Pancreatitis

“Inflammation of the pancreas by enzyme-mediated autodigestion”

Risk Factors

• Alcohol
• Gallstones
• Cancer

Aetiology

Mnemonic IGETSMASHED:

• Idiopathic
• Gallstones (most common cause)
• Ethanol (most common cause)
• Trauma
• Steroids
• Mumps – and other infections
• Autoimmune
• Scorpion venum
• Hypercalcaemia, hyperlipidaemia
• ERCP (iatrogenic)
  • Sphincterotomy in ERCP can cause localised inflammation and oedema which blocks pancreatic duct and cause backflow
• Drugs
  • e.g. azathioprine, ACE-I, statins, metformin, antibiotics (metronidazole, tetracycline), valproic acid, diuretics, sulfasalazine/mesalazine

Pathophysiology

• Premature activation of zymogen granules in pancreas → protease release and autodigestion of pancreatic tissue → inflammation of pancreas → ­ inflammation from activation of the complement cascade
• Damage to pancreatic tissue results in high lipase and amylase concentrations in blood as pancreatic enzymes are released from pancreatic acinar cells

Clinical Presentation

Investigations

• Initially:
  • ECG: indicated for every upper abdo pain and known cardiac Hx
  • ABG
  • FBC, LFT, U+Es, inflammatory markers
• Diagnosis:
  • Ultrasound: to look for gallstones or biliary obstruction
  • CT/MRCP
  • ↑ Inflammatory markers (CRP, WBC)
  • ↑ Serum amylase, lipase
    • Serum amylase 3x above the normal upper range
• Scoring systems:
  • APACHE II: Used in UHS on the ward and in ICU. Not specific for pancreatitis patients, used to stratify ICU patients
  • Modified Glasgow Score: score of 3 or more indicative of severe pancreatitis
    • PaO2 < 8 kPa
    • Age > 55
    • Neutrophils > 15
    • Calcium < 2mmol/L
    • Renal function – urea > 16
    • Enzymes – LDH > 600, AST > 200
    • Albumin <32
    • Sugar: BG > 10
  • Revised Atlanta criteria (for severity scoring) – based on organ failure, local complications, early prognostic signs
    • Mild – No organ failure, no local complications, no systemic complications
    • Moderate – Transient organ failure (<48hrs), local complications, exacerbation of comorbidity
    • Severe – Persistent Organ Failure (>48hrs)

Management

• Supportive management:
  • O2
  • Aggressive fluid resus – due to SIRS
    • 1L bolus followed by 2-3L in 24hrs based on urine output, renal function
    • SIRS (systemic response to inflammation) à cytokine storm à leaky capillaries à fluid shift out of intravascular component and sequestration of fluid in third space à hypovolaemic shock
  • Urinary catheter – monitor urine output, fluid balance
  • Analgesia
  • NO EVIDENCE FOR NBM – early oral feeding in first 24h if tolerated
    • Essential to optimise nutrition to aid response to systemic inflammation
    • Helps pancreas function normally and keeps enterocytes healthy
  • NGT/NJT/TPN if oral feeding not tolerated
  • Consider early escalation to ITU
• Surgical management:
  • ERCP with sphincterotomy, cholecystectomy – if gallstones implicated
    • Sphincterotomy: Small cut made in the sphincter of Ampulla of Vater to widen opening and aid drainage of debris/fluid/stones in the duct system
  • Surgery for complications e.g. Debridement of pancreatic necrotic tissue
• Other management:
  • Alcohol avoidance
  • Smoking cessation
  • Oral pancreatic enzyme supplements (Creon) may be needed

Complications

• Organ failure: SIRS, shock, renal failure, ARDS (pancreas inflammation can affect diaphragm and lungs above it)
• Pancreatic oedema or collection
• Pancreatic pseudocyst
• Pancreatic necrosis
• Haemorrhage (pseudoaneurysms) – can be life-threatening/catastrophic
  • Due to protease digestion of blood vessels or erosion of adjacent luminal organs around pancreas e.g. duodenum
  • Coeliac axis or gastroduodenal artery may be affected
  • Usually occurs later during hospitalisation or during procedures
• Splenic or portal vein thrombosis
  • Occur due to localised inflammation giving rise to hyperthrombotic state
  • The very common and well-recognised complication occurs even in early disease
  • Prophylactic anticoagulation
• DIC (disseminated intraarticular coagulopathy)