1) Acute pancreatitis is reversible pancreatic injury caused by inflammation that can range from mild to severe. 2) The most common causes in Western countries are biliary tract disease (35-60% of cases) and alcoholism, which together account for 80% of cases. 3) The pathogenesis involves inappropriate activation of trypsinogen within the pancreas, which triggers activation of other enzymes that cause autodigestion and inflammation through various pathways.

1. Lecture 33
All Flesh
Finger of the liver

2. ACUTE PANCREATITIS
• Acute pancreatitis is reversible
pancreatic parenchymal injury associated
with inflammation.
• Mild form
Severe form
Acute Interstitial Pancreatitis
Acute Necrotizing
Two Types:
Edematous

3. Epidemiology
• Acute pancreatitis is relatively common, with
an annual incidence rate in Western
countries of 10 to 20 cases per
100,000 people.

4. Epidemiology
• Biliary tract disease and
•alcoholismaccount for approximately
80% of cases in
Western countries.

5. Epidemiology
Gallstonesare present in 35%
to 60% of cases of acute pancreatitis,
and about 5% of patients with gallstones
develop pancreatitis.

6. Epidemiology
• The male-to-female ratio is 1 : 3 in the
group with biliary tract disease and
6 : 1 in those with alcoholism.

7. Etiologic factors

8. Tityus Trinitatis
Found in Central/ South America and
the Caribbean
»
»

9. Pathogenesis
• Pancreatic enzymes are synthesized in an inactive
proenzyme form. If trypsin is inappropriately
activated it can in turn activate other proenzymes
such as prophospholipase and proelastase.
• Prophospholipase degrade fat cells and
Proelastase damage the elastic fibers of blood
vessels.
Autodigestion

10. Pathogenesis cont.
• Trypsin also converts prekallikrein to its
activated form, thus bringing into play the kinin
system and, by activation of
• Hageman factor (factor XII),
• the clotting and
• complement systems as well.
• In this way inflammation and small-vessel
thromboses are amplified.

11. Pathogenesis cont
• The inappropriate activation of
trypsinoge
n
is an important triggering event in acute
pancreatitis.

12. Pathogenesis (Alcohol)
1. Obstruction of small pancreatic ducts
2.Contraction of Sphincter Oddi
3. Direct toxic effects on acinar cells

13. Three proposed pathways in the
pathogenesis of Acute Pancreatitis
3 possible events in the pathogenesis of
acute pancreatitis:
1.Duct obstruction
2.Acinar Cell injury
3.Defective intracellular transport

15. Morphology
• Macroscopically, the pancreatic substance
shows areas of
• red-black hemorrhage
• interspersed with
• foci of
yellow-white, chalky fat
necrosis.

18. Morphology cont.- Mild form
Milder form, acute interstitial
pancreatitis,
1.Mild inflammation,
2.Interstitial edema, and
3.Focal areas of fat necrosis
Acute Interstitial Pancreatitis

19. Morphology cont.
• A hallmark of acute pancreatitis is a
manifestation of the inflammatory response,
namely the recruitment of
neutrophils to the pancreas.

20. Morphology cont. Severe Form
• In the more severe form, acute necrotizing
pancreatitis, the acinar and ductal tissues as well
as the islets of Langerhans are necrotic. Vascular
injury can lead to hemorrhage into the
parenchyma of the pancreas.
Acute Necrotizing Pancreatitis

22. Inflammatory Spread
Due to the pancreas lacking a capsule, the inflammation and necrosis can extend to

23. SignS &
SymptomS• Severe epigastric abdominal pain - abrupt onset (may
radiate to back)
• Nausea & Vomiting
• Weakness
• Tachycardia
• +/- Fever; +/- Hypotension or shock
– Grey Turner sign - flank discoloration due to
retroperitoneal bleed in pt. with pancreatic necrosis (rare)
– Cullen’s sign - periumbilical discoloration (rare)

24. • Grey Turner sign • Cullen’s sign

25. Clinical features
• Full-blown acute pancreatitis is a medical
emergency. These patients usually have the
sudden calamitous onset of an
“acute
abdomen.”

26. DiagnoSiS
Laboratory findings include marked elevation of
1. serum amylase levels during the first 24
hours,
2. followed by a rising serum lipase level.
3.Glycosuria occurs in 10% of cases.

27. 4. Hypocalcemia may result from
precipitation of calcium soaps in necrotic fat;
if persistent, it is a poor prognostic sign.
5. Hyperglycemia
6. Increased Hematocrit
7. Leukocytosis
8. Hyperbilirubinemia
9. Inc. LDH
10. Hypertriglyceridemia

28. Diagnosis
• ↑ amylase…Nonspecific !!!
– Amylase levels > 3x normal very suggestive of pancreatitis
• May be normal in chronic pancreatitis!!!
– Enzyme level ≠ severity
– False (-): acute on chronic (EtOH); HyperTG
– False (+): renal failure, other abdominal or salivary gland
process, acidemia
• ↑ lipase
– More sensitive & specific than amylase

29. Imaging
• Direct visualization of the enlarged inflamed
pancreas by radiography is useful in the
diagnosis of pancreatitis.

30. Prognosis
• 85-90% mild, self-limited
–Usually resolves in 3-7 days
• 10-15% severe requiring ICU
admission
–Mortality may approach 50% in severe
cases

31. Complications
• Acute respiratory distress syndrome
• Acute renal failure
• A sterile pancreatic abscess
• A pancreatic pseudocyst.

32. Treatment/ Management
• The key to the management of acute
pancreatitis is “resting” the pancreas by
total restriction of oral intake and
• by supportive therapy with intravenous
fluids and analgesia.

33. Treatment