is approached endoscopically. As of yet, high-quality data comparing the efficacy of

surgical versus endoscopic treatment of symptomatic, sterile walled-off necrosis are lacking.

The most commonly performed surgical procedures used to treat pseudocysts and sterile walled-off

necrosis include cystgastrostomy, cystoduodenostomy, and Roux-en-Y cystojejunostomy.

Cystgastrostomy or cystoduodenostomy is applicable if a portion of the pseudocyst wall is adherent to

the stomach or duodenum respectively allowing for the creation of an anastomosis. Otherwise, the cyst

wall can be anastomosed to a Roux limb of jejunum. These procedures, which can be performed as open

or laparoscopic operations, should be delayed until pseudocyst wall maturation occurs. Mortality rates

associated with surgical drainage procedures average less than 5%, with pseudocyst recurrence rates

averaging 10%.

References

1. 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.

2. Peery AF, Dellon ES, Lund J, et al. Burden of gastrointestinal disease in the United States: 2012

update. Gastroenterology 2012;143:1179–1187.

3. 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.

4. Steer ML. Pathogenesis of acute pancreatitis. Digestion 1997;58 suppl 1:46–49.

5. Saluja AK, Donovan EA, Yamanaka K, et al. Cerulein-induced in vitro activation of trypsinogen in

rat pancreatic acini is mediated by cathepsin B. Gastroenterology 1997;113:304–310.

6. Leach SD, Modlin IM, Scheele GA, et al. Intracellular activation of digestive zymogens in rat

pancreatic acini. Stimulation by high doses of cholecystokinin. J Clin Invest 1991;87:362–366.

7. Hashimoto D, Ohmuraya M, Hirota M, et al. Involvement of autophagy in trypsinogen activation

within the pancreatic acinar cells. J Cell Biol 2008; 181:1065–1072.

8. Gukovsky I, Li N, Todoric J, et al. Inflammation, autophagy, and obesity: common features in the

pathogenesis of pancreatitis and pancreatic cancer. Gastroenterology 2013;144:1199–1209. e4.

9. Working Group IAP/APA Acute Pancreatitis Guidelines. IAP/APA evidence-based guidelines for the

management of acute pancreatitis. Pancreatology 2013;13:e1–e15.

10. Tenner S, Baillie J, DeWitt J, et al. American College of Gastroenterology guideline: management

of acute pancreatitis. Am J Gastroenterol 2013;108:1400–1415, 1416.

11. Nawaz H, Mounzer R, Yadav D, et al. Revised Atlanta and determinant-based classification:

application in a prospective cohort of acute pancreatitis patients. Am J Gastroenterol

2013;108:1911–1917.

12. 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;139:813–820.

13. Petrov MS, Windsor JA. Classification of the severity of acute pancreatitis: how many categories

make sense? Am J Gastroenterol 2010;105:74–76.

14. Thandassery RB, Yadav TD, Dutta U, et al. Prospective validation of 4-category classification of

1380

acute pancreatitis severity. Pancreas 2013;42:392–396.

15. Dellinger EP, Forsmark CE, Layer P, et al. Determinant-based classification of acute pancreatitis

severity: an international multidisciplinary consultation. Ann Surg 2012;256:875–880.

16. Ranson JH, Rifkind KM, Roses DF, et al. Prognostic signs and the role of operative management in

acute pancreatitis. Surg Gynecol Obstet 1974; 139:69–81.

17. Imrie CW, Benjamin IS, Ferguson JC, et al. A single-centre double-blind trial of Trasylol therapy in

primary acute pancreatitis. Br J Surg 1978;65:337–341.

18. Larvin M, McMahon MJ. APACHE-II score for assessment and monitoring of acute pancreatitis.

Lancet 1989;2:201–205.

19. Wu BU, Johannes RS, Sun X, et al. The early prediction of mortality in acute pancreatitis: a large

population-based study. Gut 2008;57:1698–1703.

20. Cho YS, Kim HK, Jang EC, et al. Usefulness of the Bedside Index for severity in acute pancreatitis in

the early prediction of severity and mortality in acute pancreatitis. Pancreas 2013;42:483–487.

21. 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.

22. Singh VK, Wu BU, Bollen TL, 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; 104:966–71.

23. Bollen TL, Singh VK, Maurer R, et al. A comparative evaluation of radiologic and clinical scoring

systems in the early prediction of severity in acute pancreatitis. Am J Gastroenterol 2012;107:612–

619.

24. Johnson CD, Stephens DH, Sarr MG. CT of acute pancreatitis: correlation between lack of contrast

enhancement and pancreatic necrosis. AJR Am J Roentgenol 1991;156:93–95.

25. Fisher JM, Gardner TB. The “golden hours” of management in acute pancreatitis. Am J Gastroenterol

2012;107:1146–1150.

26. van Brunschot S, Schut AJ, Bouwense SA, et al. Abdominal compartment syndrome in acute

pancreatitis: a systematic review. Pancreas 2014;43:665–674.

27. Marik PE, Zaloga GP. Meta-analysis of parenteral nutrition versus enteral nutrition in patients with

acute pancreatitis. BMJ 2004;328:1407.

28. 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.

29. Singh N, Sharma B, Sharma M, et al. Evaluation of early enteral feeding through nasogastric and

nasojejunal tube in severe acute pancreatitis: a noninferiority randomized controlled trial. Pancreas

2012;41:153–159.

30. Tse F, Yuan Y. Early routine endoscopic retrograde cholangiopancreatography strategy versus early

conservative management strategy in acute gallstone pancreatitis. Cochrane Database Syst Rev

2012;5:CD009779.

31. van Baal MC, Besselink MG, Bakker OJ, et al. Timing of cholecystectomy after mild biliary

pancreatitis: a systematic review. Ann Surg 2012;255:860–866.

32. Ito K, Ito H, Whang EE. Timing of cholecystectomy for biliary pancreatitis: Do the data support

current guidelines? J Gastrointest Surg 2008;12(12):2164–2170.

33. McAlister VC, Davenport E, Renouf E. Cholecystectomy deferral in patients with endoscopic

sphincterotomy. Cochrane Database Syst Rev 2007;(4):CD006233.

34. Gerzof SG, Banks PA, Robbins AH, et al. Early diagnosis of pancreatic infection by computed

tomography-guided aspiration. Gastroenterology 1987;93:1315–1320.

35. Freeman ML, Werner J, van Santvoort HC, et al. Interventions for necrotizing pancreatitis:

summary of a multidisciplinary consensus conference. Pancreas 2012;41:1176–1194.

36. 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;232:175–180.

37. Connor S, Alexakis N, Raraty MG, et al. Early and late complications after pancreatic necrosectomy.

Surgery 2005;137:499–505.

38. Mouli VP, Sreenivas V, Garg PK. Efficacy of conservative treatment, without necrosectomy, for

1381

infected pancreatic necrosis: a systematic review and meta-analysis. Gastroenterology 2013;144:333–

340.

39. van Santvoort HC, Besselink MG, Bakker OJ, et al. A step-up approach or open necrosectomy for

necrotizing pancreatitis. N Engl J Med 2010;362:1491–1502.

40. Ashley SW, Perez A, Pierce EA, et al. Necrotizing pancreatitis: contemporary analysis of 99

consecutive cases. Ann Surg 2001;234:572–579.

41. Büchler MW, Gloor B, Müller CA, et al. Acute necrotizing pancreatitis: treatment strategy according

to the status of infection. Ann Surg 2000;232:619–626.

42. Isenmann R, Runzi M, Kron M, et al. Prophylactic antibiotic treatment in patients with predicted

severe acute pancreatitis: a placebo-controlled, double-blind trial. Gastroenterology 2004;126:997–

1004.