6. Gallstone pancreatitis
• Mechanism is not entirely clear
• Common-channel theory
“Blockage below junction of biliary and
pancreatic duct cause bile flow into
pancrease”
BUT…
– short channel that stone located would
block both biliary and pancreatic duct
–Hydrostatic pressure in biliary<pancreatic
duct
7. Another proposed mechanism
• Gallstone through sphincter of Oddi
renders it incompetent. – Questionable
BUT…
–transit time through sphincter??
–sphincterotomy not routine cause
pancreatitis
8. Mechanism???
• Ductal hypertension
– Cause rupture of small ducts and
leakage of pancreatic juice
– pH in pancreatic tissue ↓
– activation of protease
– “Colocalization”
9. Alcoholic pancreatitis
• Common in pt. alcohol drinking > 2yr.
• Often much longer upto 10 yr.
• Sphincter spasm
• Decrease pancreatic blood flow
14. Diagnostic criteria
Two of following three features
•Upper abd. pain of acute onset often
radiating to back
•Serum amylase or lipase > 3times normal
•Finding on cross sectional abd. imaging
Reference : 2012 revision of atlanta classification of acute pancreatits
15. Physical exam
•Grey Turner’s Sign
- ecchymosis in 1 or both flanks
•Cullen’s sign
- ecchymosis in periumbilical area
•Associated with Necrotizing pancreatitis
• poor prognosis occurs in 1% of cases
19. Serum amylase
• Elevates within HOURS and can remain
elevated for 3-5 days
• High specificity when level >3x normal
• Many false positives (see next slide)
• Most specific = pancreatic isoamylase
(fractionated amylase)
20. Urine amylase
• urinary levels may be more sensitive
than serum levels.
• Urinary amylase levels usually remain
elevated for several days after serum
levels have returned to normal.
21. Serum lipase
• The preferred test for diagnosis
• Begins to increase 4-8H after onset of
symptoms and peaks at 24H
• Remains elevated for days
• Sensitivity 86-100% and Specificity 60-
99%
• >3X normal S&S ~100%
27. Radiologic Findings
• Plain radiographs contribute little
• Ultrasound may show the pancreas in
only 25-50%
• CT scan provides better information
–Severity and prognosis
–Exclusion of other diseases
• EUS & MRI with MRCP – cause of
pancreatitis
29. Classification of severity
- Mild : lack of organ failure and
complications
- Moderate : transient organ failure
and/or complications < 48hr
- Severe : persistent organ failure and
complications
Reference : 2012 revision of atlanta classification of acute pancreatits
33. Ranson’s Criteria (GB Pancreatitis)
• At Admission
Age > 70 yr
WBC > 18,000/mm3
Blood glucose > 220 mg/dL
Serum lactate dehydrogenase > 400IU/L
Serum aspartate aminotransferase >250IU/L
• During Initial 48 hr
Hematocrit decrease of > 10%
BUN increase of >2 mg/dL
Serum calcium <8mg/dL
Arterial pO2 NA
Serum base deficit > 5 mEq/Lio
Fluid sequestration > 4L
34. APACHE II
• Measure at during the first 24 hours
after admission
• Using a cutoff of ≥8
• The American Gastroenterological
Association (AGA) recommends:
Prediction of severe disease by the
APACHE II system
37. CT severity score
Grading based upon findings on unenhanced CT
Grade Findings Score
A Normal pancreas –without peripancreatic enhancement 0
B Focal or diffuse enlargement of the pancreas,
enhancement may be inhomogeneous on peripancreatic
1
C Peripancreatic inflammation with intrinsic pancreatic
abnormalities
2
D Intrapancreatic or extrapancreatic fluid collections 3
E Two or more large collections of gas in the pancreas or
retroperitoneum
4
Necrosis score based upon contrast enhanced CT
Necrosis, percent Score
0 0
<33 2
33-50 4
≥50 6
≥6 = severe disease.
39. Treatment
• General Considerations
- adequate IV hydration and analgesia
- NPO
- NG tube: not routinely used
* But may be used in patients with ileus or intractable N/V
• Nutrition
• Early enteral feeding
• Nasojejunal tube feeding
• PPN,TPN
40. Nutrition
• Used high protein, low fat, semi-
elemental feeding (eg, Peptamen AF)
because reduced pancreatic digestive
enzymes.
• Start at 25 cc/hr and advanced to at
least 30% of daily requirement
(25 kcal/kg IBW)
41. Nutrition
• Signs that the formula is not
tolerated include
- gastric residual volumes >400 cc
- vomiting (with nasogastric feeding)
- bloating
- diarrhea (>5 watery stools or >500 mL/d)
42. Treatment
• Metabolic Complications
- Correction of electrolyte imbalance - Ca,Mg
- Cautiously for hyperglycemia
• Cardiovascular Care
• Respiratory Care
• Deep vein thrombosis prophylaxis
43. Prophylactic antibiotics
–Although this is still an area of debate
–Not indicated for mild attack
–suggest imipenem or meropenem
for 14 days for patients with proven
necrosis
44. TREATMENT OF
ASSOCIATED CONDITIONS
• Gallstone pancreatitis
– ERCP should be performed within 72
hours in those with a high suspicion of
persistent bile duct stones
– EUS & MRCP should be considered in case
that clinical is not improving sufficiently
– Cholecystectomy +/- IOC
45. Cholecystectomy??
• should be performed after recovery in all
patient with gallstone pancreatitis
• Failure to perform a cholecystectomy
is associated with a 25-30% risk of recurrent
acute pancreatitis, cholecystitis, or cholangitis
within 6-18 weeks
46. Cholecystectomy
• In mild pancreatitis case, an usually be
performed safely within 7 days after recovery
• In severe pancreatitis case ,delaying for at
least 3 wks may be reasonable
• If high suspicion of CBD stones, preoperative
ERCP is the best test that therapeutic
intervention will be required
• If low suspicion,intraoperative cholangiogram
during cholecystectomy may be preferable to
avoid the morbidity associated with ERCP
48. Local Complications
• Pseudocyst
• Abscess
• Necrosis
–Sterile
–Infected
Mild pancreatitis severe pancreatitis
Pseudocyst abscess
Pancreatic necrosis
49. New Classification Based on
Contrast-Enhanced CT (CECT)*
• Interstitial Edematous Pancreatitis
–Acute Peripancreatic Fluid Collection
–Pancreatic Pseudocyst
• Necrotizing Pancreatitis
–Acute Necrotic Collection
–Walled-Off Necrosis
50. Interstitial Edematous VS Necrotizing
• Interstitial Edematous Pancreatitis
– Pancreatic parenchyma enhances with the
contrast agent
– Lack of peripancreatic necrosis
• Necrotizing Pancreatitis
– Pancreatic parenchymal areas without IV
contrast enhancement +/- Peripancreatic
necrosis (see below—ANC and WON)
52. Acute Peripancreatic Fluid
Collection (APFC):
Occurring within the first 4 weeks in the
setting of interstitial edematous pancreatitis.
• CECT Criteria
–Homogeneous fluid adjacent to pancreas
confined by peripancreatic fascial planes
–No recognizable wall
53. Pancreatic Pseudocyst
• An encapsulated, well-defined collection of
fluid but no or minimal solid components
• Occurs >4 weeks after onset of in interstitial
edematous pancreatitis
• CECT Criteria
– Well-defined wall , homogeneous, round
or oval fluid collection
– No solid component
– Only in interstitial edematous pancreatitis
55. Acute Necrotic Collection(ANC)
• A collection of both fluid and solid
components (necrosis) occurring during
necrotizing pancreatitis.
• This collection can involve the pancreatic
and/or the peripancreatic tissues
• CECT Criteria
– Heterogeneous
– No encapsulating wall
– Intrapancreatic and/or extrapancreatic
56. Walled-Off Necrosis(WON)
• A mature, encapsulated ANC with a well-
defined inflammatory wall
• these tend to mature >4 weeks after onset of
necrotizing pancreatitis.
• CECT Criteria
– Heterogenous
– Well-defined wall
– Intrapancreatic and/or extrapancreatic
63. Management of pseudocyst
• Watchful waiting:
- Operative intervention was recommended
following an observation period of 6 wks
- However, there are some reports support
more conservative approach
64. Management of pseudocyst
• Surgical drainage – gold standard
Open vs endoscopic
–cystgastrostomy
–Cystenterostomy
–Cystojejunostomy, Cystoduodenostomy
–Ressection
65. Management of pseudocyst
• Percutaneous catheter drainage
– As effective as surgery in draining and closing both
sterile and infected pseudocysts
– Catheter drainage is continued until the flow rate
falls to 5-10 mL/day
– If no reduction in flow, octreotide
(50 -200 µg SC q 8hr) may be helpful.
– Should follow-up CT scan when the flow rate is
reduced to ensure that the catheter is still in the
pseudocyst cavity
– more likely to be successful in patients
without duct-cyst communication
68. Timing of debridement
• The optimal timing is at least 3-4wks
following the onset of acute pancreatitis.
• Delayed debridement allows
– clinical stabilization of the patient
– resolution of early organ failure
– decreased inflammatory reaction, and
necrotic areas are demarcated
69. Surgical approach
• Open debridement with external drainage
– gold standard
• Open debridement with internal drainage and
cystgastrostomy
- only appropriate for patients with WON
• Open packing
— Open packing with planned reoperation every
48-72 hrs until the necrosis is adequately removed
• Laparoscopic debridement
-Video-assisted retroperitoneal debridement
-Laparoscopically-assisted transperitoneal
debridement
Hinweis der Redaktion
In animal flow of bile to pancreatic duct not result in pancreatitis
transit time through sphincter, sphincterotomy not routine cause pancreatitis
Colocalization In normal pancreatitis , zymogen and inactive enz found in discrete organelle
C-reactive protein (CRP) is one of the acute phase reactants made by the liver in response to interleukin-1 and interleukin-6. Its utility for predicting the severity of pancreatitis has been studied at admission and at 24, 48, and 72 hours. A review of the literature estimated that at 48 hours, it had a sensitivity, specificity, positive predictive value, and negative predictive value of 80, 76, 67, and 86 percent, respectively, using a cutoff of 150 mg/L [ 9 ]
A benefit of enteral nutrition is its ability to maintain the intestinal barrier and prevent bacterial translocation from the gut, which may be a major cause of infection
The ACG guidelines do not recommend. if used, should be restricted to patients with pancreatic necrosis (>30 %) and continue no more than 14 d. Guidelines from the Italian Association recommend antibiotics for patients with CT-proven necrosis
A, Mild acute pancreatitis showing normal enhancement of the body of pancreas after intravenous contrast. B, Severe acute pancreatitis showing pancreatic necrosis with areas of the pancreas not enhancing after IV contrast compared with areas that are normal C, Pseudocyst of the pancreas with clear-appearing fluid within the collection near the pancreas. D, Pancreatic abscess with presence of gas inside the cavity. E, Pancreatic necrosis (necrotic collection), which appears on CT scan as a clear fluid collection The same collection on MRI shows areas of necrotic debris (black arrowhead) not observed on CT scan
Pic 1 Arrows show peripancreatic stranding.
Series of 75 patients. Surgery was undertaken only for significant abdominal pain, complications, or progressive enlargement of a cyst. 52% underwent surgery for these indications, while the remaining patients were followed conservatively. Among patients in the latter group, 60% had complete resolution at one year, and only one had a pseudocyst-related complication
in one series of 52 patients, the mean duration of drainage was 42 days