Acute pancreatitis

• Self perpetuating pancreatic inflammation
• Extracellular fluid is trapped in the gut, peritoneum and retroperitoneum
• There may be rapid progression from mild oedema to necrotising pancreatitis
• In fulminating cases the pancreas is replaced by black fluid
• Contributory factors include protease induced activation of complement, kinin, fibrinolytic and coagulation cascades

Signs

• May be mild in severe disease
• Tachycardia
• Fever
• Jaundice
• Shock
• Ileus
• Rigid abdomen
• Local/generalised tenderness
• Periumbilical discolouration – Cullen’s sign
• Bruising of the flanks – Grey-Turner’s sign

Tests

• Raised serum amylase – excreted renally so renal failure results in raised levels
• Serum lipase is more sensitive and more specific
• ABG to monitor oxygenation and acid-base status
• AXR – no psoas shadow. Sentinal loop of proximal jejunum (solitary air filled dilation)
• Erect CXR can help exclude other causes e.g. perforation
• CT
• US

Management

• IV fluids
• Analgesia – pethidine or morphine
• Hourly obs
• If worsening ITU
• Keep patient NBM and pass an NG tube

Complications

• Early
  • Shock
  • ARDS
  • Renal failure
  • DIC
  • Sepsis
  • Low calcium
  • Raised glucose
• Late
  • Pancreatic necrosis and pseudosyst (fluid in the lesser sac)
  • Abscess
  • Bleeding
  • Thrombosis

Severity assessed by Glasgow criteria – PANCREAS

• Based on;
  • PaO2
  • Age
  • Neutrophils
  • Calcium
  • Renal function
  • Enzymes (LDH, AST)
  • Albumin
  • Sugar