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Acute Pancreatitis
By: Jaber Mohammed Zarbah
Supervisor: Dr. Mosaab Dahab
Physiology of Pancreas
• It is exocrine and endocrine gland.
• Produce digestive enzymes(trypsin, amylase,
lipase)
• Regulatory enzymes(insulin, glucagon)
• Water and bicarbonate.
• Digestive enzymes regulated by acetylcholine
and cholecystokinin.
• Bicarbonate and water regulated by secretin.
Definition:
• Acute pancreatitis is an inflammatory condition of
the pancreas characterized clinically by abdominal
pain and elevated levels of pancreatic enzymes in the
blood or urine.
• Because of premature activation of pancreatic
enzymes within the pancreas leads to organ injury
and pancreatitis(autodigestion).
Classification:
According to Atlanta classification:
1. Interstitial edematous acute pancreatitis w/o tissue
necrosis
2. Necrotizing acute pancreatitis
 According to the severity:
1. Mild acute pancreatitis(absence of organ failure and local
or systemic complications)
2. Moderately acute pancreatitis(no organ failure or
transient organ failure (<48 hours) and/or local
complications)
3. Severe acute pancreatitis(persistent organ failure (>48
hours) that may involve one or multiple organs)
Etiologies:
Pathogenesis:
• Pancreatic duct obstruction occurs due to biliary tract stones
(commonest), duodenal ulcer, duodenal Crohn’s, periampullary
diverticulum/tumour, trauma, pancreatic duct stricture,
ascariasis.
• OR alcohol causes direct toxicity, hypersecretion of gastric and
pancreatic juices.
• Trypsinogen gets activated forming trypsin which activates
other enzymes
• Proelastate elastate (Causes capillary rupture)
• Prolipase lipase ( metabolise TG to glycerol + fatty acid
and fatty acid combined with Ca to form saponified fat
• Extruded of toxins, saponified fat, blood across the
basolateral membrane into the interstitium, where they act
as chemoattractants for inflammatory cells.
• Activated neutrophils then exacerbate the problem by
releasing superoxide proteolytic enzymes. Finally,
macrophages release cytokines(TNF-α, IL-6,8) that further
mediate local (and, in severe cases, systemic) inflammatory
responses.
• Increase pancreatic vascular permeability hemorrhage,
edema and necrosis.
Clinical presentation:
• The cardinal symptom is abdominal pain.
• Characters of the pain:
1. Site: usually epigastrium but it may be in UQs or whole
abdomen
2. Onset: sudden and the pain has no upper limit
3. Character: dull, boring and steady
4. Radiation: to back in 50%
5. Associated with: nausea, vomiting, retching, anorexia &
hiccough.
6. Time duration: persist for hours to days
7. Exacerbate in the supine position, refractory to the usual
analgesics and may relived by sitting or leaning forward.
Cont.
• Age *
• Ask the pt about recent operative or invasive
investigations(ERCP)
• Hyperlipidemia
• Alcohol consumption
• Previous biliary colic
• Hematemesis and melena
Physical examination:
Vital signs:
Fever(76%), tachypnea (common), tachycardia(65%)
and hypotension may be present.
 Inspection:
Varies from being well till gravely ill, pale, cyanotic,
jaundice(28%), diaphoretic and listless,
distention(65%), Grey Turner`s sign, Cullen`s sign
or Fox sign.
Cont.
Superficial palpation:
Tenderness, rebound tenderness, rigidity and guarding(68%).
Deep palpation:
Epigastrium mass due to inflammation.
Percussion:
Ascites with shifting dullness, pleural effusion(15%)
Auscultation:
Absence of bowel sound due to illeus.
DDx:
• Acute peritonitis
• Perforated duodenal ulcer
• Ruptured aortic aneurysm
• Cholangitis
• Cholecystitis
• Choronic panceratitis
• Intestinal obstruction
• Cholelithiasis
• MI
• Salpingitis
• Ectopic pregnancy
Diagnosis:
• Based on clinical presentation and elevated serum amylase
level (3-4 fold).
• Diagnostic imaging is unnecessary in most cases.
Labs:
• CBC (leuckocytosis > 12.000)*
Cont.
• Elevated serum amylase(commonly used)
• CRP
• Elevated serum lipase
• LFTs (AST)*
• Electrolytes (hypocalcaemia as a complication or
hypercalcaemia as a cause)
• Hyperglycemia
• Hyperlipidemia
• Amylase creatinine clearance.
• Pregnancy test
• LDH*
• Serum urea*
• PaO2*
Assessment of severity
Imaging:
 Chest and abdominal X-ray in erect position are not
diagnostic but are useful in ddx:
Sentinel loop, colon cut-off sign, calcified gall stones, pleural
effusion, calcified pancreas…etc
 Ultrasound should performed within 24hrs to detect gall
stones, rule out cholecystitis and dilated CBD
 CT with contrast indicated in:
1. There is doubt in diagnosis
2. Sever acute pancreatitis to determine the extent of
necrosis
3. Pts with organ failure & sepsis
4. Suspicion in localized complication(fluid, pseudocyst)
Sentinel loop: a single dilated
jejunal loop in the upper
abdomen.
Colon cut-off sign: dilated colon
to the mid-transverse colon with
no air seen behind the splenic
flexure. This is due to extension
of inflammation along
mesocolon.
Management:
It is on of acute abdomen treated conservatively.
Conservative (70-90%):
• Admission to ICU.
• NPO
• Rehydration(250-400ml/hr)
• Analgesia(don`t use morphine)
• In sever hemorrhage (FFP,PCV,Platlets)
• NG tube for aspiration and feeding.
• Urinary catheterization to maintain and monitor
urine output.
Cont.
• Antibiotics( ciprofloxacin + metronidazole)
• Calcium gluconate in hypocalcaemia
• If ultrasonograms show evidence of gallstones and
if the cause of pancreatitis is believed to be biliary, a
cholecystectomy should be performed during the
same hospital admission.
Cont.
Surgery (10-30%):
• If condition of patient deteriorates in spite of good
conservative treatment.
• If there is formation of pancreatic abscess, or
infected necrosis
• In severe necrotizing pancreatitis as a trial to save
the life of the patient which has got very high
mortality
• Open surgery is the gold standard for infected
pancreatic necrosis.
Complications:
Acute fluid collection:
• In or near the pancreas
• ill-defined or lacking fibrin wall
• Sterile fluid
• Usually resolve spontaneously
• Usually no intervention
• An acute fluid collection that does not resolve can
evolve into a pseudocyst or an abscess if it becomes
infected.
Sterile and infected pancreatic necrosis:
• Focal or diffuse of non-viable parenchyma with
peripancreatic necrosis.
• Sterile and due to translocation of gut bacteria
become infected.
• Diagnosed by CT with contrast
• Mortality rate up to 50% in infected necrosis
• No need intervention in sterile necrosis
• Infected necrosis treated by needle aspiration
under CT or ultrasonography guidance
• Laprotomy necrosectomy
Pancreatic abscess:
• Demarcated intra-abdominal collection of pus
• It may be acute collection or infected pseudocyst
• Diagnosis and management as in infected
pancreatic necrosis.
Pseudocyst:
• Collection of amylase rich fluid enclosed in fibrous
tissue.
• Often single
• Diagnosed by CT or US
• Pseudocyst resolve spontaneously in most cases
• Intervention advised if the pseudocyst cause
symptoms or complications.
• Cystogastrostomy is the choice.
Acute pancreatitis
Acute pancreatitis

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Acute pancreatitis

  • 1. Acute Pancreatitis By: Jaber Mohammed Zarbah Supervisor: Dr. Mosaab Dahab
  • 2.
  • 3.
  • 4. Physiology of Pancreas • It is exocrine and endocrine gland. • Produce digestive enzymes(trypsin, amylase, lipase) • Regulatory enzymes(insulin, glucagon) • Water and bicarbonate. • Digestive enzymes regulated by acetylcholine and cholecystokinin. • Bicarbonate and water regulated by secretin.
  • 5. Definition: • Acute pancreatitis is an inflammatory condition of the pancreas characterized clinically by abdominal pain and elevated levels of pancreatic enzymes in the blood or urine. • Because of premature activation of pancreatic enzymes within the pancreas leads to organ injury and pancreatitis(autodigestion).
  • 6. Classification: According to Atlanta classification: 1. Interstitial edematous acute pancreatitis w/o tissue necrosis 2. Necrotizing acute pancreatitis  According to the severity: 1. Mild acute pancreatitis(absence of organ failure and local or systemic complications) 2. Moderately acute pancreatitis(no organ failure or transient organ failure (<48 hours) and/or local complications) 3. Severe acute pancreatitis(persistent organ failure (>48 hours) that may involve one or multiple organs)
  • 8. Pathogenesis: • Pancreatic duct obstruction occurs due to biliary tract stones (commonest), duodenal ulcer, duodenal Crohn’s, periampullary diverticulum/tumour, trauma, pancreatic duct stricture, ascariasis. • OR alcohol causes direct toxicity, hypersecretion of gastric and pancreatic juices. • Trypsinogen gets activated forming trypsin which activates other enzymes • Proelastate elastate (Causes capillary rupture) • Prolipase lipase ( metabolise TG to glycerol + fatty acid and fatty acid combined with Ca to form saponified fat
  • 9. • Extruded of toxins, saponified fat, blood across the basolateral membrane into the interstitium, where they act as chemoattractants for inflammatory cells. • Activated neutrophils then exacerbate the problem by releasing superoxide proteolytic enzymes. Finally, macrophages release cytokines(TNF-α, IL-6,8) that further mediate local (and, in severe cases, systemic) inflammatory responses. • Increase pancreatic vascular permeability hemorrhage, edema and necrosis.
  • 10. Clinical presentation: • The cardinal symptom is abdominal pain. • Characters of the pain: 1. Site: usually epigastrium but it may be in UQs or whole abdomen 2. Onset: sudden and the pain has no upper limit 3. Character: dull, boring and steady 4. Radiation: to back in 50% 5. Associated with: nausea, vomiting, retching, anorexia & hiccough. 6. Time duration: persist for hours to days 7. Exacerbate in the supine position, refractory to the usual analgesics and may relived by sitting or leaning forward.
  • 11. Cont. • Age * • Ask the pt about recent operative or invasive investigations(ERCP) • Hyperlipidemia • Alcohol consumption • Previous biliary colic • Hematemesis and melena
  • 12. Physical examination: Vital signs: Fever(76%), tachypnea (common), tachycardia(65%) and hypotension may be present.  Inspection: Varies from being well till gravely ill, pale, cyanotic, jaundice(28%), diaphoretic and listless, distention(65%), Grey Turner`s sign, Cullen`s sign or Fox sign.
  • 13.
  • 14. Cont. Superficial palpation: Tenderness, rebound tenderness, rigidity and guarding(68%). Deep palpation: Epigastrium mass due to inflammation. Percussion: Ascites with shifting dullness, pleural effusion(15%) Auscultation: Absence of bowel sound due to illeus.
  • 15. DDx: • Acute peritonitis • Perforated duodenal ulcer • Ruptured aortic aneurysm • Cholangitis • Cholecystitis • Choronic panceratitis • Intestinal obstruction • Cholelithiasis • MI • Salpingitis • Ectopic pregnancy
  • 16. Diagnosis: • Based on clinical presentation and elevated serum amylase level (3-4 fold). • Diagnostic imaging is unnecessary in most cases. Labs: • CBC (leuckocytosis > 12.000)*
  • 17. Cont. • Elevated serum amylase(commonly used) • CRP • Elevated serum lipase • LFTs (AST)* • Electrolytes (hypocalcaemia as a complication or hypercalcaemia as a cause) • Hyperglycemia • Hyperlipidemia • Amylase creatinine clearance. • Pregnancy test • LDH* • Serum urea* • PaO2*
  • 19. Imaging:  Chest and abdominal X-ray in erect position are not diagnostic but are useful in ddx: Sentinel loop, colon cut-off sign, calcified gall stones, pleural effusion, calcified pancreas…etc  Ultrasound should performed within 24hrs to detect gall stones, rule out cholecystitis and dilated CBD  CT with contrast indicated in: 1. There is doubt in diagnosis 2. Sever acute pancreatitis to determine the extent of necrosis 3. Pts with organ failure & sepsis 4. Suspicion in localized complication(fluid, pseudocyst)
  • 20. Sentinel loop: a single dilated jejunal loop in the upper abdomen. Colon cut-off sign: dilated colon to the mid-transverse colon with no air seen behind the splenic flexure. This is due to extension of inflammation along mesocolon.
  • 21.
  • 22. Management: It is on of acute abdomen treated conservatively. Conservative (70-90%): • Admission to ICU. • NPO • Rehydration(250-400ml/hr) • Analgesia(don`t use morphine) • In sever hemorrhage (FFP,PCV,Platlets) • NG tube for aspiration and feeding. • Urinary catheterization to maintain and monitor urine output.
  • 23. Cont. • Antibiotics( ciprofloxacin + metronidazole) • Calcium gluconate in hypocalcaemia • If ultrasonograms show evidence of gallstones and if the cause of pancreatitis is believed to be biliary, a cholecystectomy should be performed during the same hospital admission.
  • 24. Cont. Surgery (10-30%): • If condition of patient deteriorates in spite of good conservative treatment. • If there is formation of pancreatic abscess, or infected necrosis • In severe necrotizing pancreatitis as a trial to save the life of the patient which has got very high mortality • Open surgery is the gold standard for infected pancreatic necrosis.
  • 26. Acute fluid collection: • In or near the pancreas • ill-defined or lacking fibrin wall • Sterile fluid • Usually resolve spontaneously • Usually no intervention • An acute fluid collection that does not resolve can evolve into a pseudocyst or an abscess if it becomes infected.
  • 27. Sterile and infected pancreatic necrosis: • Focal or diffuse of non-viable parenchyma with peripancreatic necrosis. • Sterile and due to translocation of gut bacteria become infected. • Diagnosed by CT with contrast • Mortality rate up to 50% in infected necrosis • No need intervention in sterile necrosis • Infected necrosis treated by needle aspiration under CT or ultrasonography guidance • Laprotomy necrosectomy
  • 28. Pancreatic abscess: • Demarcated intra-abdominal collection of pus • It may be acute collection or infected pseudocyst • Diagnosis and management as in infected pancreatic necrosis.
  • 29. Pseudocyst: • Collection of amylase rich fluid enclosed in fibrous tissue. • Often single • Diagnosed by CT or US • Pseudocyst resolve spontaneously in most cases • Intervention advised if the pseudocyst cause symptoms or complications. • Cystogastrostomy is the choice.