This document provides an overview of acute pancreatitis, including its definition, epidemiology, etiology, pathophysiology, clinical features, investigations, and assessment of disease severity. Acute pancreatitis is defined as acute inflammation and autodigestion of the pancreas presenting with abdominal pain and elevated pancreatic enzymes. Gallstones and alcohol abuse are the most common causes. Clinical features include epigastric pain radiating to the back. Investigations include serum amylase, lipase, imaging like CT scan. Disease severity is assessed using criteria like Ranson score, APACHE II score, CT severity index, and Atlanta criteria.

1. ACUTE PANCREATITIS
DR SUJAN PANDEY
SURGERY RESIDENT
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2. OUTLINE
• INTRODUCTION
• DEFINITION
• EPIDEMIOLOGY
• ETIOLOGY
• PATHOPHYSIOLOGY
• CLINICAL FEATURES
• INVESTIGATION
• ASSESSMENT OF SEVERITY OF DISEASE
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3. INTRODUCTION
• The name ‘pancreas’ is derived from the greek ‘pan’ (all) and
‘kreas’ (flesh).
• The average gland weighs between 75 and 125 gm and
measures 10 to 20 cm.
• Retroperitoneal organ that lies in an oblique position, sloping
upward from the C-loop of the duodenum to the splenic
hilum.
• Due to its retroperitoneal location, pain associated with
pancreatitis often is characterized as penetrating through the
back.
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4. Anatomically divided into 4 parts :
① Head
② neck
③ Body
④ Tail
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5. 5

6. Arterial supply of pancreas
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7. Main pancreatic duct:wirsung duct
Acessory duct: santorini duct 7

8. PANCREATITIS
• Inflammation of the pancreatic parenchyma.
Types:
1. Acute: Emergency condition.
2. Chronic: Prolonged & frequently lifelong disorder
resulting from the development of fibrosis within the
pancreas.
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9. DEFINITION
• ACUTE PANCREATITIS: Acute condition of diffuse
pancreatic inflammation & autodigestion, presents with
abdominal pain, a threefold or greater rise in the serum
levels of the pancreatic enzymes amylase and lipase, and
or characteristic findings of pancreatic inflammation on
contrast enhanced CT.
• Reversible inflammation of the pancreas
• Ranges from mild to severe.
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10. EPIDEMIOLOGY
• Acute pancreatitis accounts for 3% of all cases of abdominal
pain among patients admitted to hospital in the UK.
• The hospital admission rate for acute pancreatitis is 9.8 per
year per 100 000 population in the UK, although
worldwide, the annual incidence may range from 5 to 50
per 100 000.
• Women are affected more the men, but men are more
likely to suffer recurrent attacks.
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11. ETIOLOGY
Two major causes are :
• Biliary calculi (50–70%)
• Alcohol abuse (25%)
The remaining cases may be due to rare causes
or be idiopathic.
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12. 12

13. Mnemonic for the causes of Acute
Pancreatitis:
‘I get smashed‘
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion / Snakes
Hyperlipidaemia / Hypercalcaemia
ERCP
Drugs 13

14. Biliary Pancreatitis:
1. Common channel theory
2. Incompetent sphincter of
Oddi
3. Obstruction of the
pancreatic duct
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15. Alcoholic Pancreatitis:
-Direct toxic effect on the
pancreatic acinar cells
-Stimulation of the
pancreatic secretion
-Constriction of the
sphincter of Oddi
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16. PATHOPHYSIOLOGY
• Exact mechanism of AP not completely known.
• Most researchers believe that AP begins with the activation
of zymogens inside acinar cells, which causes acinar cell
injury .
• Severity of AP may be determined by the events that occur
subsequent to acinar cell injury, which include release of
cytokines and other chemical mediators of inflammation.
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17. 17

18. Events of pathogenesis of Acute
Pancreatitis include:
A. Precipitating Initial Events
B. Intrapancreatic Events
C. Systemic Events
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19. A. Precipitating Initial Events
 Acinar Cell Events.
 When acinar cells are pathologically stimulated, their
Lysosomal(L) & Zymogen(Z) contents colocalize,
consequently trypsinogen is activated to trypsin by
cathespin B.
 Increased cytosolic Calcium is required .
 Cathespin B and other contents of these colocalized
organelles are released .
 Cathespin B activates apoptosis by causing
cytochrome c to be released from mitochondria.
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20. • Activation of PKC results in a
sudden activation of NF Kappa
beta
• Which triggers release of
Cytokines
• Cytokines attract
inflammatory response cells
which mediate local & syst.
inflammation
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21. Intrapancreatic Events
• After activation of superoxides (“Respiratory burst”) and release of
proteolytic enzymes (cathespin, elastase and collagenase),
activated neutrophils are attracted to focus of tissue injury .
• Macrophages release TNF-alfa, IL-6 & IL-8 which mediate the local
and systemic inflammatory response
• The inflammatory mediators cause increased pancreatic vascular
permeability – leading to edema, hemorrhage & microthrombi
• Failure of pancreatic microcirculation resulting in pancreatic
hypoperfusion & necrosis
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22. Systemic Events
• Organ failure can develop at any stage of acute pancreatitis.
• The development pancreatic necrosis, the breakdown of the
interstitial barrier and suppression of immune response
contribute to the development of infected pancreatic
necrosis .
• This may associated with late development of SIRS or MODS
• Organ failure is scored using the Marshall or Sequential
Organ Failure Assessment system(SOFA).
• The 3 organ system most frequently involved are
Cardiovascular, Respiratory an Renal.
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23. SIRS
23

24. • Having a persistent SIRS throughout hospital
admission, having a transient SIRS, or never
meeting SIRS criteria has been associated with
mortality rates of 25%, 8%, and 0%,
respectively.
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25. MODIFIED MARSHALL SCORE
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26. 26

27. DIAGNOSIS
A. Clinical presentation
B. Investigation
c.Imaging
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28. Revised Atlanta Criteria
Diagnosis of acute pancreatitis, which states that acute
pancreatitis requires at least 2 of the following three
criteria:
1) Abdominal pain and physical exam consistent
with pancreatitis
2) lipase or amylase levels three times the upper limit of
normal and
3) imaging (CT, MRI, ultrasound) findings that are
consistent with acute pancreatitis.
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29. CLINICAL PRESENTATION
History and Physical Examination:
Abdominal Pain – ( SOCRATES)
• Site: Diffuse, upper abdominal pain (epigastric)
• Onset: Sudden
• Character: Boring Pain
• Radiation: Radiates to the back
• Associated factor: Nausea, vomiting, dyspnea
• Timing: Pain escalates in intensity and peaks
within 10-20 minutes of onset.
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30. • Aggravating and relieving factor: Aggravated
by breathing with increased chest expansion
and relieved by leaning forward.
• Severity: Depending on severity, patient may
present in shock( Tachypnea, tachycardia and
hypotension may be present )
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31. Physical Examination
• Elevation of body temperature is often in
acute pancreatitis .
• In gallstone pancreatitis icterus may be
present .
31

32. Abdominal Examination
1. Inspection: abdominal distension (ileus,ascites)
2. Palpation:
Hepatomegaly
Tenderness (epigastric region)
Cullen sign
Gray turner sign
FOX’S sign
Guarding/Rigidity
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33. 33

34. Percussion : shifting dullness suggesting ascites
Auscultation: hypoactive or an absent bowel
sounds . Ileus is common in pancreatitis.
Ausculation of lungs: 10-20% of patients have
pulmonary findings, commonly left sided
findings.
1. Basilar rales
2. Atelectasis
3. Pleural effusion
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35. Differential Diagnosis
 Perforated viscus (DU)
 Acute cholecystits, Biliary colic
 Acute intestinal obstruction
 Esophageal rupture
 Mesenteric vascular obstruction
 Renal colic
 Dissecting aortic aneurysm
 Myocardial infarction
 Basal pneumonia
 Diabetic ketoacidosis
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36. INVESTIGATIONS
Serum Amylase:
• Sensitivity: 72%
• Specificity: 99%
• Released within 6-12 hours of the onset, & Remains elevated for 3-
5 days.
• Elevation ˃ 3X normal is significant.
• Undergoes renal clearance. After its serum levels decline, its urinary
level remains elevated.
• Its level doesn't correlate with the disease activity.
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37. Other Causes of Increased Serum
Amylase
Renal Failure
Liver Cirrhosis
Peritonitis
GIT Inflammation
Mesentric ischemia
Ruptured Ectopic Pregnancy/Salphingitis
Salivary Gland Inflammation (Parotitis)
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38. Serum Lipase:
 More pancreatic-specific than s. Amylase.
 Sensitivity: about 100% , Specificity: 96%
 Remains elevated longer than amylase (7 to 14 days).
 Useful in patients presenting late to the physician.
 S. Amylase tends to be higher in gallstone pancreatitis
 S. Lipase tend to be higher in alcoholic pancreatitis
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39. • Other Blood Tests..
• Full Blood Count : Elevated Leucocytes count for
Ranson’s Criteria and to predict prognosis.
• LFT: To asses cause of Pancreatitis/obstructive
jaundice .
• Random Blood Glucose: Damage to beta cells
interferes with insulin production causing
Hyperglycemia (in severe cases)
• Serum Calcium :Hypocalcaemia suggests
saponification
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40. • Serum albumin is low in 10% of patients and
indicates severe pancreatitis.
• Markedly elevated LDH (>500U/dl) suggests poor
prognosis.
• Serial assessment of C-reactive is a good
indicator of progress .
• ABGs show hypoxia.
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41. IMAGING
Role of Imaging in Acute Pancreatitis:
• To clarify diagnosis when the clinical picture is
confusing
• To determine possible causes
• To assess severity (Balthazar Score) and thus
to determine prognosis
• To detect complications
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42. Chest x-ray
• Not diagnostic of AP but are useful in differential
diagnosis.
• Non specific findings in Pancreatitis : Generalized
or local ileus (Sentinel Loop), a colon cut off sign,
and calcified gallstones.
• Erect CXR: Look for pleural effusion. In severe
cases, a diffuse alveolar shadowing (Acute
Respiratory Distress Syndrome)
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43. A focal dilated proximal jejunal loop in LUQ
SENTINEL LOOP SIGN
COLON CUT OFF SIGN
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44. 44
PLEURAL EFFUSION

45. USG
Trans abdominal USG : Does not establish a diagnosis.
• USG should be performed within 24 hours in all patients
- To detect gallstones
- To rule out Acute Cholecystitis
- To determine whether the common bile duct is dilated
- To evaluate change on pancreas i.e. edema, mass in
Pancreas
45

46. • Transverse Transbadominal Ultrasound shows
a swollen pancreatic body with ill- defined
heterogeneous hypoechoic pattern.
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47. • USG cannnot clearly delineate extrapancretic
spread of pancreatic inflammation or identify
necrosis within the pancreas; these important
findings are the best seen by CECT.
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48. CT SCAN
• Gold standard.
• Done 72 hours after acute attack.
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49. A contrast-enhanced CT is indicated in following :
 If there is diagnostic uncertainty
 severe acute Pancreatitis to distinguish interstitial from
necrotizing pancreatitis.
 In Pt. with organ failure(MODS), signs of sepsis or progressive
clinical deterioration
 Local complication is suspected I.e. fluid collection, pseudo
cyst.
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50. Peripancreatic stranding (arrow). Multiple gallstones in the
gallbladder
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51. Pancreatic edema with peri-pancreatic
inflammatory changes.
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52. Contrast-enhanced CT: acute necrotising pancreatitis.
Pancreatic area of reduced enhancement,
peripancreatic edema and stranding of the fatty tissue
52

53. Pancreatic Necrosis. Lack of gland
enhancement following IV contrast
administration is diagnostic.
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54. Pancreatic abscess. Large, relatively
well-circumscribed heterogeneous
collection containing gas bubbles
inferior to the pancreatic head. 54

55. Pancreatic pseudocyst
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56. ERCP
• Diagnostic and therapeutic
• To look for Gallstones, CBD stones or CBD
dilatation
• In patient with severe acute gallstone
pancreatitis & signs of on going biliary
obstruction and cholangitis – an urgent ERCP
should be sought.
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57. ERCP
57

58. ERCP IN ACUTE PANCREATITIS
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59. ERCP: GALLSTONE PANCREATITIS
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60. MRCP
 Both enhanced and non enhanced ,has a strong
correlation with contrast-enhanced CT in acute
pancreatitis.
 Greater sensitivity compared to CT to detect mild acute
pancreatitis.
 Better categorize fluid collection ,necrosis,
abscess,hemorrhage and pseudocyst.
 Delineates the pancreatic and bile ducts.
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61. MRCP
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62. ASSESSMENT OF SEVERITY OF DISEASE
A. Ranson Prognostic criteria
B. Acute Physiology And Chronic Health
Evaluation (APACHE II)score
C. Computed Tomography Severity Index (CTSI)
D. Atlanta Criteria for Acute Pancreatitis
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63. 63

64. Acute Physiology and Chronic Health
Evaluation (APACHE II) Score :
• Based on patient’s age, previous health status and 12
routine physiologic measurements.
• The main advantage is that it can be used on admission
and repeated at any time.
• APACHE II score of 8 or higher defines severe
pancreatitis .
• APACHE II has a positive predictive value of 43% and a
negative predictive value of 89%.
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65. 65

66. Atlanta Criteria for Acute Pancreatitis
Organ Failure, as Defined by
• Shock (SBP <90mm Hg)
• Pulmonary insufficiency (PaO2 <60 mm Hg)
• Renal failure (creatinine level >2 mg/dl after fluid resuscitation)
• Gastrointestinal bleeding (>500 ml/24 hrs)
Systemic Complication
• DIC ( platelet ≤10,000)
• Fibrinogen <1 g/L
• Fibrin split products >80 mcg/dl
• Metabolic disturbance (calcium level ≤7.5 mg/dl)
Local Complications
• Necrosis
• Abscess
• Pseudocyst
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67. Based on the severity of the disease
Acute pancreatitis is divided into the following types;
• In mild acute pancreatitis, there is the absence of local
or systemic complications and organ failure.
• In moderately severe acute pancreatitis are local
complications with or without organic failure for less
than 48 hours.
• In severe acute pancreatitis, there is persistent organ
failure for more than 48 hours with the involvement of
one or more than one organ.
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68. C –REACTIVE PROTEIN
• Inflammatory marker , peaks 48 to 72 hours after the onset of
pancreatitis .
• Correlates with the severity of the disease.
• A CRP level of >=150 mg/mL defines severe pancreatitis.
• The major limitation is that it cannot be used on admission;
sensitivity decreases if CRP levels are measured within 48 hours
after the onset of symptoms. In addition to CRP, a number of
studies have shown.
• Biochemical markers (e.g., serum levels of procalcitonin, IL-6, IL-
1, elastase) that correlate with the severity of the disease.
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69. REFERENCE
• SABISTON 21TH EDITION
• BAILEY AND LOVE 27TH EDITION
• SCHWARTZ’S 10TH EDITION
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70. • THANK YOU
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