Lecture 33

All Flesh

Finger of the liver

ACUTE PANCREATITIS • Acute pancreatitis is reversible pancreatic

parenchymal injury associated with inflammation.

• Mild form

Severe form

Acute Interstitial Pancreatitis

Acute Necrotizing Pancreatitis

Two Types:

Edematous

Epidemiology• Acute pancreatitis is relatively common, with

an annual incidence rate in Western countries of 10 to 20 cases per 100,000 people.

Epidemiology• Biliary tract disease and

• alcoholism account for approximately

80% of cases in

Western countries.

EpidemiologyGallstones are present in 35% to

60% of cases of acute pancreatitis, and about 5% of patients with gallstones develop pancreatitis.

Epidemiology• The male-to-female ratio is 1 : 3 in the

group with biliary tract disease and

6 : 1 in those with alcoholism.

Etiologic factors

Tityus TrinitatisFound in Central/ South America and the Caribbean

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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

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.

Pathogenesis cont

• The inappropriate activation of

trypsinogen is an important triggering event in acute

pancreatitis.

Pathogenesis (Alcohol)

1. Obstruction of small pancreatic ducts 2.Contraction of Sphincter Oddi 3. Direct toxic effects on acinar cells

Three proposed pathways in the pathogenesis of Acute Pancreatitis3 possible events in the pathogenesis of

acute pancreatitis:

1.Duct obstruction2.Acinar Cell injury3.Defective intracellular transport

Morphology

• Macroscopically, the pancreatic substance shows areas of

• red-black hemorrhage • interspersed with • foci of yellow-white, chalky fat necrosis.

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

Morphology cont.

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

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

Inflammatory Spread

Due to the pancreas lacking a capsule, the inflammation and necrosis can extend to include fascial layers in the immediate vicinity of the pancreas.

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)

• Grey Turner sign • Cullen’s sign

Clinical features• Full-blown acute pancreatitis is a medical

emergency. These patients usually have the sudden calamitous onset of an

“acute abdomen.”

DiagnosisLaboratory 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.

4. Hypocalcemia may result from precipitation of calcium soaps in necrotic fat; if persistent, it is a poor prognostic sign.

5. Hyperglycemia6. Increased Hematocrit7. Leukocytosis8. Hyperbilirubinemia9. Inc. LDH10. Hypertriglyceridemia

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

Imaging• Direct visualization of the enlarged inflamed

pancreas by radiography is useful in the diagnosis of pancreatitis.

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

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

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.

Treatment