Acute Pancreatitis

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
  1. The resulting pancreatic inflammatory response causes an increase in vascular permeability and subsequent fluid shifts → hypovolemic shock
  1. 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
  1. Severe end-stage pancreatitis will eventually result in partial or complete necrosis of the pancreas (due to compromised blood supply)
  1. The necrotic tissue can become infected → release of toxic metabolites into the blood (shock, pulmonary compromise, acute renal failure) and peritoneal cavity (abscess formation)

Clinical presentation

Symptoms

  • Severe acute onset epigastric pain
    • Classically pain radiates through to back
    • Worse with eating, relieved by leaning forward
  • Nausea and vomiting
  • Jaundice indicates gallstone aetiology

Signs

  • Diffuse upper abdominal tenderness +/- guarding
  • Normal bowel sounds
  • If severe - widespread guarding and absent bowel sounds
  • Skin changes (less common, represent retroperitoneal haemorrhage)
    • Cullen’s sign - periumbilical bruising
    • Grey Turner’s sign - flank bruising
notion image

Investigations

Bloods

  • Serum amylase - 3x the upper limit of normal is diagnostic
  • LFTs - if cholestatic indicates gallstone aetiology
  • Others:
    • ↑ CRP, WBC, urea, AST/ALT, glucose
    • ↓ calcium

Imaging

  • USS - if underlying cause is unknown, typically used to identify gallstones
  • AXR - not routinely performed, can show a sentinel loop sign
  • CT may be required if initial assessment and investigations prove inconclusive - only use 6-10 days after admission in patients with features of persistent inflammatory response or organ failure

Management

  • Supportive - fluid resuscitation, O2, broad spectrum prophylactic antibiotics in confirmed pancreatic necrosis
  • Treat underlying cause once patient stabilized e.g. cholecystectomy if gallstones

Complications

Pancreatic pseudocyst

  • Fluid collections become surrounded with granulation tissue
  • May cause biliary obstruction or gastric outlet obstruction
  • Presents with pain, nausea and vomiting, jaundice, weight loss, fullness in epigastrium
  • Management - nothing, drainage, resection

Pancreatic abscesses

  • Larger pseudocysts/areas of necrosis may become infected
  • Should be drained to control sepsis - CT/US guided

Haemorrhage

  • Due to pseudoaneurysm, necrosis or pseudocysts