Acute inflammation of the pancreas most commonly caused by gallstones and alcohol excess

Aetiology

'I GET SMASHED'

• Idiopathic
• Gallstones - up to 65% of cases
• Ethanol
• Trauma
• Steriods
• Mumps - and other infections e.g. coxsackie B, viral hepatitis
• Autoimmune - IgG4 related disease, polyarteritis nodosa
• Scorpion bite
• Hypercalcaemia; Hyperparathyroidism, Hyperlipidaemia
• ERCP
• Drugs e.g. azathioprine

Pathophysiology

1. Each cause will trigger a premature and exaggerated activation of the digestive enzymes within the pancreas
2. The resulting pancreatic inflammatory response causes an increase in vascular permeability and subsequent fluid shifts → hypovolemic shock
3. Enzymes are released from the pancreas into the systemic circulation, causing autodigestion of fats and blood vessels
   1. Fat necrosis affects Ca2+ binding → hypocalcaemia
   2. Autodigestion of blood vessels → retroperitoneal haemorrhage
4. Severe end-stage pancreatitis will eventually result in partial or complete necrosis of the pancreas (due to compromised blood supply)
5. The necrotic tissue can become infected → release of toxic metabolites into the blood (shock, pulmonary compromise, acute renal failure) and peritoneal cavity (abscess formation)