acute and chronic pancreatitis

1. PancreatitisPancreatitis
Int. Kornbongkot Bunyuenyongsakun
Int. Thanadet Phongchomporn
Ext. Nattavut Wongdeethai

2. Pancreas
• an exocrine and endocrine organ
• It is a retroperitoneal organ, except for the
distal tail, which is in contact with the spleen.

3. Anatomical relations

4. Blood supply

7. Parasympathetic system
Sympathetic system
Exocrine and endocrine
secretion

8. Pancreatic ducts
Main pancreatic duct
Common bile duct
Hepatopancreatic ampulla (of Vater)
Acinar cells
Pancreatic ductal cells
Exocrine secretion is under vagus nerve
and hormonal control

9. Development of Pancreas

10. Exocrine secretions

11. Endocrine secretions

12. Acute pancreatitisAcute pancreatitis
• ETILOGY
• PATHOLOGY
• MACROSCOPIC PATHOLOGY
• CLINICAL FEATURES
• DIFFERENTIAL DIAGNOSIS
• INVESTIGATION: ASSESS SEVITTY &
CONFIRMATION
• MANAGEMENT: SEVERE PANCREATITIS
• COMPLICATION

13. Heavy alcohol drinker
คือบริโภค alcohol มากกว่า 50 gm ต่อวัน
เป็นเวลาอย่างน้อย 5 ปี
Increase secretory function
Induce spasm of the sphincter of Oddi
Induce pancreatic ductal permeability, which
would allow prematurely activated enzymes to
cause damage to the pancreatic parenchyma.

17. autosomal dominant disorder
usually related to mutations of the cationic
trypsinogen gene (PRSS1), causing premature
activation of trypsinogen to trypsin and cause
abnormalities of ductal secretion, both of which
promote acute pancreatitis

18. Hyperparathyroidism
most likely involves hypersecretion and
the formation of calcified stones
intraductally

19. หลังจากการทำา Endoscopic retrograde
cholangiopancreatography (ERCP) ความเสี่ยงในการเกิด
ได้แก่
•การทำา ERCP ที่มีการฉีด contrast ไปยัง pancreatic duct,
•การทำา pancreatic sphincterotomy,
•ผู้ป่วยอายุน้อย,
•ผู้ป่วยที่สงสัยว่าจะมี sphincter of Oddi dysfunction

22. thiazide diuretics,
furosemide,
estrogens,
azathioprine,
methyldopa,
l-asparaginase,
6-mercaptopurine,
tetracycline,
pentamidine,
procainamide,
nitrofurantoin,
dideoxyinosine,
valproic acid, and
acetylcholinesterase
inhibitors

23. Pathophysiology
Trypsinogen activation
Trypsin
Autodigestion
Co-localization theory
Acinar cell event
Intrapancreatic event
Systemic event

24. Acinar cell event
Intrapancreatic event
Systemic event
Zymogen
+
Lysosomal enzyme
“Cathepsin B”
Trypsinogen Trypsin
Apoptotic program
cell death

25. Acinar cell event
Intrapancreatic event
Systemic event
Apoptotic program
cell death
Neutrophil & Macrophage
Cytokines
tumor necrosis factor-alpha (TNF-α), inter-
leukin (IL)-6, and IL-8
Increase pancreatic
vascular permeability
Edema,
Hemorrhage,
Microthrombus

26. Acinar cell event
Intrapancreatic event
Systemic event
NFkappaB
cytokines & chemokines
TNF-α; IL-1, IL-2, IL-6
Systemic
inflammation

27. Definition of types of acute pancreatitis

28. Definition of types of acute pancreatitis
Revised Atlanta classification 2012 by international consensus
1. Interstitial edematous pancreatitis
2. Necrotizing pancreatitis
3. Acute peripancreatic fluid collection
4. Acute necrotic collection
5. Pancreatic pseudocyst
6. Walled-off necrosis

29. 1. Interstitial edematous pancreatitis

30. 2. Necrotizing pancreatitis

31. 3. Acute peripancreatic fluid collection (APFC)

32. 4. Pancreatic pseudocyst

33. 5. Acute necrotic collection (ANC)

34. 6. Walled-off necrosis (WON)

35. Symptoms&Signs
•Acute onset of persistent upper abdominal pain, at epigastric and
periumbilical regions
•Nausea and vomiting
•The pain may radiate to the back, chest, flanks, and lower abdomen.
•Patients are usually restless and bend forward (the knee-chest position) in an
effort to relieve the pain
•Physical examination findings are variable but may include fever, hypotension,
severe abdominal tenderness, guarding, respiratory distress, and abdominal
distention.

36. Cullen sign
: Periumbilical ecchymosis associated with both severe necrotizing
pancreatitis and retroperitoneal hemorrhage of various causes.
Severe necrotizing
pancreatitis

37. Grey Turner sign
: An ecchymosis of the flank due to retroperitoneal hemorrhage.
: When present, it usually occurs 3-7 days after the onset of pain and is
indicative of severe pancreatitis.

39. Require 2 out of following 3 features:
1.abdominal pain consistent with acute pancreatitis
(acute onset of a severe constant epigastric pain which often
radiates through to the mid back)
2.The elevation of serum amylase or lipase
(>3 times upper limit of normal).
3.Imaging (usually by contrast enhanced CT scanning)
is only required for the diagnosis of acute pancreatitis when
these diagnostic criteria are not met.
Diagnosis
Revised Atlanta classification 2012 by
international consensus

40. Diagnostic Imaging Modalities
1. CXR
• pleural effusions, atelectasis, or hemidiaphragm elevation
(suggestive of fluid sequestration),
• To exclude free air (pneumoperitoneum)
2. Plain and upright abdominal X-rays
• possible calcifications ( indicating chronic pancreatitis),
• gallstones (though only about 15% of gallstones are radio-
opaque),
• local dynamic ileus (or sign of bowel obstruction),
• “cutoff sign” : the gas in the transverse colon appears to end abruptly.
• “sentinel loop”: a single dilated jejunal loop in the upper abdomen

42. 3. Ultrasound
Features to be detected in acute pancreatitis on
ultrasound are as follow:
• Pancreatic swelling
• Peripancreatic fluid collection
• Extrapancreatic soft tissue edema
• Gallstones or CBD stones (Gallstones pancreatitis)
By the way, U/S may be of limited value in obese patients
or in patients with significant amounts of bowel gas
overlying the pancreas

43. 4. CT scan:
Features to be detected in acute pancreatitis on CT scan
are as follow:
•Pancreatic edema
•Peripancreatic fluid collection
•Extrapancreatic soft tissue edema
•Pancreatic necrosis
: hypodensity area in pancreatic parenchyma
•Air bubble in peripancreatic area
•Gallstones or CBD stones (Gallstones pancreatitis)
The primary purpose of cross sectional imaging is the diagnosis of
local complications, in particular the development and extent of
pancreatic necrosis or the presence of different fluid collections.

44. Severity assessment

45. Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus
1. Classification of the Severity of Acute Pancreatitis

46. Definition of organ failure
Three organ systems should be assessed to define organ failure:
respiratory, cardiovascular and renal.
Organ failure is defined as a score of 2 or more for one of these three
organ systems using the Modified Marshall scoring system
Classification of acute pancreatitis—2012:
revision of the Atlanta classification and definitions by
international consensus
Respiratory
Renal
Cardiovascular

47. Definition of local complications
Local complications are
acute peripancreatic fluid collection,
Pancreatic pseudocyst,
acute necrotic collection
walled-off necrosis
gastric outlet dysfunction,
splenic and portal vein thrombosis,
colonic necrosis
Classification of acute pancreatitis—2012:
revision of the Atlanta classification and definitions by
international consensus

48. 2. Multifactorial severity system
1. Ranson’s criteria
2. APACHE ( Acute Physiologic And Chronic Health Evaluation ) II score
3. BISAP score ( the Bedside Index for Severity in Acute Pancreatitis )

49. 3 or more positive criteria,
the disease is considered
“predicted severe.”
Ranson’s criteria
Ranson’s score
0 - 2 : mortality rate nearly 0 %
3 - 5 : mortality rate 10 - 20 %
> 7 : mortality rate > 50 %

50. APACHE ( Acute Physiologic
And Chronic Health Evaluation ) II score
1. Physiologic points :
Temperature
MAP (Mean Arterial Pressure)
Heart rate
Respiratory rate
Oxygenation (PaO2)
Arterial pH
Serum sodium
Serum potassium
Hematocrit
White cell count
Glasgow coma score
1+2+3 = Total Score
2. Age points
3. Chronic health points :
Liver
Cardiovascular
Respiratory
Renal
Immunocompromised
The main advantage of the APACHE II
system is that a score can be derived at any
time during the patient’s hospital course,
while the Ranson’s criteria are only
prognostic during the initial 48 hours.
Score >_ 8 indicate severe pancreatitis

52. Bedside Index for Severity of Acute Pancreatitis
(BISAP)
Although it has the
advantage of simplicity
and can be performed
within the first 24 hours
of admission,
it has performed no better
than other predictors
in comparison studies

53. Single parameter system
•C-RP (C-reactive protein)
•PMN elastase
•Trysinogen activation peptides
•Interleukin

54. Unfortunately !!!
these and many other single and combined predictors
of severity have an accuracy of only around 70%.
This means that there is misclassification error of 30%

55. Imaging severity assessment system
CT severity index score (CTSI)
score 0 - 3 : morbidity 3 % mortality 8 % : mild form
score 4 - 6 : morbidity 6 % mortality 35 % : moderate form
score 7 - 10 : morbidity 17 % mortality 92 % : severe form

56. Score 0-2: mild pancreatitis
Score 4-6: moderate pancreatitis
Score 8-10: severe pancreatitis

57. American collage of
Gastroentrology(ACG) Guideline 2013:
Management of Acute Pancreatitis

60. Management

61. Severe pancreatitis
• One of the following:
– Presence of local complication
– Pancreatic necrosis/pseudocyst/abscess
– Presence of organ failure
– SBP < 90 mmHg,
– PaO2 < 60 mmHg,
– Cr > 2 mg/dl
– GI bleeding > 500 ml/24 hr
– Ranson’s score: ≥ 3
– APACHE II: ≥ 8 points
– CRP ≥ 150, cutaneous sign, CXR change,
hemoconcentration, obesity

62. Mild acute pancreatitis
• Analgesic : Pethidine
• Aggressive fluid resuscitation with
isotonic crystalloid solution
• Monitoring : V/S , U/O , SaO2 , CVP
• NPO ในช่วงแรกๆ
• NG tube for decompression and
N/V
• Early enteral nuitrition เร็วที่สุดที่ผู้ป่วย
สามารถรับได้

63. Severe acute pancreatitis
• Admit ICU
• Urgent ERCP in 72 hours for GS
pancreatitis
• Systemic ATB: Imipenem,
fluoroquinolone ในรายที่ CT- พบ
necrosis
• Surgery: Infected pancreatic
necrosis
– FNA culture positive

64. tt
EARLY AGGRESSIVE INTRAVENOUS
HYDRATION

65. NUTRITION IN AP

66. ERCP IN AP

67. THE ROLE OF ANTIBIOTICS IN AP

69. THE ROLE OF SURGERY IN AP

70. Enteral nutrition should be commenced after
initial fluid resuscitation and within the first
24 hours of admission.
To avoid development of intestinal ileus and
feeding intolerance.
Route: Nasogastric or Nasojejunal
เพื่อวินิจฉัย pancreatic necrosis
เวลาที่เหมาะสมคือช่วงปลายสัปดาร์แรกของโรค
Revised Atlanta classification
1.Interstitial edematous pancreatitis
+/- acute peripancreatic fluid collection
(APFC)
2.Necrotizing pancreatitis ( parenchymal necrosis or peripancreatic
necrosis ) +/- acute necrotic collection (ANC)
ผู้ป่วยที่ควรได้ Antibiotics:
1.Necrosis > 30% of pancreas
2.มี Organ failure
3.ไม่สามารถรับ enteral feeding ได้
Preferred ATB: Carbapenem group
Percutaneous drainage
Endoscopic necrosectomy

72. Chronic pancreatitisChronic pancreatitis
• ETILOGY
• PATHOLOGY
• CLINICAL FEATURES
• DIFFERENTIAL DIAGNOSIS
• INVESTIGATION: ASSESS SEVITTY &
CONFIRMATION
• MANAGEMENT: SEVERE PANCREATITIS

73. • Defined as chronic inflammatory condition
that causes irreversible damage to pancreatic
structure and function
• Causes: ETOH abuse, malnutrition, hyperPTH,
pancreas divisum, ampullary stenosis, cystic
fibrosis, hereditary, trauma, idiopathic
Chronic pancreatitisChronic pancreatitis

75. Etiologic factors ass. With CP: TIGAR-O

76. • Chronic pancreatitis results in interstitial
inflammation w/duct obstruction and dilation
leading to parenchymal loss and fibrosis.
• Loss of both exocrine and endocrine
• Clinicically significant malabsorption occurs
when 90% of pancreas is lost.
Chronic pancreatitisChronic pancreatitis

77. • Presents as mild epigastric abdominal pain,
nausea, vomiting
• Pts. May appear chronically ill, w/sign of
pancreatic insufficiency such as weight loss,
steatorrhea, clubbing, polyuria
• Differentiating acute vs chronic pancreatitis is
difficult b/c primary distinction is based on
disease reversibility
Chronic pancreatitisChronic pancreatitis

79. DIFFERENTIAL DIAGNOSIS
• Pancreatic cancer (most important)
– older age
– absence of a history of alcohol use
– weight loss
– a protracted flare of symptoms
– onset of significant constitutional symptoms
– pancreatic duct stricture greater than 10 mm in length on ERCP
– Markers such as CA 19-9 and CEA
• peptic ulcer disease
• gallstones
• irritable bowel syndrome
• Acute pancreatitis

80. • Tests of function – hormone stimulation
– Secretin/ secretin CCK test
– Fecal elastase
– Fecal chymotrypsin
– Serum trypsinogen (trypsin)
– Fecal fat
– Blood glucose
–Tests of structure
– Endoscopic US
– ERCP
– MRI/MRCP/CT
– Abdominal US
– Plain abdominal film

81. US or CT grading system
• Normal – no abnormality on good quality study
• Equivocal – mild parenchymal duct dilatation (2-4mm)
– gland enlargement <2 fold
• Mild –moderate - + duct dilatation >4mm,
» duct irregularity,
» cavity < 10mm,
» parenchymal heterogenity,
» increased echo of duct wall,
» irregular head and body,
» focal parenchymal necrosis
• Severe - + cavity >10mm,
» intraductal filling defects,
» caliculi/ pancreatic calcification,
» ductal obstruction/stricture,
» severe ductal dilatation or irregularity,
» contiguous organ invasion

83. Complications
• Cobalamin malabsorption
– Excess binding by cobalamin binding proteins other than
intrinsic factor which were degraded by pancreatic
enzymes
• DM – but end organ damages of DM and DKA are rare
• Non DM retinopathy (peripheral) due to Vit A and Zn defc.
• Pleural, peritoneal and pericardial effusions with high
amylase
• GI bleeding – PUD, gastritis, pseudocyst, varies (SV
thrombosis)
• Cholestasis, icterus, cholangitis, biliary cirrhosis
• Fistula – internal or external
• Subcutaneous fat necrosis – tender red nodules on the shins
• Pseudocyst, obstruction
• Pancreatic carcinoma – 4% life time risk
•

84. Chronic Pancreatitis
• Nonoperative management
– Control of abdominal pain
• Can be a problem (drug dependency)
• In some patients total abstinence from alcohol relieves
the pain
• Dietary changes are also recommended
– Treatment of endocrine insufficiency
– Treatment of exocrine insufficiency

85. Chronic Pancreatitis
• Operative management
– Ampullary procedures
• Designed to eliminate pancreatitis by preventing bile reflux into
the pancreatic duct (results have not been favorable)
– Ductal drainage procedures
• Designed to decompress the pancreatic duct in a retrograde
manner
– Pancreaticojejunostomy (success rates of 60-90%)
– Ablative procedures (last step)
• Pancreatectomy (total or subtotal)
– Most obtain adequate pain relief however these procedures can
cause IDDM

86. T h a n k y o u