The document provides a comprehensive overview of acute pancreatitis, detailing its anatomy, aetiology, pathophysiology, clinical evaluation, differential diagnoses, and management strategies. It emphasizes the importance of history and physical examination in diagnosing the condition, common causes such as biliary calculi and alcohol abuse, and the various complications that may arise. The document also outlines the severity assessment using various scoring systems and discusses diagnostic imaging techniques involving ultrasound, CT scans, and ERCP.

1. Acute Pancreatitis

2. Outline of Presentation
• Anatomy of Pancreas
• Aetiology
• Pathophysiology
• Clinical Approach – History and Physical
Examination
• Differential Diagnosis
• Investigation
• Assessment of Severity
• Management of Acute Pancreatitis
• Complications

3. ANATOMY OF PANCREAS

4. Anatomy
• Retroperitoneal organ
• In adults- 15cm long & 70-100 weighs
• 3 portions- head, body and tail
• Relations:
Head
Neck
Uncinate
Body
Tail

7. • Main pancreatic duct- Wirsung duct
• Acessory duct – Santorini duct

10. Pancreatitis
Acute
presenting with abdominal pain and is usually
associated with raised pancreatic enzyme levels
in the blood or urine as a result of pancreatic
inflammation.
Chronic

11. Incidence
• 3 % of all cases of abdominal pain
• Hospital admission rate for is 9.8 per 100 000
population anually
• Worldwide, 50 per 100 000 cases anually.
• The disease may occur at any age, with a peak
in young men and older women.

12. Etiology
Two major causes are :
• biliary calculi (50–70%)
• alcohol abuse (25%)
The remaining cases may be due to rare causes
or be idiopathic

15. Gallstone Pancreatitis
• Transient blockage of common bile duct 
reflux of bile into pancreatic duct and impair
flow of normal pancreatic juice  premature
activation of pancreatic enzymes within duct
system.

16. Alcohol Pancreatitis
• High risk in:
1. Long standing alcohol intake for at least 2 years
or single session of heavy drinking
2. Consumption >80g/day
• What Happened ?
1. Direct toxic effect of alcohol in genetically
predisposed individuals
2. Viscid secretion of pancreatic juice  formation
of protein plugs and impairment of flow

17. Pathophysiology
• Premature activation of pancreatic enzymes
within the pancreas, leading to a process of
autodigestion.
• Anything that injures the acinar cell and impairs
the secretion of zymogen granules, or damages
the duct epithelium and thus delays enzymatic
secretion, can trigger acute pancreatitis.
• Once cellular injury has been initiated, the
inflammatory process can lead to pancreatic
oedema, haemorrhage and, eventually, necrosis.
• As inflammatory mediators are released into the
circulation, systemic complications can arise.

19. ACUTE PANCREATITIS
History and Physical Examination

20. Purpose of History Taking
• Pain
• Causes
• Complications

21. History Taking
1) Abdominal Pain - Remember SOCRATES!
• Site: Diffuse, upper abdominal pain
• 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.

22. • 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

23. 2) History of underlying causes
‘I GET SMASHED’
• Idiopathic (10%)
• Gallstone (45%)
• Ethanol (35%)
• Trauma (10%)
• Steroids
• Mumps
• Autoimmune
• Scorpion / Snake
• Hyperlipidemia
• ERCP
• Drugs (10%)

24. 3) History of Complications
Systemic :
• ARDS
• Renal Failure
• Shock, arrythmias
• Metabolic: hypocalcemia, hyperglycemia
• Encephalopathy

25. Local :
• Mostly develop silently
• Pancreatic abscess – high grade fever
• Pseudocyst
• Pancreatic effusion

26. Physical Examination: Acute
Pancreatitis
• Elevation of body temperature is often is
acute pancreatitis

27. • Abdominal Examination
1. Inspection: abdominal distension
2. Palpation:
• Hepatomegaly
• Tenderness
• Cullen sign
• Gray turner sign
• Peritoneal signs
• Rigidity
• Guarding

29. • Percussion : Dullness suggesting ascites
• Auscultation: auscultate the abdomen for
hypoactive or an absent bowel sounds or an
abdominal bruit. 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

30. Presented by Siti Nur Rifhan Kamaruddin
DIFFERENTIAL DIAGNOSIS
INVESTIGATIONS
SEVERITY SCORING

31. Differential Diagnosis
For Mild Acute Pain For Severe Acute Pain
Acute Cholecystitis Fecal Peritonitis due to
Perforated Colon
Peptic Ulcer Disease Ruptured Abdominal Aortic
Aneurysm
Inferior Myocardial Infarction Ruptured Ectopic Pregnancy
Acute Appendicitis Massive Bowel Infarction

32. INVESTIGATIONS

33. Investigations
• The diagnosis if made on basis of clinical
presentation, an elevated serum Amylase level and
characteristic Imaging features.
• Biological :
- Serum Amylase increase 3x than normal or
more than 1000IU/mL (Peak within the first
24hours after onset of Symptom)
- Serum Lipase has longer half life thus more
useful in delayed cases.
- Serum Lipase: more sensitive & specific for
Pancreatitis than Amylase

34. Other Causes of Increased Serum Amylase :
• Renal Failure
• Liver Cirrhosis
• Peritonitis
• GIT Inflammation
• Ruptured Ectopic Pregnancy/Salphingitis
• Salivary Gland Inflammation (Parotitis)

35. 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
BUSE To determine level of dehydration
Random
Blood
Glucose
Damage to beta cells interferes with insulin
production causing Hyperglycemia (in severe cases)
Serum
Calcium
Hypocalcaemia suggests saponification

36. 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

37. Imaging : Ultrasound
• 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

38. • Transverse
Transbadominal
Ultrasound shows a
swollen pancreatic
body with ill-
defined
heterogeneous
hypoechoic
pattern.

39. 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.

40. ERCP : Gallstone Pancreatitis

41. Plain Abdominal X-Ray
• Plain erect chest & abdominal X-ray are not diagnostic of
Acute Pancreatitis 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)

42. A focal dilated proximal jejunal loop in the left upper quadrant. A focal
area of adynamic ileus close to an intraabdominal inflammatory process
The sentinel loop sign may aid in localizing the source of inflammation.
Sentinel Loop in upper abdomen may indicate Pancreatitis

43. -Colon Cut-off Sign describes gaseous distension seen in proximal colon
- Associated with narrowing of splenic flexure in cases of Acute
Pancreatitis
- This Appearance results from inflammatory process extending from
Pancreas into the phrenicolic ligament via transverse mesocolon

44. CT Scan
• Not necessary for all patients.
• May reveal pseudo cyst or abscess (complication
of acute pancreatitis)
• A contrast-enhanced CT is indicated in following :
 If there is diagnostic uncertainty
 In Pt. with severe acute Pancreatitis to distinguish
interstitial from necrotizing pancreatitis.
 In Pt. with organ failure, signs of sepsis or
progressive clinical deterioration
 When a localized complication is suspected I.e. fluid
collection, pseudo cyst.

45. CT Anatomy Pancreatic Level

46. CT shows significant swelling &
Inflammation of the Pancreas

47. Morphologic Types of Acute
Pancreatitis
THE REVISED ATLANTA CLASSIFICATION
1) Interstitial Edematous Pancreatitis
2) Necrotizing Pancreatitis
• Parenchymal necrosis
• Peripancreatic necrosis
• Combined Type

48. Interstitial Edematous Pancreatitis
• Pancreatic Enlargement
due to edema
• Pancreatic Parenchyma
shows relatively
homogenous enhancement
& peripancreatic fat
stranding
• Outcome : Symptoms
usually resolve within first
week

49. - Inflammation associated
pancreatic parenchymal
necrosis orperipancreatic
necrosis
- Cause impairment of
pancreatic perfusion
- Impairment evolve
over several days
- Early CECT may
underestimate extent
of disease
Necrotizing Pancreatitis
(5-10%)

50. Pancreatic Fluid Collection : Revised Atlanta 2012
85% 15%

51. Local Complications should be suspected if :
 Persistence or recurrence of abd. pain
 Secondary increases in Serum Pancreas activity
 Increasing organ dysfunction
 Development of clinical signs of Sepsis i.e. fever,
leucocytosis
Prompt CECT to be done in these cases.
Pancreatic Fluid Collection : REVISED ATLANTA 2012
•Acute Peripancreatic Fluid Collection (APFC)
•Pancreatic Pseudocyst (PP)
•Acute Necrotic Collection (ANC)
•Walled-off Necrosis (WOPN)

52. 1) Acute Peripancreatic
Fluid Collection (APFC)
• Peripancreatic Fluid
associated with IEP with
no necrosis
• Usually seen within first 4
weeks
• Homogenous collection of
fluid
• Usually resolve
spontaneously
• When a localised APFC
persists > 4 weeks –
develop into a Pseudocyst

53. 2) Pancreatic
Pseudo cyst
• Encapsulated
collection of fluid
with a well defined
inflammatory wall
usually outside the
pancreas
• With minimal or no
necrosis
• Usually round or oval
• Appears after 4
weeks of onset IEP
-Note the two round, homogenous fluid
collection with a well defined borders
- White stars denote normal enhancing
pancreas

54. 3) Acute Necrotic
Collection (ANC)
• A collection
containing of both
fluid & necrosis
• < 4 weeks
• Occurs only in
setting of NP
• Single or multiple
heterogeneous
collection
• No defined wall -Note enhancement of entire pancreatic
Parenchyma (Whitestars)
- Note the heterogeneous, non-liquid component
in retroperitoneum (White arrows pointing at the
borders of ANC)

55. 4) Walled-off
Necrosis (WON)
• A mature, encapsulated
collection of pancreatic
/peripancreatic necrosis
• that has developed a
well-defined
inflammatory wall
• Appears >4 weeks after
onset of NP
• Heterogeneous with
liquid & non-liquid
density
-Note the Area of non-liquid components of
high attenuation (black arrows) in the collection
- It has a well defined, enhancing wall (White
arrows)

56. - Homogenous,
low attenuation fluid density
- NO solid component
Pseudocyst (PC) vs. Walled-off Necrosis (WON)
-Heterogeneous with liquid
and solid densities

57. SUMMARY: Local Complications of AP

58. CT Severity Index: Balthazar + Necrosis Score
A
B
C
D
E

59. Assessment of
Severity
 Ranson Score
 Glasgow Scale
 APACHE II Score

60. Severity: RANSON’S SCORE
To predict severity of acute pancreatitis.
On Admission (LEGAL)
L – Leucocytes >16000
E – Enzyme AST > 250
G – Glucose > 200
A – Age > 55
L – LDH > 350
During Next 48 Hours (C.HOBBS)
C – Calcium 8mg/dl
H – Hematocrit fall of >10%
O2– Pa02 < 60mmHG
B – Base deficit > 4mmol/L
B – BUN rise > 5
S – Sequestration (Fluid) > 6 litres
3 or more factors
present – SEVERE

61. Glasgow Scale
3 OR MORE FACTORS
PRESENT - SEVERE

62. APACHE II SCORE
Score > 8 : Severe
Acute Pancreatitis

63. Management of Acute
Pancreatitis
Presented By Fariza Asilah Ahmad Rahim

64. Mild Acute Pancreatitis
1. Nil by mouth
2. Fluid resuscitation : 4 pints
3. Analgesia : IM Tramal 50mg TDS
4. Treat underlying cause
5. No role for antibiotics

65. Severe Acute Pancreatitis
• Admission to intensive care or high-
dependency unit
1. Oxygen supplementation
2. Analgesia
3. Aggressive fluid rehydration
4. Monitor vital signs
5. Monitor haematological & biochemical
parameters

66. 6. Nasogastric drainage
7. Antibiotic prophylaxis –imipenem, cefuroxime
8. CT scan
9. ERCP within 72 hours
10. Supportive therapy for organ failure
11. Nutritional support

67. Complications of Acute
Pancreatitis

68. SYSTEMIC
• Cardiovascular - shock
- arrhythmia
• Pulmonary - ARDS
• Renal failure
• Haematological - DIC
• Gastrointestinal - Ileus

69. SYSTEMIC
• Metabolic - Hypocalcaemia
- Hyperglycaemia
- Hyperlipidaemia
• Neurological - Visual disturbance
- Confusion
- Encephalopathy
• Miscellaneous - Arthralgia

70. • Acute fluid collection
• Sterile pancreatic necrosis
• Infected pancreatic necrosis
• Pacreatic abscess
• Pseudocyst
LOCAL

71. • Pancreatic ascites
• Pleural effusion
• Portal or systemic vein thrombosis
• Pseudocyst
LOCAL

72. Complications & their Management
Acute fluid collection
 No intervention unless pressure effect
 Aspirate under US or CT guidance OR
 Transgastric drainage under EUS guidance
Pancreatic necrosis
 No intervention

73. Infected pancreatic necrosis
 Aspirate under CT guidance
 Percutaneous drainage
 Prophylactic antibiotic

74. If patient deteriorates
 Necrosectomy
 Closed continuous lavage
 Closed drainage
 Open packing
 Closure and relaparotomy

75. Pancreatic abscess
 Percutaneous drainage
 Antibiotic cover
Pancreatic ascites
 Drainage
 Parenteral or jejunal feeding

76. Pancreatic effusion
 Percutaneous drainage under CT guidance
Portal or systemic vein thrombosis
 Aspirin in the early process

77. Pseudocyst
 Percutaneous transgastric cystogastrotomy
and place double-pigtail drain
 Endoscopic under EUS guidance and place
tube drain
 Surgical drainage – internal drainage into
gastric or jejunum lumen

78. Cystogastrotomy

79. Reference
 BAILEY, H., LOVE, R. J. M., MANN, C. V., & RUSSELL, R. C. G.
(1992). Bailey and Love's short practice of surgery. London,
Chapman & Hall Medical.
 COLLEDGE, N. R., WALKER, B. R., RALSTON, S., & DAVIDSON, S.
(2010). Davidson's principles and practice of medicine.
Edinburgh, Churchill Livingstone/Elsevier.