Acute pancreatitis

Recent changes in management of acute
pancreatitis , common misunderstanding
& areas of ongoing controversies

 Causes of acute pancreatitis
 Epidimiology
 Revised definations of morphological features of acute
pancreatitis
 Management
• Fluid resuscitation
• Nutrition
• WOPN
• Pseudoaneurysm
 Long term consequences
 Prevention of relapse

Gallstones Pancreatitis
 Most common cause
 Mechanism is not entirely clear
 Common-channel theory
“Blockage below junction of biliary and
pancreatic duct cause bile flow into pancrease”
BUT…
 short channel in which stone located would
block both biliary and pancreatic duct
 Hydrostatic pressure in biliary<pancreatic duct

 Mechanism???
Ductal hypertension
 Cause rupture of small ducts and leakage of pancreatic
juice
 pH in pancreatic tissue ↓
 activation of protease
 “Co-localization”

 There are no convincing data from controlled trials that
either pancreatic sphincter of Oddi dysfunction or
pancreas divisum plays a role in acute pancreatitis
 Pancreas divisum is not a cause of pancreatitis by itself
but acts as a partner of CFTR mutations
 PD frequency is 47 % in subjects CFTR-associated
pancreatitis
Am J Gastroenterol. 2012 Feb;107(2):311-7. doi:
10.1038/ajg.2011.424. Epub 2011 Dec 13
 DiMagno MJ et al suggested that CFTR mutations
influence pancreatic duct embryogenesis & if CFTR
mutations are found, then refer patients for genetic
counseling and withhold endoscopic/surgical therapy

Alcohol induced acute
pancreatitis
 Alcohol is the second most common cause
 Dose : 4 to 5 drinks daily for > 5 years
 Overall lifetime risk among heavy drinkers is 2 to 5%.
 The type of alcohol does not affect risk
 Binge drinking in the absence of long-term use does not
precipitate acute pancreatitis

 Intra-acinar cell activation of the transcriptional activator
nuclear factor-κB (NF-κB) occurs simultaneous to, but
independent of trypsinogen activation
 NF-κB regulates a wide variety of genes involved in cell
survival, cellular replication, immunity, and inflammation
 NF-κB-mediated inflammatory response appears to be
responsible for up to half of the pancreatic tissue damage
 Ethanol oxidation-mediated decrease in the NAD+/NADH
ratio leads to decreased sirtuin-3 activity and
consequently, hyperacetylation of cyclophilin-D.

World J Gastrointest Pathophysiol 2016 February
15; 7(1): 48-58

Drug induced pancreatitis Trivedi CD J Clin Gastroenterol.2005
Sep;39(8):709-16
Class I medications Class II medications
 didanosine
 asparaginase
 azathioprine
 valproic acid
 pentamidine
 mercaptopurine
 mesalamine
 estrogen preparations
 opiates
 Tetracycline
 cytarabine
 steroids
 Cotrimoxazole
 sulfasalazine
 furosemide
 rifampin
 lamivudine
 octreotide
 carbamazepine
 Acetaminophen
 phenformin
 interferon alfa-2b
 Enalapril
 Hydrochlorothiazide
 Cisplatin
 Erythromycin

Drug induced pancreatitis
 < 5% of all cases of acute pancreatitis
 Usually mild.
 Recent data do not support a role for glucagon-like peptide
1 mimetics in causing pancreatitis
Pancreatology.2016 Jan-Feb;16(1):10-3. doi:
10.1016/j.pan.2015.11.009. Epub 2015 Dec 1.
 Rarely is accompanied by clinical or laboratory evidence of
a drug reaction, such as rash, lymphadenopathy, or
eosinophilia.

 3 pathogenic mechanisms of drug-induced
pancreatitis
1. Hypersensitivity reaction
2. Accumulation of a toxic metabolite
3. Intrinsic toxicity
 Hypersensitivity reaction
 occur 4 to 8 weeks after starting drug
 not dose related
 On rechallenge with the drug, pancreatitis recurs within
hours to days.
 Examples: aminosalicylates, metronidazole, and
tetracycline

 Accumulation of a toxic metabolite
 after several months of use
 Examples: valproic acid , didanosine (DDI), drugs that
induce hypertriglyceridemia (e.g., thiazides, isotretinoin,
tamoxifen)
 Intrinsic toxicity
 d/t overdose
 Examples : erythromycin, acetaminophen

Postoperative pancreatitis
 Occur after thoracic or abdominal surgery
 Lefor AT et al retrospectively reviewed 5621 patients who
underwent cardiopulmonary bypass
 25 (0.44%) sustained pancreatic complications.
 There were 15 cases of acute pancreatitis & 10 cases of
pancreatic necrosis
 11 deaths with a mortality rate of 44%
Lefor AT, Vuocolo P, Parker FB Jr, Sillin LF. Arch Surg. 1992
Oct;127(10):1225-30

 Pancreatitis occurs in 6% of liver transplantations with 40
percent mortality rate
 The incidence of AP was significantly higher in patients
with hepatitis B (17 %) than in patients without hepatitis B
(3 %) (p < 0.01)
Camargo CA Jr, Greig PD, Levy GA, Clavien PAJ Am
Coll Surg.1995 Sep;181(3):249-56

 Risk factors for post operative pancreatitis
 Preoperative hypotension
 Preoperative use of inotropic agents
 Renal failure (preoperative and postoperative)
 Fluid sequestration
 Respiratory failure
 Sepsis
 Tachycardia
 Hypocalcemia
 Age >55 years

Epidemiology
 Admissions have increased by at least 20% over the past 10
years
 Studies worldwide have shown a rising incidence acute
pancreatitis
 D/t worldwide obesity epidemic and increasing rates of
gallstone

 Death is more likely in certain subgroups of patients
 Elderly
 Those with more numerous and more severe coexisting
conditions (particularly obesity)
 Hospital acquired infections
 Those with severe episodes of acute pancreatitis

 Overall mortality is approximately 2%
 It approaches 30% among patients with persistent
organ failure
Classification of acute pancreatitis—2012:
revision of the Atlanta classification and definitions by international
consensus
 “critical pancreatitis” i.e. presence of both persistent
organ failure and infected pancreatic necrosisis -
associated with the highest mortality
Ann Surg. 2012 Dec;256(6):875-80. doi:
10.1097/SLA.0b013e318256f778.

Definition of organ failure
A score of 2 or more in any system defines the presence
of organ failure

Revised definitions of morphological
features AP
 Interstitial oedematous pancreatitis: Acute
inflammation of the pancreatic parenchyma and
peripancreatic tissues, but without recognisable
tissue necrosis
 CECT criteria
▸ Pancreatic parenchyma enhancement by
intravenous contrast agent
▸ No findings of peripancreatic necrosis

Necrotising pancreatitis :
Inflammation associated with
pancreatic parenchymal necrosis
and/or peripancreatic necrosis
CECT criteria
▸ Lack of pancreatic parenchymal
enhancement by intravenous
contrast agent and/or
▸ Presence of findings of
peripancreatic necrosis

 APFC (acute peripancreatic fluid collection)
Peripancreatic fluid associated with interstitial
oedematous pancreatitis with no associated peripancreatic
necrosis.
 Seen within the first 4 weeks after onset of interstitial
oedematous pancreatitis & without the features of
pseudocyst.
 CECT criteria
▸ Occurs in the setting of interstitial oedematous
pancreatitis
▸ Homogeneous collection with fluid density
▸ Confined by normal peripancreatic fascial planes
▸ No definable wall encapsulating the collection
▸ Adjacent to pancreas (no intrapancreatic extension)

(A) Interstitial oedematous
pancreatitis and APFC in the left
anterior pararenal space . The
pancreas enhances completely, is
thickened, and has a
heterogeneous appearance due
to oedema. APFC has fluid density
without an encapsulating wall.
(B) A few weeks later, a follow up
CT
shows complete resolution of the
APFC with minimal residual
peripancreatic fat stranding.

 Pancreatic pseudocyst :An encapsulated collection of
fluid with a well defined inflammatory wall usually outside
the pancreas with minimal or no necrosis.
 This entity usually occurs more than 4 weeks after onset of
interstitial oedematous pancreatitis .
 CECT criteria
▸ Well circumscribed, usually round or oval
▸ Homogeneous fluid density
▸ No non-liquid component
▸ Well defined wall (completely encapsulated)
▸ Maturation usually requires >4 weeks after onset of
acute pancreatitis

 ANC (acute necrotic collection): A collection
containing variable amounts of both fluid and necrosis
associated with necrotising pancreatitis; the necrosis
can involve the pancreatic parenchyma and/or the
peripancreatic tissues
 CECT criteria
▸ Occurs only in the setting of acute necrotising
pancreatitis
▸ Heterogeneous (some appear homogeneous early n
their course)
▸ No definable wall
▸ Location—intrapancreatic and/or extrapancreatic

 WON (walled-off necrosis): A mature, encapsulated
collection of pancreatic and/or peripancreatic necrosis that
has developed a well defined inflammatory wall.
 Usually occurs >4 weeks after onset of necrotising
pancreatitis.
 CECT criteria
▸ Heterogeneous with liquid and non-liquid density with
varying degrees of loculations (some may appear
homogeneous)
▸ Well defined wall
▸ Location—intrapancreatic and/or extrapancreatic
▸ Maturation usually requires 4 weeks after onset of
acute
necrotising pancreatitis

Non-liquid components of high attenuation (black arrowheads) in the
collection are noted. The collection has a thin, well defined, and
enhancing wall (thick white arrows)

 Serum amylase
 Elevates within HOURS and can remain elevated for 3-5
days
 High specificity when level >3x normal
 Many false positives
 Most specific = pancreatic isoamylase (fractionated
amylase)

Serum lipase
 The preferred test for diagnosis
 Begins to increase 4-8H after onset of symptoms and
peaks at 24H
 Remains elevated for days
 Sensitivity 86-100% and Specificity 60-99%
 >3X normal S&S ~100%

Plain Abdominal Radiograph
 Bowel ileus
 “Sentinel Loop”
 “Colon cut off sign”
 Loss of psoas shadow
 Helps exclude other causes of abdominal pain: bowel
obstruction and perforation

 localized ileus from nearby inflammation
Sentinel loop

 Plain radiographs contribute little
 Ultrasound show the pancreas in only 25-50%
 CT scan provides better information
 Severity and prognosis
 Exclusion of other diseases
 EUS & MRI with MRCP – cause of pancreatitis

Early in the course of the disease
• Extravasation of protein-rich intravascular fluid into
the peritoneal cavity and retroperitoneum
• Hemoconcentration and decreased renal perfusion
with the associated elevation in BUN.
• Decreased perfusion pressure into the pancreas leads
to microcirculatory changes that result in pancreatic
necrosis

 On admission hematocrit of more than 44% & a failure of the
admission hematocrit to decrease at 24 hours are predictors
of necrotizing pancreatitis
Lankisch PG, Pflichthofer D, Lehnick D Pancreas.3:319322 2000
• Elevation or rising BUN is associated with increased mortality.
Wu BU Gastroenterology.2009 Jul;137(1):129-35. doi:
10.1053/j.gastro.2009.03.056
 The goal is to provide enough intravascular volume to
decrease the hematocrit and the BUN, thereby increasing
pancreatic perfusion

Fluid Resuscitation
 Crystalloid solution recommended at a rate of 200 to 500
ml per hour, or 5 to 10 ml/ kg of body weight/hour
 Amounts to 2500 to 4000 ml within the first 24 hours
 Ringer’s lactate is superior to NS in reducing inflammatory
markers
Wu BU, Hwang JQ, Gardner TH, et al. Clin Gastroenterol
Hepatol 2011; 9(8): 710-717.e1

 Ways to gauge the adequacy of fluid therapy:
 Clinical cardiopulmonary monitoring for fluid status
 Hourly measurement of urine output
 Monitoring of the blood urea nitrogen level and
hematocrit
 Aggressive fluid administration during the first 24 hours
reduces morbidity and mortality
 Fluid therapy is most important during the first 12 to 24
hours after the onset of symptoms and is of little value
after 24 hours

Feeding
• In mild acute pancreatitis : there is no need for complete
resolution of pain or normalization of pancreatic enzyme
to start oral feeding
Eckerwall GE Clin Nutr. 2007 Dec;26(6):758-63. Epub
2007 Aug 24.
 Low fat or solid diet is safe & associated with shorter
hospital stays than a clear-liquid diet
 Nasogastric or nasoduodenal feeding is clinically
equivalent Chang YS, Fu HQ, Xiao YM, Liu
JC.Nasogastric or nasojejunal feeding in predicted severe acute
pancreatitis: a metaanalysis. Crit Care 2013; 17: R118

 Randomised controlled trial ( Jiang RL et al Parenteral & Enteral
Nutrition 2011; 18: 82-84)
 Suggest NJ feeding is superior to NG feeding
 27 patients with SAP were randomized to NG routes (14
patients) or NJ routes (13 patients).
 Patients recover slowly in the index such as amylase, lipase and
CRP & the symptom of abdominal pain in NG groups.
 4 pts dropped out of because of failure tolerate NG
 Highly individual and specialized management may be required
in the nutrition support considering the potential of gastric
dysmotility.
 Sample number is small in this clinical test

 Singh N, Sharma B, Sharma M, Sachdev V, Bhardwaj
P, Mani K, Joshi YK, Saraya A. Pancreas. 2012
Jan;41(1):153-9. (AIIMS, New Delhi)
 NG was not inferior to NJ
 Infectious complication in the NG was 23.1% & in NJ
groups was 35.9% (significantly different)
 Meta analysis by Ying-Jie et al suggested that NG feeding is
as effective and safe as NJ in patients with SAP
 ACG has recommend NG feeding in patients with SAP

Nutrition in mild AP
 Low-fat solid diet is safe compared with clear liquids,
providing more calories
 Jacobson BC Clin Gastroenterol Hepatol. 2007
Aug;5(8):946-51
 Randomized 121 patients: 66 to CLD and 55 to LFSD.
 The number of patients requiring cessation of feeding
because of pain or nausea was similar in both groups
(6% for CLD, 11% for LFSD; P = .51).
 The median LOH after refeeding was identical in both
groups . Patients in the LFSD arm consumed significantly
more calories and grams of fat than those in the CLD
 There was no difference in the 28-day re-admission rates
between the 2 arms

 Oral refeeding with a full solid diet in mild AP was well
tolerated and resulted in a shorter LOH , without
abdominal pain relapse
Moraes JMJ Clin Gastroenterol.2010 Aug;44(7):517-
22
 In severe pancreatitis continuous enteral nutrition is
better in all patients who tolerate it
ESPEN Guidelines on Enteral Nutrition: Pancreas

Type of formula ??
 Elemental (Monomeric) Formulas
 Indivisual amino acids, are low in fat, especially LCTs
 Require minimal digestive function and cause less stimulation
of exocrine pancreatic secretion.
 In many products, MCT is the predominant fat source
 Semi-elemental (Oligomeric) Formulas
 Oligopeptides of varying lengths, dipeptides and tripeptides
 Silk et al found that individual and free amino acid residues,
were poorly absorbed while amino acids provided as
dipeptides and tripeptides were better absorbed

 Polymeric formulas/ standert formula contain intact proteins,
complex carbohydrates and LCTs
 Specialized formulas contain biologically active substances or
nutrients such as glutamine, arginine, nucleotides or essential
fatty acids
 Most EN studies utilized the more expensive elemental formulas
 No studies have compared elemental or semi-elemental
formulas to polymeric formulas
 Start with a standard formula and if this is not tolerated a
peptide-based formula can be used
ESPEN GUIDELINES Clinical Nutrition (2006) 25, 275–284

 TPN should be reserved for the rare cases in which enteral
nutrition is not tolerated or nutritional goals are not met.
 Early initiation of nasoenteric feeding (within 24 hours
after admission) is not superior to oral diet at 72 hours
 Tube feeding should be started only if oral feeding is not
tolerated over the ensuing 2 to 3 days
 Patients predicted to have severe or necrotizing
pancreatitis do not benefit from very early initiation of
enteral nutrition through a tube.

Endoscopic Therapy
 Indications of ERCP
 Evidence of cholangitis superimposed on gallstone
pancreatitis
 Documented choledocholithiasis on imaging
 Findings strongly suggestive of a persistent bile duct
stone
Jaundice
Progressive rise in the results of liver biochemical
studies
Persistently dilated bile duct

Treatment of Fluid Collections and
Necrosis
 Acute peripancreatic fluid collections do not require
therapy
 Sterile necrosis does not require therapy except in the
rare case of a collection that obstructs a nearby viscus
(e.g., duodenal, bile duct, or gastric obstruction)
 Drainage of these symptomatic sterile or infected
pseudocysts or WON should be done after 4 weeks
 to allow for encapsulation
 better definition of the margins
 To reduce adverse events if drainage is performed
ASGE
guideline 2016

 The development of infection is the main indication for
therapy
 The infection is usually monomicrobial and can involve
gram-negative rods, enterobacter species, or gram-positive
organisms
 Aspiration and culture of the collection are not required
 EUS-FNA is not recommended to determine whether a
PFC is infected.
 Performing this diagnostic procedure is a/w a high false-
negative rate and may contaminate a previously sterile
fluid collection.
ASGE
guideline 2016

 Santvoort et al, NEJM 2010 (PANTER study)
 Intervened on patients solely based on a clinical
suspicion of infected necrosis without using FNA and
was accurate in >90% of cases
 Signs of infected necrosis include
 Increasing abdominal pain
 new-onset or persistent sepsis
 clinical deterioration despite adequate support
 no alternative source of infection
 gas bubbles within necrosis on radiologic imaging

A 47-year-old man with acute necrotising pancreatitis complicated by infected
pancreatic necrosis. There is a heterogeneous, acute
necrotic collection (ANC) in the pancreatic and peripancreatic area (white
arrows pointing at the borders of the ANC) with presence of gas bubbles
(white arrowheads), usually a pathognomonic sign of infection of the necrosis
(infected necrosis).

 Therapy begins with the initiation of broad spectrum
antibiotics that penetrate the necrotic tissue
 Efforts are made to delay any invasive intervention for at
least 4 weeks
 Delayed intervention is possible in mostly stable pts
 In patients whose condition is not stable, the initial
placement of a percutaneous drain in the collection is
often enough to reduce sepsis and allow the 4-week delay
to be continued

 Nearly 60% of patients with necrotizing pancreatitis can be
treated noninvasively and will have a low risk of death
van Santvoort HC, Bakker OJ,
Bollen TL, et al. Gastroenterology2011; 141: 1254-63
 A step-up approach with a delay in definitive treatment is
now standard of therapy
 Step-up approach consists of antibiotic administration,
percutaneous drainage as needed, and after a delay of
several weeks, minimally invasive debridement, if required
 This approach is superior to traditional open necrosectomy
with respect to the risk of major complications or death

van Santvoort HC, Besselink MG, Bakker OJ, et al. N Engl J Med 2010; 362:
1491-502

 Randomized controlled trial comparing direct endoscopic
necresectomy (DEN) vs surgical necresectomy
 DEN reduced the postprocedural IL-6 levels compared with
surgical necrosectomy (P = .004)
 Endoscopic necrosectomy did not cause new-onset multiple
organ failure (0% vs 50%)
 Reduced number of pancreatic fistulas in DEN (10% vs 70%)
 Conclusion : endoscopic necrosectomy reduced the
proinflammatory response as well as the composite clinical
end point
Endoscopic transgastric vs surgical necrosectomy JAMA. 2012
Mar 14;307(10):1053-61 (PENGUIN trial )

 Clinical resolution after DEN was 92% versus 25% after initial PCD
(P = 0.003)
 75% of step-up patients required surgical intervention
 One DEN patient proceeded to PCD after 26 weeks (because of a
persistent collection that was endoscopically not accessible)
 9 of 12 patients in the step-up approach group proceeded to
minimally invasive surgical necrosectomy
 Seven of the 9 patients undergoing surgical necrosectomy
experienced a total of 8 complications
Direct Endoscopic Necrosectomy Versus Step-Up Approach for
Walled-Off Pancreatic Necrosis Nitin Kumar, Darwin L. Conwell,
and Christopher C. Thompson Pancreas. 2014 Nov; 43(8): 1334–1339.

 Retrospective, comparative study.
 25 underwent direct endoscopic necrosectomy, and 20
underwent standard endoscopic drainage
 Successful resolution - 88% in DEN vs 45% who received
standard drainage (P < .01)
 The maximum size of tract dilation was larger in the direct
endoscopic necrosectomy group (17 mm vs 14 mm, P < .02)
 Fewer postprocedural LOH stay and a decrease in the rate of
cavity recurrence in DEN
DEN Vs transmural endoscopic drainage for the treatment of
walled-off pancreatic necrosis Gardner TB Gastrointest Endosc. 2009
May;69(6):1085-94

 EUS facilitates the creation of multiple internal conduits
for better drainage of necrotic debris in patients with
WOPN- Multiple transluminal gateway technique (MTGT)
 In a study of 60 patients with WOPN, the treatment was
successful in 91.7% of pts treated with multiple internal
conduits compared with only 52.1% in patients treated by
using standard transluminal drainage
Varadarajulu S, Phadnis MA, Christein JD, Wilcox CM
Gastrointest Endosc. 2011 Jul; 74(1):74-80

Long-Term Consequences
of Acute Pancreatitis
 Pancreatic exocrine and endocrine dysfunction develops in
approximately 20 to 30% of patients
 Chronic pancreatitis develops in one third to one half of
those patients
 Risk factors for the transition to recurrent attacks and
chronic pancreatitis
The severity of the initial attack
The degree of pancreatic necrosis
Long-term, heavy alcohol
Smoking

Prevention of Relapse
 da Costa DW et al. Lancet 2015; 386: 1261-8
 Multicentre, RCT in patients recovering from mild
gallstone pancreatitis
 Randomly to cholecystectomy within 3 days of
randomisation (same-admission cholecystectomy.
N=129) orcholecystectomy 25-30 days after
randomisation (interval cholecystectomy. N=137)
 Primary end point : composite of readmission for
recurrent gallstone-related complications (pancreatitis,
cholangitis, cholecystitis, choledocholithiasis needing
endoscopic intervention, or gallstone colic) or mortality
within 6 months after randomisation
 The primary endpoint occurred in 23 (17%) in interval
group and in six (5%) in the same-admission group

 Cholecystectomy performed during the initial
hospitalization for mild pancreatitis due to gallstones
reduces the rate of subsequent gallstone-related
complications by 75%, as compared with cholecystectomy
performed 25 to 30 days after discharge
 Endoscopic biliary sphincterotomy will reduce the risk of
recurrent biliary pancreatitis but may not reduce the other
risk of gall stone
 For patients with severe or necrotizing pancreatitis,
cholecystectomy may be delayed

 Continued alcohol drinking is a/w recurrent pancreatitis
& chronic pancreatitis
 Smoking cessation are effective prevention
 In drug induced pancreatitis, in absence of any alternative
causes, withdrawal of an implicating medication may
prevent relapse
 Serum TG levels will fall in the absence of oral intake
 Repeated measurements of TG levels after discharge can
be informative.

 Primary prevention of pancreatitis is possible only in
the case of pancreatitis caused by ERCP
 Two therapies are
 Temporary placement of pancreatic duct stents
Mazaki T, Mado K, Masuda H, Shiono M J
Gastroenterol. 2014 Feb;49(2):343-55. doi: 10.1007/s00535-013-0806-
1. Epub 2013 Apr 24.
 Pharmacologic prophylaxis with nonsteroidal
antiinflammatory drugs
Elmunzer BJ, Scheiman JM, Lehman GA,
et al. A randomized trial of rectal indomethacin to prevent post-ERCP
pancreatitis. N Engl J Med 2012; 366: 1414-22

Conclusion
 New approaches to fluid resuscitation, antibiotic use,
nutritional support, and treatment of necrosis have
changed management but have not yet been widely
adopted
 The accurate description of local complications, the time
course of progression, and the presence or absence of
infection, will improve the stratification of patients
 The management of acute pancreatitis should continue to
improve, as new consensus definitions help to guide
clinical research

References
 N Engl J Med 2016;375:1972-81. DOI: 10.1056/NEJMra1505202
 Am J Gastroenterol. 2012 Feb;107(2):311-7. doi:
10.1038/ajg.2011.424. Epub 2011 Dec 13
 World J Gastrointest Pathophysiol 2016 February 15; 7(1): 48-58
 Trivedi CD J Clin Gastroenterol.2005 Sep;39(8):709-16
 Pancreatology.2016 Jan-Feb;16(1):10-3. doi:
10.1016/j.pan.2015.11.009. Epub 2015 Dec 1.
 Classification of acute pancreatitis—2012: revision of the Atlanta
classification and definitions by international consensus
 Ann Surg. 2012 Dec;256(6):875-80. doi:
10.1097/SLA.0b013e318256f778
 Lankisch PG, Pflichthofer D, Lehnick D Pancreas.3:319322 2000
 Wu BU Gastroenterology.2009 Jul;137(1):129-35. doi:
10.1053/j.gastro.2009.03.056
 Wu BU, Hwang JQ, Gardner TH, et al. Clin Gastroenterol Hepatol 2011;
9(8): 710-717.e1

 Eckerwall GE Clin Nutr. 2007 Dec;26(6):758-63. Epub 2007 Aug 24.
 Chang YS, Fu HQ, Xiao YM, Liu JC.Nasogastric or nasojejunal feeding in
predicted severe acute pancreatitis: a metaanalysis. Crit Care 2013; 17:
R118
 Am J Gastroenterol advance online publication, 30 July 2013; doi:
10.1038/ajg.2013.218
 ESPEN Guidelines on Enteral Nutrition: Pancreas
 Mazaki T, Mado K, Masuda H, Shiono M J Gastroenterol. 2014
Feb;49(2):343-55. doi: 10.1007/s00535-013-0806-1. Epub 2013 Apr 24.
 Elmunzer BJ, Scheiman JM, Lehman GA, et al. A randomized trial of
rectal indomethacin to prevent post-ERCP pancreatitis. N Engl J Med
2012; 366: 1414-22
 da Costa DW et al. Lancet 2015; 386: 1261-8
 van Santvoort HC, Besselink MG, Bakker OJ, et al. N Engl J Med 2010;
362: 1491-502

 Gardner TB Gastrointest Endosc. 2009 May;69(6):1085-94
 JAMA. 2012 Mar 14;307(10):1053-61
 Nitin Kumar, Darwin L. Conwell, and Christopher C. Thompson
Pancreas. 2014 Nov; 43(8): 1334–1339
 Lankisch PG, Pflichthofer D, Lehnick D Pancreas.3:319322 2000
 Moraes JMJ Clin Gastroenterol.2010 Aug;44(7):517-22

Acute pancreatitis

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