In Focus

Update on the Management of Acute Pancreatitis and Its Complications


Management of pancreatic necrosis

Although this topic has generated much debate, the majority of available evidence shows no clinical benefit from using prophylactic antibiotics to prevent infection in pancreatic necrosis46.

Infectious complications are the major cause of late mortality in AP. The predominant source is bacterial translocation from the GI tract47,48. Infected pancreatic necrosis should be suspected in patients with imaging evidence of pancreatic or extrapancreatic necrosis, who have a sudden deterioration in clinical status, typically 2-3 weeks after onset of symptoms or if gas bubbles are seen within a necrotic collection (Figure 2). When infected pancreatic necrosis is suspected or established, antibiotics such as carbapenems, fluoroquinolones, metronidazole, and cephalosporin should be started, which have better penetrance into ischemic pancreatic tissue. CT guided aspiration has lost much of its utility, since there has been a paradigm shift to delaying drainage of infected (suspected or established) pancreatic necrosis. A negative or positive CT aspirate does not dictate timing of intervention and is only recommended if a fungal or drug resistant infection is suspected15. As mentioned above, when debridement of an infected necroma is contemplated, the two guiding principles are to delay drainage and use minimally invasive approaches.

Vascular complications

Vascular complications such as splanchnic vein thrombosis can occur in up to a quarter of AP patients49. Anticoagulation is not usually indicated unless thrombosis is extensive and causes bowel ischemia. Arterial pseudoaneurysms are rare but life threatening complications of AP. They typically require interventional radiology guided coil embolization to prevent massive bleeding50.

Abdominal compartment syndrome

Abdominal compartment syndrome is an end result of third spacing of fluid into the abdominal cavity secondary to inflammation and fluid resuscitation in severe pancreatitis. Abdominal pressure in patients can be monitored by measuring bladder pressures. Intra-abdominal hypertension is defined as a sustained pressure greater than 12 mm Hg, while abdominal compartment syndrome is defined as sustained intra-abdominal pressure greater than 20 mm Hg with new organ failure51. Intra-abdominal hypertension (IAH) is present in up to 75% of patients with severe AP. While all conservative measures to prevent development or worsening of IAH should be implemented (adequate sedation, decompression of bowel in patients with ileus, etc.), current guidelines do not recommend aggressive interventions to treat it. On the other hand, abdominal compartment syndrome is a life-threatening complication that requires urgent intervention to decrease intra-abdominal pressure, such as percutaneous drain placement or surgical fasciotomy52,53.


The key principles in the management of acute pancreatitis are aggressive hydration and preventing development of end organ failure. In the last two decades there has been a paradigm shift in the guidelines for management of peripancreatic fluid collections and pancreatic necrosis. When feasible, drainage of these collections should be delayed and be performed using minimally invasive interventions. There is still an urgent need for developing and testing disease-specific treatments targeting control of the inflammatory response in the early phase of acute pancreatitis and prevention of development of severe disease with end-organ dysfunction.

Dr. Gulati is a gastroenterology and hepatology fellow at Allegheny Health Network, Pittsburgh, and Dr. Papachristou is professor of medicine, University of Pittsburgh School of Medicine, Pittsburgh.


1. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Chapter 55, 923-33.

2. Morgagni G.B. [Fie Books on the Seats and Causes of Diseases as Discovered by the Anatomist]. Venice, Italy: Typographia Remondiniana;1761.

3. Fitz R.H. Boston Med Surg J. 1889;120:181-8.

4. Comfort M., Gambill E., Baggesnstoss A. Gastroenterology. 1946;6:238-76.

5. Bollen T.L., van Santvoort H.C., Besselink M.G., et al. Br J Surg. 2008;95:6–21.

6. Dellinger E.P., Forsmark C.E., Layer P., et al. Ann Surg. 2012 Dec;256[6]:875-80.

7. Kochar B., Akshintala V.S., Afghani E., et al. Gastrointest Endosc. 2015 Jan;81[1]:143-9.

8. Choudhary A., Bechtold M.L., Arif M., et al. Gastrointest Endosc. 2011 Feb;73[2]:275-82.

9. Shi Q.Q., Ning X.Y., Zhan L.L., Tang G.D., Lv X.P. World J Gastroenterol. 2014 Jun 14;20[22]:7040-8.

10. Elmunzer B.J., Waljee A.K., Elta G.H., Taylor J.R., Fehmi S.M., Higgins P.D. Gut. 2008 Sep;57[9]:1262-7.

11. Sethi S., Sethi N., Wadhwa V., Garud S., Brown A. Pancreas. 2014 Mar;43[2]:190-7. 
12. Elmunzer B.J., Serrano J., Chak A., et al. Trials. 2016 Mar 3;17[1]:120.

13. Lowenfels A.B., Maisonneuve P., Sullivan T. Curr Gastroenterol Rep. 2009;11:97-103.

14. Agarwal N., Pitchumoni C.S., Sivaprasad A.V. Am J Gastroenterol. 1990;85:356-66.

15. Tenner S., Baillie J., DeWitt J. Vege S.S. Am J Gastroenterol. 2013;108:1400-15.

16. Papachristou G.I., Muddana V., Yadav D., et al. Am J Gastroenterol. 2010;105:435-41.

17. Mounzer R., et al. Gastroenterology 2012;142:1476-82.

18. Working Group IAP/APA Acute Pancreatitis Guidelines. Pancreatology. 2013 Jul-Aug;13(4 Suppl 2):e1-15.

19. Koutroumpakis E., Wu B.U., Bakker O.J., et al. Am J Gastroenterol. 2015 Dec;110[12]:1707-16.

20. Bang U.C., Semb S., Nojgaard C., Bendtsen F. World J Gastroenterol. 2008 May 21;14[19]:2968-76.

21. Warndorf M.G., Kurtzman J.T., Bartel M.J., et al. Clin Gastroenterol Hepatol. 2011 Aug;9[8]:705-9.

22. Hotz H.G., Foitzik T., Rohweder J., et al. J Gastrointest Surg. 1998 Nov-Dec;2[6]:518-25.

23. Brown A., Baillargeon J.D., Hughes M.D., et al. Pancreatology 2002;2:104-7.

24. Wu B.U., Hwang J.Q., Gardner T.H., et al. Clin Gastroenterol Hepatol. 2011 Aug;9[8]:710-7.

25. Forsmark C.E., Baillie J., AGA Institute Clinical Practice and Economics Committee, AGA Institute Governing Board. Gastroenterology. 2007 May;132[5]:2022-44.

26. Lankisch P.G., Mahlke R., Blum T., et al. Am J Gastroenterol. 2001;96:2081-5.

27. Wu B.U., Johannes R.S., Sun X., et al. Gastroenterology 2009;137:129-35.

28. Scherer J., Singh V.P., Pitchumoni C.S., Yadav D. J Clin Gastroenterol. 2014 Mar;48[3]:195-203.

29. Gubensek J., Buturovic-Ponikvar J., Romozi K., Ponikvar R. PLoS One. 2014 Jul 21;9[7]:e102748.

30. Chen J.H., Yeh J.H., Lai H.W., Liao C.S. World J Gastroenterol. 2004 Aug 1;10[15]:2272-4.

31. Tse F., Yuan Y. Cochrane Database Syst Rev. 2012 May 16;[5]:CD009779.

32. Folsch U.R., Nitsche R., Ludtke R., et al. N Engl J Med. 1997;336:237-42.

33. Al-Omran M., Albalawi Z.H., Tashkandi M.F., Al-Ansary L.A. Cochrane Database Syst Rev. 2010 Jan 20;[1]:CD002837.


Next Article:

Insurance-mandated diet pre–bariatric surgery deemed harmful