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Pancreatitis
Acute or Chronic
inflammation of pancreas
Types
 Acute-
 Acute onset, boring epigastric pain
 Associated with nausea & vomiting
 Lipase & amylase >3 times elevated
 Chronic-
 Recurrent or persistent boring epigastric pain
 Associated with steatorrhea ± glucose intolerance
 ± elevated amylase/lipase
Causes
 Gallstones or biliary sludge
 Alcoholism
 Others-
 Hypertriglyceridemia- TG >1000 mg/dl
 Hypercalcemia
 Mumps, coxsackie virus
 Trauma or post-ERCP
 Pancreas divisum
 Drugs- didanosine, pentamidine, HCTZ, Na valproate,
L-asparaginase, estrogen etc.
Pathophysiology
 Whatever the etiology,
causes raised pancreatic ductal pressure
 Premature activation of pancreatic enzymes-
trypsin, phospholipase, elastase
 Local tissue destruction &
activate inflammatory cascade
 Inflammation, edema, hemorrhage, necrosis
 Acute- SIRS with multiorgan dysfunction,
Chronic- fibrosis &
loss of function
Diagnosis
 History & examination
 Lipase ± amylase
 CBC, RBS, Ca, TG, bilirubin, SGOT, ABG
 AxR- calcification, gallstones, ileus
 CxR- atelectasis, effusion, ARDS
 US- gallstones, biliary tract
 CT scan- necrosis, fluid collection,
pseudocyst
 MRI/MRCP
 ERCP/EUS- in chronic pancreatitis
Ranson’s prognostic criteria- Acute
 On admission-
 Age >55 years
 Blood glucose >200
 LDH >350
 SGOT >250
 WBC/TLC >16000
 Px-
 <3- mortality ~5%
 >3- mortality 15-20%
 After 48 hours-
 Hct drop >10%
 BUN increase >5
 Ca <8
 PaO2 <60
 Base deficit >4
 Estimated fluid sequestration
>6 litres
Balthazar CT grading- Acute
CT severity index based on
CT appearance & %age necrosis
Treatment
 Pain control- opioids
 Bowel rest & IV fluids
 Antiemetics & PPI
 Post-pyloric enteral feeding- NG feed
 IV Abx- if necrosis >30% or abscess
 Enzyme & dietary supplementation- chronic
 ERCP with sphincterotomy, if required- acute
 Surgery-
 Infected necrosis- acute
 Pseudocyst drainage, possible endoscopically too
 Bypass or partial/total resection for pain control- chronic

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Pancreatitis

  • 2. Types  Acute-  Acute onset, boring epigastric pain  Associated with nausea & vomiting  Lipase & amylase >3 times elevated  Chronic-  Recurrent or persistent boring epigastric pain  Associated with steatorrhea ± glucose intolerance  ± elevated amylase/lipase
  • 3. Causes  Gallstones or biliary sludge  Alcoholism  Others-  Hypertriglyceridemia- TG >1000 mg/dl  Hypercalcemia  Mumps, coxsackie virus  Trauma or post-ERCP  Pancreas divisum  Drugs- didanosine, pentamidine, HCTZ, Na valproate, L-asparaginase, estrogen etc.
  • 4. Pathophysiology  Whatever the etiology, causes raised pancreatic ductal pressure  Premature activation of pancreatic enzymes- trypsin, phospholipase, elastase  Local tissue destruction & activate inflammatory cascade  Inflammation, edema, hemorrhage, necrosis  Acute- SIRS with multiorgan dysfunction, Chronic- fibrosis & loss of function
  • 5. Diagnosis  History & examination  Lipase ± amylase  CBC, RBS, Ca, TG, bilirubin, SGOT, ABG  AxR- calcification, gallstones, ileus  CxR- atelectasis, effusion, ARDS  US- gallstones, biliary tract  CT scan- necrosis, fluid collection, pseudocyst  MRI/MRCP  ERCP/EUS- in chronic pancreatitis
  • 6. Ranson’s prognostic criteria- Acute  On admission-  Age >55 years  Blood glucose >200  LDH >350  SGOT >250  WBC/TLC >16000  Px-  <3- mortality ~5%  >3- mortality 15-20%  After 48 hours-  Hct drop >10%  BUN increase >5  Ca <8  PaO2 <60  Base deficit >4  Estimated fluid sequestration >6 litres
  • 7. Balthazar CT grading- Acute CT severity index based on CT appearance & %age necrosis
  • 8. Treatment  Pain control- opioids  Bowel rest & IV fluids  Antiemetics & PPI  Post-pyloric enteral feeding- NG feed  IV Abx- if necrosis >30% or abscess  Enzyme & dietary supplementation- chronic  ERCP with sphincterotomy, if required- acute  Surgery-  Infected necrosis- acute  Pseudocyst drainage, possible endoscopically too  Bypass or partial/total resection for pain control- chronic