This document provides tips for using a PowerPoint presentation on acute pancreatitis. It recommends: 1. Freely editing and modifying the slides to add your own name. 2. Not worrying about the number of slides, as many are blank except for the title to facilitate active learning sessions. 3. Showing blank slides first to elicit what students already know, then showing the content slide. 4. Repeating this process of blank slide then content slide at the end for review. 5. This format allows for active learning through three revisions of content.

1. Tips on using my ppt.
1. You can freely download, edit, modify and put your
name etc.
2. Don’t be concerned about number of slides. Half the
slides are blanks except for the title.
3. First show the blank slides (eg. Aetiology ) > Ask
students what they already know about ethology of
today's topic. > Then show next slide which enumerates
aetiologies.
4. At the end rerun the show – show blank> ask questions >
show next slide.
5. This will be an ACTIVE LEARNING SESSION x
three revisions.
6. Good for self study also.
7. See notes for bibliography.

2. Learning Objectives

3. Learning Objectives
1. Introduction & History
2. Relevant Anatomy, Physiology
3. Aetiology
4. Pathophysiology
5. Pathology
6. Classification
7. Clinical Features
8. Investigations
9. Management
10. Prevention
11. Guidelines
12. Take home messages

4. Acute Pancreatitis
Definition

5. Acute Pancreatitis
Definition
• Auto digestion of pancreas.
• Usually painful and self-limited
• Isolated event or a recurring illness
• Pancreas returns to normal after (or
between) attacks

6. Relevant Anatomy
•

7. Relevant Anatomy and
Physiology
• neutralize chyme
• digestive enzymes
• hormones

8. Relevant Physiology
•

9. Exocrine Function
pancreatic duct
common bile
duct
ampulla
pancreatic enzymes
TAIL
BODY
HEAD
UNCINATE

10. Aetiology

11. Aetiology
• Idiopathic
• Congenital/ Genetic
• Nutritional Deficiency/excess
• Traumatic
• Infections /Infestation
• Autoimmune
• Neoplastic (Benign/Malignant)
• Degenerative
• Iatrogenic
• Psychosomatic
• Poisoing/ Toxins/ Drug induced..

12. Aetiology
• Biliary tract disease
• Alcohol
• Endoscopic retrograde cholangiopancreatography
• Trauma
• Drugs
• Infection
• Hereditary pancreatitis
• Hypercalcemia
• Developmental abnormalities of pancreas
• Hypertriglyceridemia
• Tumors
• Toxins
• Surgical procedures
• Vascular abnormalities
• Autoimmune pancreatitis

13. EtOH
35%
Idiopathic
10%
Other
10%
Gallstones
45%
Acute Pancreatitis
Etiology

14. • Cholelithiasis
• Ethanol abuse
• Idiopathic
• Medications
• Hyperlipidemia
• ERCP
• Trauma
• Pancreas divisum
• Hereditary
• Hypercalcemia
• Viral infections
– Mumps
– Coxsackievirus
• End-stage renal failure
• Penetrating peptic
ulcer
Acute Pancreatitis
Associated Conditions

15. Pathophysiology

16. Acute Pancreatitis: Pathophysiology
• Localized destruction in the pancreas and
systemic inflammatory response.
• The inciting event is the premature
activation of trypsinogen to trypsin within
the acinar cell as opposed to in the duct
lumen.
• It is postulated that this can be caused by
elevated ductal pressures (such as in duct
obstruction) as well as problems with
calcium homeostasis and pH.

17. Acute Pancreatitis: Pathophysiology
• Early activation of these zymogens leads to
localized tissue damage and release of
Damage Associated Molecular Patterns
(DAMPs)
• Lead to increase capillary permeability and
damage of endothelium with microvascular
thrombosis that causes multiorgan
dysfunction syndrome (MODS), the main
cause of morbidity and mortality in acute
pancreatitis.

18. • STAGE 1: Pancreatic Injury
– Edema
– Inflammation
• STAGE 2: Local Effects
– Retroperitoneal edema
– Ileus
• STAGE 3: Systemic
Complications
– Hypotension/shock
– Metabolic disturbances
– Sepsis/organ failure
SEVERITY
Mild
Severe
Acute Pancreatitis
Pathogenesis

19. Protective Measures
• COMPARTMENTALIZATION - digestive
enzymes are contained within zymogen granules
in acinar cells
• REMOTE ACTIVATION - digestive enzymes
are secreted as inactive proenzymes within the
pancreas
• PROTEASE INHIBITORS – trypsin inhibitor is
secreted along with the proenzymes to suppress
any premature enzyme activation
• AUTO “SHUT-OFF” – trypsin destroys trypsin
in high concentrations

20. Clinical Features
•

21. Clinical Features
• Demography
• Symptoms
• History
• Signs
• Prognosis
• Complications

22. Demography

23. Demography
• Incidence & Prevalence
• Geographical distribution.
• Race
• Age
• Sex
• Socioeconomic status
• Temporal behaviour

24. Demography
• Incidence of acute pancreatitis ranges
between 5 and 80 per 100,000
• Age-related demographics
• Alcohol-related - 39 years
• Biliary tract–related - 69 years
• Trauma-related - 66 years
• Drug-induced etiology - 42 years
• ERCP-related - 58 years
• AIDS-related - 31 years
• Vasculitis-related - 36 years

25. Demography
• Generally, acute pancreatitis affects males
more often than females. In males,
– In males, the etiology is more often related to
alcohol
– in females, it is more often related to biliary
tract disease.
– Idiopathic pancreatitis has no clear predilection
for either sex.

26. Demography
• Race-related demographics
• 3 to 4 times higher for blacks than whites.

27. Demography
• Overall, the frequency of acute pancreatitis
has been noted to be rising in the United
States and the rest of the world.
• Whether this trend is related to a true
increase in incidence or simply increased
detection is difficult to determine.

28. Symptoms

29. Symptoms
• Abdominal pain
– Dull,
– Boring, and steady; usually sudden in onset
and gradually becoming more severe until
reaching a constant ache
– In the upper abdomen and may radiate directly
through to the back
– Discomfort frequently improves with the
patient sitting up and bending forward.
• Nausea and vomiting, sometimes with anorexia
• Diarrhea
• Fever

30. History
• Similar complaints
• Recent operative or other invasive
procedures
• Family history of hypertriglyceridemia
• Previous biliary colic and binge alcohol
consumption (major causes of acute
pancreatitis)

31. Signs

32. Signs
• Fever
• Tachycardia
• hypotension
• Abdominal tenderness, muscular guarding
distention diminished or absent bowel
sounds
• Jaundice
• Dyspnea tachypnea; basilar rales, especially
in the left lung

33. Signs
• In severe cases, hemodynamic instability
and hematemesis or melena
• Occasionally, extremity muscular spasms
secondary to hypocalcemia
Uncommon-
• Cullen sign
• Grey-Turner sign
• Erythematous skin nodules

34. Grey-Turner sign

35. Cullen sign

36. Prognosis

37. Prognosis
• The mortality in mild acute pancreatitis is
less than 1%
• The mortality in severe acute pancreatitis
is 10%-15%.
• Patients with biliary pancreatitis tend to
have a higher mortality than patients with
alcoholic pancreatitis.
• In patients with severe disease (organ
failure), who account for about 20% of
presentations, mortality is approximately
30%.

38. Complications

39. Compilcations
• Systemic
• Local

40. Systemic Compilcations
• Cardiovascular: hypotension,Arrhythmias
• Pulmonary: pleural effusions, ARDS
• Renal: acute tubular necrosis
• Hematologic: disseminated intravascular
coag.
• Metabolic: hypocalcemia,
hyperglycemia,Hyperlipidemia
• GI: ileus, hemorrhage
• Purtscher retinopathy causing temporary or
permanent blindness.

41. Local Compilcations
• Acute fluid collections
• Pancreatic necrosis
• Pseudocyst
• Ascites
• Portal/Splenic vein thrombosis
• Pseudoaneurysm
• Pancreatic abscess / Infected necrosis

42. Classification:Predictors of Severity
• Why are they needed?
– appropriate patient triage & therapy
– compare results of studies of the impact of
therapy
• When are they needed?
– optimally, within first 24 hours (damage control
must begin early)
• Which is best?

43. Severity Scoring Systems
• Ranson and Glasgow Criteria (1974)
– based on clinical & laboratory parameters
– scored in first 24-48 hours of admission
– poor positive predictors (better negative predictors)
• APACHE Scoring System
– can yield a score in first 24 hours
– APACHE II suffers from poor positive predictive
value
– APACHE III is better at mortality prediction at > 24
hours
• Computed Tomography Severity Index
– much better diagnostic and predictive tool
– optimally useful at 48-96 hours after symptom onset

44. CT Severity Index
appearance normal enlarged inflamed
1 fluid
collection
2 or more
collections
grade A B C D E
score 0 1 2 3 4
necrosis none < 33% 33-50% > 50%
score 0 2 4 6
score morbidity mortality
1-2 4% 0%
7-10 92% 17%
Balthazar et al. Radiology 1990.

45. Ranson Criteria
Alcoholic Pancreatitis
AT ADMISSION
1. Age > 55 years
2. WBC > 16,000
3. Glucose > 200
4. LDH > 350 IU/L
5. AST > 250 IU/L
WITHIN 48 HOURS
1. HCT drop > 10
2. BUN > 5
3. Arterial PO2 < 60 mm Hg
4. Base deficit > 4 mEq/L
5. Serum Ca < 8
6. Fluid sequestration > 6L
Number
Mortality
<2
1%
3-4
16%
5-6
40%
7-8
100%

46. Glasgow Criteria
Non-alcoholic Pancreatitis
1. WBC > 15,000
2. Glucose > 180
3. BUN > 16
4. Arterial PO2 < 60 mm Hg
5. Ca < 8
6. Albumin < 3.2
7. LDH > 600 U/L
8. AST or ALT > 200 U/L

47. Atlanta classification
• Acute pancreatitis is broadly classified as
either mild or severe

48. Atlanta classification
Severe Acute Pancreatitis
• Scoring systems
–  3 Ranson criteria
–  8 APACHE II points
–  5 CT points
• Organ failure
– Shock (SBP < 90 mmhg)
– Pulmonary edema / ARDS (pao2 < 60 mmhg)
– Renal failure (cr > 2.0 mg/dl)
• Local complications
– Fluid collections  pseudocysts
– Necrosis (mortality 15% if sterile, 30-35% if
infected)
– Abscess

49. Investigations
•

50. Investigations
• Laboratory Studies
– Routine
– Special
• Imaging Studies
• Tissue diagnosis
– Cytology
• FNAC
– Histology
• Diagnostic Laparotomy.

51. Diagnostic Studies
Imaging Studies
• X-Ray
• USG
• CT
• Angiography
• MRI
• Endoscopy
• Nuclear scan

52. Laboratory Studies

53. Laboratory Studies
• Serum amylase and lipase
• Liver-associated enzymes
• Blood urea nitrogen (BUN), creatinine, and electrolytes
• Blood glucose
• Serum cholesterol and triglyceride
• Complete blood count (CBC) and hematocrit; NLR
• C-reactive protein (CRP)
• Arterial blood gas values
• Serum lactic dehydrogenase (LDH) and bicarbonate
• Immunoglobulin G4 (IgG4): elevated in autoimmune
pancreatitis

54. Imaging Studies

55. Imaging Studies
• Diagnostic imaging is unnecessary in most
cases
• When the diagnosis is in doubt,
• When pancreatitis is severe,
• When a given study might provide specific
information required

56. Imaging Studies
• Xray- To exclude du perforation, Pleural
effusion
• USG- To detedct Gall Stones
• CECT- In Severe cases.
• MRI- MRCP
• Endoscopy ERCP, EUS
• CT-guided or EUS-guided aspiration and
drainage
• Genetic testing

57. Acute Pancreatitis
Differential Diagnosis
• Choledocholithiasis
• Perforated ulcer
• Mesenteric ischemia
• Intestinal obstruction
• Ectopic pregnancy
• Peptic ulcer disease
• Cholangitis
• Cholecystitis
• Bowel perforation
•
•
• Mesenteric ischemia
• Acute hepatitis
• Diabetic ketoacidosis
• Basilar pneumonia
• Myocardial infarction
• Renal colic
• Aortic dissection

58. Differential Diagnosis

59. • Symptoms
– Abdominal pain
• Laboratory
– Elevated amylase or lipase
• > 3x upper limits of normal
• Radiology
– Abnormal sonogram or CT
Acute Pancreatitis
Diagnosis

60. Causes of Increased
Serum Pancreatic Enzymes
Amylase Lipase
Pancreatitis ↑ ↑
Parotitis ↑ Normal
Biliary stone ↑ ↑
Intestinal injury ↑ ↑
Tubo-ovarian
disease ↑ Normal
Renal failure ↑ ↑
Macroamylasemia ↑ Normal

61. Management

62. Management
• Analgesics
• Fluid resuscitation
• Nutritional support

63. Non Operative Therapy

64. Goals of Treatment
• Limit systemic injury
– support and resuscitation – effective
– decrease pancreatic secretion – ineffective / harmful?
– inhibit inflammatory mediators – ineffective
– inhibit circulating trypsin – ineffective (too late)
– removing gallstones – mostly ineffective
• Prevent necrosis – how?
• Prevent infection
– antibiotics (imipenem and ciprofloxacin) – probably
effective in necrotic pancreatitis
– prevent colonic bacterial translocation
– removing gallstones – variably effective
• Identify and treat complications

65. Treatment of Mild Pancreatitis
• Pancreatic rest
• Supportive care
– fluid resuscitation – watch BP and urine output
– pain control
– NG tubes and H2 blockers or PPIs are usually not
helpful
• Refeeding (usually 3 to 7 days)
– bowel sounds present
– patient is hungry
– nearly pain-free (off IV narcotics)
– amylase & lipase not very useful here

66. Treatment of Severe Pancreatitis
• Pancreatic rest & supportive care
– Fluid resuscitation* – may require 5-10 liters/day
– Careful pulmonary & renal monitoring – ICU
– Maintain hematocrit of 26-30%
– Pain control – PCA pump
– Correct electrolyte derangements (K+, ca++, mg++)
• Rule-out necrosis
– CECT in 2nd week.
– Prophylactic antibiotics if present
– Surgical debridement if infected
• Nutritional support
– May be NPO for weeks
– TPN vs. Enteral support (ten)nasojujunal feeding.

67. Role of ERCP
• Gallstone pancreatitis
– Cholangitis
– Obstructive jaundice
• Recurrent acute pancreatitis
– Structural abnormalities
– Neoplasm
– Bile sampling for microlithiasis
• Sphincterotomy in patients not suitable for
cholecystectomy

68. Enteral Nutrition in Severe
Pancreatitis
• May start as early as possible
– When emesis has resolved
– Ileus is not present
• Nasojejunal route preferred over
nasoduodenal
• Likely decreases risk of infectious
complications by reducing
transmigration of colonic bacteria

69. Antibiotics
• Antibiotics (usually of the imipenem class)
should be used in any case of pancreatitis
complicated by infected pancreatic necrosis
but should not be given routinely for fever,
especially early in the presentation
• Antibiotic prophylaxis in severe pancreatitis
is controversial; routine use of antibiotics as
prophylaxis against infection in severe acute
pancreatitis is not currently recommended

70. Operative Therapy

71. Operative Therapy
• Gallstone pancreatitis: Cholecystectomy
• Pancreatic duct disruption: Image-guided
percutaneous placement of a drainage tube
into the fluid collection
• Stent or tube placement via ERCP
• In refractory cases, distal pancreatectomy or
a whipple procedure
• Pseudocysts:

72. Operative Therapy
• Pseudocysts:
– None necessary in most cases;
– For large or symptomatic pseudocysts,
• Percutaneous aspiration
• Endoscopic transpapillary or transmural techniques
• Surgical management
• Infected pancreatic necrosis: Image-guided
aspiration; necrosectomy
• Pancreatic abscess: Percutaneous catheter
drainage and antibiotics; if no response,
surgical debridement and drainage

73. Prevention

74. Prevention
• Screening
• Risk reduction

75. Prevention
• Avoid alcohol
• Avoid fatty meals
• Prevent Abd trauma.
• In gallstone pancreatitis, early
cholecystectomy is strongly recommended.
• In the setting of hypertriglyceridemia, the
goal of specific treatment is to bring down
and maintain triglyceride levels to less than
500 mg/dL.

76. Guidelines
•

77. Guidelines
• ACG Guidelines 2013, the American
College of Gastroenterology (ACG) issued
guidelines for the management of acute
pancreatitis
• AGA Guidelines 2018 AGA guidelines
(initial AP management)
• WSES Guidelines In June 2019, the World
Society of Emergency Surgery (WSES)
released updated guidelines for the
management of severe acute pancreatitis.

78. ConclusionsTake home messages
• Acute pancreatitis is a self-limited disease
in which most cases are mild.
• Gallstones and alcohol are the leading
causes of acute pancreatitis.
• Abdominal pain with S.Amylase S.Lipase
raised >3 times is diagnostic.
• CECT is usually not required. If needed do
in 2nd week.
• Treatment is Agressive fluid resuscitation,
analgesia and early enteral feeding.

79. ConclusionsTake home messages
• PPIs are not indicated.
• Antibiotics are not indicated.
• Octreotide is not indicated.

80. Webinar
• >Raised amylase lipase 3 times.
• Abd. Pain
• Atlanta Classification 2012
• Apache score
• Obsolete terms hemorrhagic pancreatitis,
• Amylase lipase has no severity correlation,
prognosis- no serial monitoring.
• CT no need if diagnosis is clear . Do it 2nd
week..

81. Webinar
• CT Eevaluatioon of complications, severity
• CT severity grades.
• Modified severity index.
• MRI if contrast allerrgy
• TT- no role of colloids. Give RL 20ml.kg
bolus 3ml/kg/hour watch ivc diameter/ cvp
• Respiratory support.
• Pain conntrol NSAIDs, Tramodol,
Narcotics
• Eearly enteral feeding nasojejunal tube

82. Webinar
• ERCP – cholangitis, bile duct obstruction
• Surgery
• Compartment syndrome >20mm of mercury
• No necrosectomy

83. Lessons From Criticon 2022
D Nageshwar Reddy on acute pancreatitis
in ICU-
• Cause of death Infected necrosis organ
failure SIRS
• Modified Marshall score
• Elderly
• Comorbidity obesity
• BUN is a good predictor of severity
• Aggressive fluid therapy RL/NS use USG
to monitor.

84. D Nageshwar Reddy
• Early enteral feeding prevents infection
• Low fat solid diet. Oral or tube.
• Avoidance of prophylactic antibiotics
• TARGET 0.5- 1 ML urine output
• MAP 65 TO 85
• No benefit of Rules tube
• No benefit of Foley catheter
• Early ERCP if cholangitis (raised SGOT,
SGPT.)
• Don't use PPIs.

85. Modified Marshall Organ Failure Score
•
Organ
system Score 0* Score 1 Score 2 Score 3 Score 4
Cardiovasc
ular
(systolic
blood
pressure)†
> 90 mm
Hg
< 90 mm
Hg (fluid
responsive)
< 90 mm
Hg (not
fluid
responsive)
< 90 mm
Hg (pH <
7.3)
< 90 mm
Hg (pH <
7.2)
Renal
(serum
creatinine)
‡
< 1.4
mg/dL (≤
134
micromol/L
)
1.4–1.8
mg/dL
(134–169
micromol/L
)
1.9–3.6
mg/dL
(170–310
micromol/L
)
3.6–4.9
mg/dL
(311–439
micromol/L
)
> 4.9
mg/dL (>
439
micromol/L
)
Respiratory
(PaO2/FiO
2)§
> 400 mm
Hg
301–400
mm Hg
201–300
mm Hg
101–200
mm Hg
≤ 101 mm
Hg

86. MCQs

87. MCQs
• Which of the following is the most
common cause of acute pancreatitis?
A.Alcoholism
B.Gallstones
C.Smoking
D.Viral infection

88. MCQs
• Which of the following is the most
common cause of acute pancreatitis?
A.Alcoholism
B.Gallstones
C.Smoking
D.Viral infection

89. MCQs
• Which of the following tests has a
sensitivity and specificity of > 90% for
acute pancreatitis?
A.Amylase:creatinine clearance ratio test
B.Serum amylase level
C.Serum lipase level
D.Urine trypsinogen-2 dipstick test

90. MCQs
• Which of the following tests has a
sensitivity and specificity of > 90% for
acute pancreatitis?
A.Amylase:creatinine clearance ratio test
B.Serum amylase level
C.Serum lipase level
D.Urine trypsinogen-2 dipstick test

91. MCQs
• Basic treatment of acute pancreatitis
includes early fluid resuscitation,
analgesia, and which of the following?
A.Antibiotics
B.Endoscopic retrograde
cholangiopancreatography (ERCP)
C.Enteral nutrition
D.Total parenteral nutrition

92. MCQs
• Basic treatment of acute pancreatitis
includes early fluid resuscitation,
analgesia, and which of the following?
A.Antibiotics
B.Endoscopic retrograde
cholangiopancreatography (ERCP)
C.Enteral nutrition
D.Total parenteral nutrition

93. MCQs
• Basic treatment of acute pancreatitis
includes early fluid resuscitation,
analgesia, and which of the following?
A.Antibiotics
B.Endoscopic retrograde
cholangiopancreatography (ERCP)
C.Enteral nutrition
D.Total parenteral nutrition

94. MCQs
• Which of the following physical findings
may indicate severe necrotizing
pancreatitis?
A. Jaundice
B. Erythematous skin nodules
C. Fever
D. Hypotension

95. MCQs
• Which of the following physical findings
may indicate severe necrotizing
pancreatitis?
A. Jaundice
B. Erythematous skin nodules
C. Fever
D. Hypotension

96. MCQs
• Which of these findings is the most
common in acute pancreatitis?
A. Distention
B. Jaundice
C. Dyspnea
D. Hematemesis

97. MCQs
• Which of these findings is the most
common in acute pancreatitis?
A. Distention
B. Jaundice
C. Dyspnea
D. Hematemesis

98. MCQs
• Which of the following is accurate about
the workup of patients with suspected acute
pancreatitis?
A. Aggressive hydration is rarely necessary
B. Contrast-enhanced CT scanning and/or MRI
should be performed in all cases
C. Routine use of prophylactic antibiotics is
indicated
D. Intervention in patients with infected necrosis
may be delayed through the use of antibiotics
that do not penetrate the necrotic tissue

99. MCQs
• Which of the following is accurate about
the workup of patients with suspected acute
pancreatitis?
A. Aggressive hydration is rarely necessary
B. Contrast-enhanced CT scanning and/or MRI
should be performed in all cases
C. Routine use of prophylactic antibiotics is
indicated
D. Intervention in patients with infected necrosis
may be delayed through the use of antibiotics
that do not penetrate the necrotic tissue

100. MCQs
• Which of the following should not be used
in the short term in patients suspected of
having autoimmune pancreatitis who
present with acute pancreatitis?
A. Corticosteroids
B. Analgesics
C. Enteral feeding
D. Mechanical ventilation

101. MCQs
• Which of the following should not be used
in the short term in patients suspected of
having autoimmune pancreatitis who
present with acute pancreatitis?
A. Corticosteroids
B. Analgesics
C. Enteral feeding
D. Mechanical ventilation

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