1. ACUTE PANCREATITIS
DR.BARUN KUMAR

2. At a glance
• Etiology
• Pathogenesis
• Diagnostic assessment

3. DEFINITIONS
• An acute inflammatory process of pancreas that
may also involve peripancreatic tissue or remote
organ system
• Requires 2 out of following 3 features:
1. Abdominal pain characteristic of acute
pancreatitis
2. Serum amylase and/or lipase level >/ 3 times the
upper limit of normal
3. Characteristic findings of acute pancreatitis on
ultrasonography or CT scan

4. ETIOLOGY
• Alcohol
• Gallstone
• Post-ERCP
• Drugs
• Autoimmune
• Genetic
• Abdominal trauma
• Post operative
• Infections
• Metabolic - hypercalcemia, hyperparathyroidism,
hypertriglyceridemia
• Miscellaneous- scorpion bite, worm infestations

5. A.ALCOHAL
• Along with gallstone, alcohol is the major
etiological agent of acute pancreatitis
• Heavy ethanol abuse >100g/day for at least 5
years, smoking and genetic predisposition
bears strong risk for alcohol induced injury.
• Alcohol has both direct(caspases ,sphincter of
oddi obst,dec perfusion) and indirect (nf-kb,
tnf-alpha, IL-1) effects on exocrine pancreas
• N34S , SPINK-1 mutation association

6. B.GALLSTONE
• Responsible for as many as 40% of cases,
especially in northern belts of india and woman
aged 50-70 years.
• OBSTRUCTIVE THEORY: excessive pressure inside
the pancreatic duct due to obstruction and
subsequent activation of enzymatic and
inflammatory cascade
• REFLUX THEORY: stones impacted in ampulla of
vater resulting in reflux of bile in pancreatic duct.

7. C.POST-ERCP
• Occurs in as high as upto 5% of patients
• Most common complication of ERCP
• More common in therapeutic ERCP than diagnostic
• Major risk factors include use of precut
sphincterotomy, number of pancreatic duct
cannulation, and duct opacification.
• 2 theories have been proposed:
a)Traumatic intubatiuon of ampulla causing sphincter
spasm
b)Excessive hydrostatic pressure during contrast injection
causing acinar cell damage

8. D.MICROLITHOIASIS : association with idiopathic recurrent acute
pancreatitis
E.GENETICS : IRAP and idiopathic chronic pancreatitis shows strong
genetic association
PRSS1 (cationic trypsinogen gene) ,
SPINK1 (42% association) ,
CFTR (9% association)
F. HYPERTRIGLYCERIDEMIA: a level of >1000 mg/dl is suggestive
>2000 mg/dl is diagnostic
G.CONGENITAL ANAMOLIES: pancreas divisum
needs modifiers or cofactors

9. H. DRUG INDUCED PANCREATITIS:
I. HYPERSENSITIVITY : 5-aminosalicyclic acid,
azathioprine, 6-mercaptopurine,metronidazole,
tetracycline
II.DURG INDUCED HYPERTRIGLYCERIDEMIA:
thiazide, isotretinoin, tamoxifen
III. TOXIC METABOLITE: pentamidine, valproic acid,
didanosine
IV. OVERDOSE REACTION: acetaminophen,
erythromycin

10. I. INFECTIONS: hep A , HEP B (well recognised)
HEP C, HEV
mumps, EBV,VZ,CMV
J. ASCARIASIS: KASHMIR is the most affected
area with as high as 23% cases of acute
pancreatitis due to ascariasis
K. HYPERPARATHYROIDISM: the primary
mechanism is calcium mediated activation of
trypsinogen or calcium depostion in pancreatic
duct

11. L. AUTO-IMMUNE PANCREATITIS:
• auto immune infiltration of pancreas
lymphoplasmacytic cells resulting in focal or diffuse
enlargement of pancreas.
• However, there is no features of pancreatitis.
Instead there are features of obstructive jaundice.
• Serum IgG4 levels > 1400 mg/l OR
IgG4 positive cells in IHC

12. PATHOGENESIS
• The exact mechanism and detailed
understanding is still unknown.
• However, most researchers believe abnormal
activation of pancreatic enzymes inside the
pancreatic acinar cells is the basic pathology
• This further leads to immune response which
then is responsible for both local changes and
systemic response

13. FIG.
pathophysiology
of acute
pancreatitis

14. MAJOR STEPS IN PATHOPHYSIOLOGY :
A.INTRA-ACINAR EVENTS
B. INNATE IMMUNE RESPONSE
C. MICROCIRCULATORY DISTURBANCES
D.BACTERIAL INFECTIONS

15. A. INTRA – ACINAR EVENTS
The key event is intra pancreatic activation of the digestive
enzymes either through :
i. Ach mediated vagal stimulation
ii. Enterokinase activation under pH dependant reaction
iii. Trypsin is the first enzyme to get activated which then in turn
activates other enzymes
Protecting factors:
i. SPINK 1 : packing of inactive intracellular enzymes away from
proteolytic enzymes
ii. Low intracellular pH- prevents trypsin activation
iii. Maintenance of particulate subcellular Ca gradient
COLOCALIZATION THEORY: colocalization of zymogen granules and
lysosomes in presence of increased cytosolic Ca gradient

16. B. INNATE IMMUNE RESPONSE :
Activation of vascular adhesion molecules
Attraction of neutrophils
neutrophil elastase mediated injury ( measured by MPO)
Monocyte mediated injury (through IL-1, IL-6 and TNF-alpha)
Results in damage and further inactivation and the cycle continues
(Levels of TNF-alpha and IL-6 correlates with the degree of severe
pancreatitis )

17. C. MICROCIRCULATORY DISTURBANCE
Leucocyte adhesion, hemoconcentration and vasoconstriction
Reduced capillary perfusion and ischemia
Further pancreatic injury
Pancreatic necrosis
Effects on systemic circulation with circulatory failure,
hypotension and acute renal failure

18. D. BACTERIAL INFECTION
The necrosed pancreatic tissue and peripancreatic fluid
collection are susceptible sites for bacterial infection
The most common source of infection is gut through
transmigration of bacteria
Most common organsim : E.Coli , pseudomonas, klebsiella
Infected pancreatic necrosis carries a high mortality of as high as
40%
Institution of early enteral feeding is instrumental of preventing
transmigration of bacteria

19. DIAGNOSTIC ASSESSMENT
A. CLINICAL DIAGNOSIS
B.LABOROTORY DIAGNOSIS
C. ASSESSMENT OF SEVERITY

20. Clinical Presentation
• Pain (95%)
– Acute onset
– Mid-abdominal or mid-epigastric
– Radiates to the back (50%)
– Peak intensity in 30 minutes
– Lasts for several hours
• Nausea and vomiting (80%)
• Fever
• Shock
• Abdominal distension (75%)
• Abdominal guarding and tenderness (50%)
• Restlessness and agitation
• Grey-Turner's sign (hemorrhagic discoloration of the flanks)
• Cullen's sign (hemorrhagic discoloration of the umbilicus)

21. Cullen's sign Grey-Turner's sign

22. LABORATORY DIAGNOSIS
• Serum amylase : alone cannot be used reliably for the
diagnosis of AP and serum lipase is preferred.
• Serum lipase is more specific and remains elevated
longer than amylase after disease presentation.
• Increased amylase and/or lipase >3 times
– Amylase levels rise w/in 2-12h
• Peak w/in first 48hr
• Remain elevated 3-5days before return to baseline
– Lipase much more specific

23. .• Abdominal ultrasound US should be performed in
all patients with AP
• In the absence of gallstones and / or history of
significant history of alcohol use, a serum
triglyceride should be obtained and considered
the etiology if >1000 mg/dl
• In a patient > 40 years old, a pancreatic tumor
should be considered as a possible cause of AP

24. CT SCAN/ MRI
• CT/MRI is the modality of choice for diagnosis and
evaluation and diagnosis of acute pancreatitis
• However, patients with mild acute pancreatitis need not
undergo ct/mri
• CT/MRI is indicated when:
1. Clinical diagnosis is doubtful
2. Failure to respond to medical management in 48-72
hrs
3. Any change in clinical status suggestive of
complication
CT/MRI offers the advantage of evaluation of extent
and severity of disease

25. MDCT PROTOCOL FOR ACUTE PANCREATITIS
60 SEC DELAY
Dome of
diaphragm to
symphysis
pubis
PORTAL
VENOUS PHASE
35 SEC DELAY
COVERAGE
THROUGH
PANCREAS
TO LOOK FOR
NECROSIS
PANCREATIC
PARENCHYMAL
PHASE
10 SEC DELAY
Top of the
vertetbral
body T12 to
sup edge of L4
(in suspected
vascular
complications)
Arterial phase
CONTRAST
– 150 ml of
60%
iodinated
non-ioinc
iv @3-4
ml/sec

27. MODIFIED CT SEVERITY INDEX
PROGNOSTIC INDICATOR POINTS
PANCREATIC INFLAMMATION
• NORMAL PANCREAS
• INTRINSIC PANCREATIC ABNORMALITIES WITH/WITHOUT
INFLAMMATORY CHANGES IN PERIPANCREATIC FAT
0
2
• PANCREATIC OR PERIPANCREATIC FLUID COLLECTION OR
PERIPANCREATIC FAT NECROSIS 4
PANCREATIC NECROSIS
• NONE 0
• <30% 2
• >=30% 4
EXTRAPANCREATIC COMPLICATIONS
one or more of pleural effusion, ascites , vascular complications,
parenchymal complications, or gastrointestinal tract involvement
2

28. .
• Higher CTSI score associated with protracted
clinical course, a higher complication rate and a
higher mortality
• CTSI 0-1 = no morbidity or mortality
• CTSI 2 = morbidity rate of 4% and no mortality
• CTSI 7-10% = 17% mortality and 92%
complication rate

29. CT Findings
Tail Indistinct
Intraperitoneal fluid

30. CT Findings
Severe Pancreatitis
Nonenhancin
g
Necrosis
Peripancreatic edema
and inflammation

31. CLINIAL ASSESSMENT
HISTORY PLUS EXAMINATIONS
SYMPTOMPS OUT OF PROPORTION THAN SIGNS
SERUM AMYLASE + SERUM LIPASE
USG W/A
CT SCAN / MRI
ASSESSEMENT OF RISK

32. RISK ASSESSMENT
A.
ATLANTA
SCORING

33. ATLANTA CRITERIA ( CONTD.)
CHARACTERISTICS DEFINING POINT
ORGAN FAILURE SHOCK (SBP <90mm of Hg)
Pulmonary insufficiency (PaO2<60 mm oh Hg)
Renal failure (serum creatinine level >2mg/dl after rehydration)
Gastrointestinal bleeding (>500 mL/24 hr)
LOCAL
COMPLICATIONS
PANCREATIC NECROSIS
(>30% of the parenchyma or >3 cm)
PANCREATIC ABSCESS
( circumscribed collection of pus containing little or no
pancreatic necrosis)
PANCREATIC PSEUDOCYST
(collection of pancreatic juices enclosed by a wall of fibrous
tissue or granulation tissue)
UNFAVOURABLE
PROGNOSTIC SIGNS
RANSONS SCORE >=3
APACHE II SCORE >=8

34. ATLANTA CRITERIA ( CONTD.)
CHARACTERISTIC DEFINING POINT
SYSTEMIC
COMPLICATIONS
DIC (platelet count <100000)
FIBRINOGEN (1GR/L
FIBRIN SPLIT PRODUCTS >80 ug/dl
METABOLIC DISTURBANCE ( calcium level
<7.5 mg/dl)

35. B.RANSON SCORE
At admission
• age in years > 55 years
• white blood cell count > 16000 cells/mm3
• blood glucose > 11 mmol/L (> 200 mg/dL)
• serum AST > 250 IU/L
• serum LDH > 350 IU/L
At 48 hours
• Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL)
• Hematocrit fall > 10% (as compared with admission value)
• Oxygen (hypoxemia PO2 < 60 mmHg)
• BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV
fluid hydration
• Base deficit (negative base excess) > 4 mEq/L
• Sequestration of fluids > 6 L

36. C.APACHE-II SCORE
• ACUTE PHYSIOLOGY AND CHRONIC HEALTH
EVALUATION
• predicts severity of any acute disease
• consists of 11 parameters reflecting functions of
major organ system also taking age amd baseline
chronic disease into account
• allow for monitoring of disease progression and
response to therapy
• Has been shown superior to ranson and glasgow

37. I.MARSHALL SCORING SYSTEM
ORGAN SYSTEM 0 1 2 3 4
RESPIRATORY (P02/FiO2) >400 301-400 201-300 101-
200
<=100
RENAL
Serum creatinine, mg/dl
<1.4 1.4-1.8 1.9-3.6 3.6-4.9 >4.9
CARDIOVASCULAR
Systolic blood pressure, mm oh
Hg
>90 <90
Fluid
responsive
<90
Not fluid
responsive
<90
pH<7.3
<90
pH<7.2

38. .
D. SIRS SCORE
• hr>90/min,
• TEMP >38 or <36 celcius
• Resp rate >20 breaths/min or PaCO2>32 mm oh Hg
• Blood cell count >12000 or <4000 cells/microlit
or >10% band form
E. BISAP SCORE
o BUN> 25 mg/Dl
o Impaired mental status (gcs<15)
o SIRS >=2
o Age>60 yrs
o Pleural effusion

39. .F. Panc 3 score
• Hemotocrit >44 , bmi>30kg/m2, pleural effusion
G.JAPANESE SEVERITY SCORE
• Has 9 components
• Score of 3 or more reflects severe acute pancreatitis
H. HARMLESS ACUTE PANCREATITIS SCORE
• Absence of rebound tenderness and/or guarding
• Normal hematocrit
• Normal serum creatinine
 Enables scoring within 30 mins of admn
 In a cohort of 394 patients, has shown the accuracy to
predict a mild course of acute pancreatitis as high as 98%

40. BIOCHEMICAL PREDICTORS OF PANCREATIC NECROSIS
AND SEVERITY
1. C-reactive protein (CRP) - >150 mg/ml
2. Proclcitonin (PCT)
3. Serum amyloid –a (SAA)
4. Serum macrophage migration inhibitory factor
(MIF)
5. Trypsionogen activation peptide (TAP)
6. Polymorphonuclear granulocyte elastase (PMN)
7. Interleukin
8. Hematocrit
9. Bun

41. THANK YOU
• ,