This document provides information on acute pancreatitis including: - Etiology is often gallstones or alcohol use. Other causes include drugs, genetics, obesity, and diabetes. - Diagnosis requires abdominal pain consistent with pancreatitis plus serum lipase or amylase 3x upper limit and findings on imaging. CT scan is useful for assessing severity. - Treatment involves aggressive IV fluids, monitoring for complications, enteral nutrition, and antibiotics only if infection is present. Severe cases may require endoscopic or minimally invasive drainage of pancreatic fluid and necrosis. - Complications include pancreatic pseudocysts, abscesses, and sterile or infected pancreatic necrosis. Severity is classified based on organ failure

1. Acute Pancreatitis
Kurdistan Board GEH/GIT Surgery J Club 2016
Supervised by:
Professor Mohamed Alshekhani

2. Anatomy

3. Introduction:
• The incidence is increasing
• One of the most common reasons for hospitalization
with a GI condition.
• 80% have mild, self-limited disease &discharged
with several days.
• Mortality has decreased over time&the overall
mortality is 2%.
• Death is more likely in certain subgroups ; elderly,
those with more numerous &more severe coexisting
conditions (obesity), hospitalacquired infections,
severe episodes of acute pancreatitis (persistent
failure of one or more organ systems or infected
pancreatic necrosis).

4. Etiology

7. Gallstone pancreatitis:
• Most common cause.
• Migrating gallstones cause transient obstruction of
the pancreatic duct, a mechanism shared by other
recognized causes (e.g., ERCP).
• SOD contributed to post-cholecystectomy biliary pain,
but no convincing data that either pancreatic SOD or
pancreas divisum plays a role in acute pancreatitis.

8. Alcoholic pancreatitis
• Common in pt. alcohol drinking > 2yr.
• Often much longer upto 10 yr.
• Sphincter spasm
• Decrease pancreatic blood flow

9. Alcoholic pancreatitis
• The second most common cause.
• Prolonged alcohol use (four to five drinks daily >5
years) is required for alcohol-associated pancreatitis;
• The overall lifetime risk of pancreatitis among heavy
drinkers is 2 - 5%.
• In most cases, chronic pancreatitis has already
developed&the acute clinical presentation represents a
flare.
• The risk is higher for men than for women.
• The mechanisms include both direct toxicity &
immunologic mechanisms.
• Binge drinking in the absence of long-term, heavy
alcohol use does not appear to precipitate AP.

12. AGA Institute

13. Drugs:
• Cause <5% of all cases.
• The drugs most strongly associated are azathioprine,
6-mercaptopurine, didanosine, valproic acid, ACEIs,
mesalamine.
• Usually mild.
• GLP Not linked.

14. Genetics:
• Genes are associated with acute (and chronic)
pancreatitis, including mutations in the genes
encoding cationic trypsinogen (PRSS1 ), serine
protease inhibitor Kazal type 1 (SPINK1 ), cystic
fibrosis transmembrane conductance regulator
(CFTR ), chymotrypsin C, calcium-sensing receptor&
claudin-2.
• These mutations may serve as cofactors, interacting
with other causes as claudin-2 mutations work
synergistically with alcohol.

15. Obesity/DM:
• Morbid obesity is a risk factor for acute
pancreatitis2&severe acute pancreatitis.
• Type 2 diabetes increases the risk of acute
pancreatitis by a factor of 2 or 3.
• Both obesity & diabetes are also risk factors for
chronic pancreatitis & pancreatic cancer.

16. Diagnosis

17. Diagnosis:
• At least two of the following three :
• Abdominal pain consistent with acute pancreatitis,
• serum lipase or amylase at least 3 times the upper
limit of the normal
• Findings of on cross-sectional imaging ( CT or MRI).

18. Diagnosis:
• Cross-sectional imaging role:
• Confirming an initial diagnostic impression.
• Assessing patients for mimics.
• Evaluating patients with atypical symptoms or small
elevations in serum pancreatic enzyme levels.

19. Classifications:
• Classifications of moderately severe pancreatitis &
severe pancreatitis are defined by the presence of
complications that are systemic, local, or both.
• Systemic complications include failure of an organ
system (respiratory, cardiovascular, or renal) &
exacerbation of a preexisting disorder (e.g.,COPD, HF,
or CLD).
• Local complications comprise peripancreatic fluid
collections or pseudocysts &pancreatic or
peripancreatic necrosis, sterile or infected.
• Persistent organ failure(i.e.>48 hs) is the prime
determinant of a poor outcome with mortality 30%.
• Both persistent organ failure & infected pancreatic
necrosis is associated with the highest mortality.

20. Predicting severity:
• Clinical factors increasing the risk of complications or
death include:
• Advanced age (≥60 years),
• Numerous / severe coexisting conditions (obesity
BMI>30 &long-term, heavy alcohol use.
• Hemoconcentration&azotemia
• Markers of inflammation (e.g., elevated CRP
interleukins 6, 8, 10).
• The most useful predictors are elevated BUN
&creatinine &elevated hematocrit, particularly if they
do not return to the normal with fluid resuscitation.
The degree of elevation of the serum amylase or lipase
level has no prognostic value.

21. Scoring systems:
• All have a high false positive rate (i.e., in many
patients with high scores, severe pancreatitis does not
develop.
• The presence of SIRS is usually obvious.
• SIRS can be diagnosed on the basis of four routine
clinical measurements, with findings of two or more of
the following values:
• Temperature, <36C or >38 C
• Pulse>90 /minute
• RR>20 /minute (or Pa CO2, <32 mm Hg).
• WBC<4000 or > 12,000.
• SIRS that persists for 48 hours or more after the onset
of symptoms is indicative of a poor prognosis.

22. Scoring systems:
• Recent guidelines uses demographic/clinical factors at
admission (advanced age, BMI,coexisting conditions),
• Simple labvalues at admission&during the next 24 to
48 hours (hematocrit,>44%; BUN, >20 or creatinine
>1.8 &* the presence of SIRS to identify patients who
are at greatest risk for severe disease & most likely to
benefit from a high-intensity nursing unit.
• During the first 48 to 72 hours, a rising hematocrit or
blood urea nitrogen or creatinine level, persistent
SIRS after adequate fluid resuscitation, or the
presence of pancreatic or peripancreatic necrosis on
cross-sectional imaging constitutes evidence of
evolving severe pancreatitis

23. Physical exam
•Grey Turner’s Sign
- ecchymosis in 1 or both flanks
•Cullen’s sign
- ecchymosis in periumbilical area
•Associated with Necrotizing pancreatitis
• poor prognosis occurs in 1% of cases

24. Grey Turner’s Sign

25. Cullen’s Sign

26. Serum markers

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

28. Urine amylase
• urinary levels may be more sensitive
than serum levels.
• Urinary amylase levels usually remain
elevated for several days after serum
levels have returned to normal.

29. 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%

30. Slide 189

31. Plain Abdominal Radiograph

32. 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

33. Sentinel Loop
•
- localized ileus from nearby inflammation

34. Colon cutoff sign

35. Radiologic Findings
• Plain radiographs contribute little
• Ultrasound may 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

36. Assessment of severity

37. Classification of severity
- Mild : lack of organ failure and
complications
- Moderate : transient organ failure
and/or complications < 48hr
- Severe : persistent organ failure and
complications
Reference : 2012 revision of atlanta classification of acute pancreatits

38. Complication

39. Early prognostic sign
• Ranson’s score
• APACHE II

41. Ranson’s Criteria (GB Pancreatitis)
• At Admission
Age > 70 yr
WBC > 18,000/mm3
Blood glucose > 220 mg/dL
Serum lactate dehydrogenase > 400IU/L
Serum aspartate aminotransferase >250IU/L
• During Initial 48 hr
Hematocrit decrease of > 10%
BUN increase of >2 mg/dL
Serum calcium <8mg/dL
Arterial pO2 NA
Serum base deficit > 5 mEq/Lio
Fluid sequestration > 4L

42. APACHE II
• Measure at during the first 24 hours
after admission
• Using a cutoff of ≥8
• The American Gastroenterological
Association (AGA) recommends:
Prediction of severe disease by the
APACHE II system

43. APACHE II

44. Biochemical marker
• CRP at 48hr
– cutoff 150mg/L
– Sens. 80%
– Spec. 76%
• TAP
• Interleukins
• ???

45. CT severity score
Grading based upon findings on unenhanced CT
Grade Findings Score
A Normal pancreas –without peripancreatic enhancement 0
B Focal or diffuse enlargement of the pancreas,
enhancement may be inhomogeneous on peripancreatic
1
C Peripancreatic inflammation with intrinsic pancreatic
abnormalities
2
D Intrapancreatic or extrapancreatic fluid collections 3
E Two or more large collections of gas in the pancreas or
retroperitoneum
4
Necrosis score based upon contrast enhanced CT
Necrosis, percent Score
0 0
<33 2
33-50 4
≥50 6
≥6 = severe disease.

46. Treatment

49. Treatment
• The essential requirements:
• Accurate diagnosis
• Appropriate triage
• High-quality supportive care,
• Monitoring for & treatment of
complications
• Prevention of relapse

50. Fluids:
• Aggressive fluid administration during first 24 hs
reduces morbidity & mortality.
• Guidelines provide directions for early& vigorous
fluid administration.
• Most important during the first 12 - 24 hours after the
onset of symptoms &of little value after 24 hours.
• A balanced crystalloid solution at a rate of 200-500
ml / hour, or 5 -10 ml / Kgm; 2500 - 4000 ml within the
first 24 hours.
• Ringer’s lactate reduces inflammatory markers.
• Clinical cardiopulmonary monitoring for fluid status,
hourly measurement of urine output&BUN/PCV are
practical ways to gauge the adequacy of fluid therapy.

51. Fluids:
• Excessive fluid administration results in increased
risks of the abdominal compartment syndrome, sepsis,
need for intubation, & death.

52. Feeding:
• Most patients with mild acute pancreatitis can be
started on a low-fat diet soon after admission, in the
absence of severe pain, nausea, vomiting&ileus
unusual in mild case.
• Total parenteral nutrition is now known to be more
expensive, riskier&no more effective than enteral
nutrition.
• Nasogastric or nasoduodenal feeding is clinically
equivalent
• Total parenteral nutrition should be reserved for the
rare cases in which enteral nutrition is not tolerated or
nutritional goals are not met.

53. Antibiotics:
• No benefit of prophylactic antibiotics.
• Prophylaxis with antibiotic therapy is not
recommended for any type of acute pancreatitis unless
infection is suspected or has been confirmed.

54. Endoscopic therapy:
• ERCP is used primarily in patients with gallstone
pancreatitis &indicated in those who have evidence of
cholangitis superimposed on gallstone pancreatitis.
• Also a reasonable treatment in patients with
documented choledocholithiasis on imaging or
findings strongly suggestive of a persistent bile duct
stone (e.g., jaundice, a progressive rise in the results of
liver biochemical studies, or a persistently dilated bile
duct).

55. Pancreatic fluid & necrosis:
• EUS is used as a platform for minimally invasive
treatment of a pancreatic pseudocyst or walled-off
pancreatic necrosis.
• Acute peripancreatic fluid collections do not require
therapy.
• Symptomatic pseudocysts are managed primarily with
the use of endoscopic techniques, depending on local
expertise.
• Necrotizing pancreatitis includes pan necrosis&
peripancreatic fat necrosis.
• Over 4 wks or longer, becomes more liquid & becomes
encapsulated by visible wall(WOPN)
• Sterile necrosis not require therapy except in rare case
of collection that obstructs a nearby viscus.

56. Pancreatic fluid & necrosis:
• The development of fever, leukocytosis, increasing
abdominal pain suggests infection of the necrotic
tissue.
• A CT scan may reveal evidence of air bubbles in the
necrotic cavity.
• Therapy begins with the initiation of broadspectrum
antibiotics that penetrate the necrotic tissue.
• Aspiration / culture of the collection are not required.
• In current practice, efforts are made to delay any
invasive intervention for at least 4 week.
• Nearly 60% of patients can be treated noninvasively
and will have a low risk of death.

57. Pancreatic fluid & necrosis:
• The step-up approach consists of antibiotic
administration, percutaneous drainage as needed&
after a delay of several weeks, minimally invasive
debridement, if required.
• A number of minimally invasive techniques (e.g.,
percutaneous, endoscopic,
laparoscopic,retroperitoneal approaches) are
available to debride infected necrotic tissue in patients
with WOPN.
• Ssmall proportion of patients with infected necrosis
can be treated with antibiotics alone.

58. Treatment
• General Considerations
- adequate IV hydration and analgesia
- NPO
- NG tube: not routinely used
* But may be used in patients with ileus or intractable N/V
• Nutrition
• Early enteral feeding
• Nasojejunal tube feeding
• PPN,TPN

59. Treatment
• Metabolic Complications
- Correction of electrolyte imbalance - Ca,Mg
- Cautiously for hyperglycemia
• Cardiovascular Care
• Respiratory Care
• Deep vein thrombosis prophylaxis

60. Prophylactic antibiotics
–Although this is still an area of debate
–Not indicated for mild attack
–suggest imipenem or meropenem
for 14 days for patients with proven
necrosis

61. TREATMENT OF
ASSOCIATED CONDITIONS
• Gallstone pancreatitis
– ERCP should be performed within 72
hours in those with a high suspicion of
persistent bile duct stones
– EUS & MRCP should be considered in case
that clinical is not improving sufficiently
– Cholecystectomy +/- IOC

62. Complication

63. Local Complications
• Pseudocyst
• Abscess
• Necrosis
–Sterile
–Infected
Mild pancreatitis severe pancreatitis
Pseudocyst abscess
Pancreatic necrosis

64. New Classification Based on
Contrast-Enhanced CT (CECT)*
• Interstitial Edematous Pancreatitis
–Acute Peripancreatic Fluid Collection
–Pancreatic Pseudocyst
• Necrotizing Pancreatitis
–Acute Necrotic Collection
–Walled-Off Necrosis

65. Interstitial Edematous VS Necrotizing
• Interstitial Edematous Pancreatitis
– Pancreatic parenchyma enhances with the
contrast agent
– Lack of peripancreatic necrosis
• Necrotizing Pancreatitis
– Pancreatic parenchymal areas without IV
contrast enhancement +/- Peripancreatic
necrosis (see below—ANC and WON)

66. Interstitial Edematous VS Necrotizing

67. Acute Peripancreatic Fluid
Collection (APFC):
Occurring within the first 4 weeks in the
setting of interstitial edematous pancreatitis.
• CECT Criteria
–Homogeneous fluid adjacent to pancreas
confined by peripancreatic fascial planes
–No recognizable wall

68. Pancreatic Pseudocyst
• An encapsulated, well-defined collection of
fluid but no or minimal solid components
• Occurs >4 weeks after onset of in interstitial
edematous pancreatitis
• CECT Criteria
– Well-defined wall , homogeneous, round
or oval fluid collection
– No solid component
– Only in interstitial edematous pancreatitis

69. APFC vs Pseudocyst

70. Acute Necrotic Collection(ANC)
• A collection of both fluid and solid
components (necrosis) occurring during
necrotizing pancreatitis.
• This collection can involve the pancreatic
and/or the peripancreatic tissues
• CECT Criteria
– Heterogeneous
– No encapsulating wall
– Intrapancreatic and/or extrapancreatic

71. Walled-Off Necrosis(WON)
• A mature, encapsulated ANC with a well-
defined inflammatory wall
• these tend to mature >4 weeks after onset of
necrotizing pancreatitis.
• CECT Criteria
– Heterogenous
– Well-defined wall
– Intrapancreatic and/or extrapancreatic

72. ANC vs WON

73. Infected pancreatic necrosis.
• The most common organisms include E.coli,
Pseudomonas, Klebsiella, and Enterococcus

74. Guideline management of
severe pancreatitis

75. AGA Guideline

76. Surgical debridement

77. Management of pseudocyst

78. Management of pseudocyst
• Watchful waiting:
- Operative intervention was recommended
following an observation period of 6 wks
- However, there are some reports support
more conservative approach

79. Management of pseudocyst
• Surgical drainage – gold standard
Open vs endoscopic
–cystgastrostomy
–Cystenterostomy
–Cystojejunostomy, Cystoduodenostomy
–Ressection

80. Management of pseudocyst
• Percutaneous catheter drainage
– As effective as surgery in draining and closing both
sterile and infected pseudocysts
– Catheter drainage is continued until the flow rate
falls to 5-10 mL/day
– If no reduction in flow, octreotide
(50 -200 µg SC q 8hr) may be helpful.
– Should follow-up CT scan when the flow rate is
reduced to ensure that the catheter is still in the
pseudocyst cavity
– more likely to be successful in patients
without duct-cyst communication

81. Management of local
complication of pancreatitis

82. Indication for
pancreatic debridement
• Infected pancreatic necrosis
• Symptomatic sterile pancreatic necrosis
• chronic low grade fever
• Nausea
• Lethargy
• Inability to eat
• * Fail medical treatment

83. Timing of debridement
• The optimal timing is at least 3-4wks
following the onset of acute pancreatitis.
• Delayed debridement allows
– clinical stabilization of the patient
– resolution of early organ failure
– decreased inflammatory reaction, and
necrotic areas are demarcated

84. Surgical approach
• Open debridement with external drainage
– gold standard
• Open debridement with internal drainage and
cystgastrostomy
- only appropriate for patients with WON
• Open packing
— Open packing with planned reoperation every
48-72 hrs until the necrosis is adequately removed
• Laparoscopic debridement
-Video-assisted retroperitoneal debridement
-Laparoscopically-assisted transperitoneal
debridement

85. Long-term complications:
• Pancreatic exocrine/endocrine dysfunction develops
in 20- 30% &clear-cut chronic pancreatitis develops in
one third to one half of those patients.
• Risk factors include:
• The severity of the initial attack
• The degree of pancreatic necrosis.
• The cause of acute pancreatitis,Sp long-term, heavy
alcohol use as the cause & smoking as a cofactor
dramatically increase the risk.

86. Prevention of relapse:
• Cholecystectomy prevents recurrent gallstone
pancreatitis.
• A delay of cholecystectomy for >few weeks places the
patient at a high (up to 30%) risk for relapse.
• Cholecystectomy during the initial hospitalization for
mild pancreatitis due to gallstones reduces the rate of
subsequent gallstone-related complications by almost
75%
• In severe or necrotizing pancreatitis endoscopic
surgery can be delayed &biliary sphincterotomy will
reduce (but not eliminate) the risk of recurrent biliary
pancreatitis but may not reduce the risk of subsequent
acute cholecystitis &biliary colic..

87. Prevention of relapse:
• Alcohol & smoking quitting.
• Withdrawing an implicated medication may prevent
relapse.
• Tight control of hyperlipidemia can prevent a relapse.
• Serum triglyceride levels will fall in the absence of oral
intake of food & fluids,so repeated measurements
after dischargecan be informative.
• For PERCPP temporary placement of pancreatic duct
stents& pharmacologic prophylaxis with NSAIDs.
• ERCP should be avoided in patients who are not likely
to benefit from it (e.g., those with suspected SODD)

88. Conclusion:
• Acute pancreatitis is an increasingly common clinical
problem.
• New approaches to fluid resuscitation,antibiotic use,
nutritional support, treatment of necrosis have
changed management but have not yet been widely
adopted.
• More effective prevention of post-ERCP pancreatitis is
possible, & gallstone pancreatitis can be prevented
with timely cholecystectomy.