Key Facts

Acute pancreatitis is a common and potentially life-threatening condition. Early recognition, severity assessment, and supportive care are crucial. Gallstones and alcohol account for >75% of cases.

Epidemiology

Incidence is approximately 30-50 per 100,000 per year in the UK and is increasing. Hospital admissions for acute pancreatitis have doubled over 20 years. Gallstone pancreatitis is more common in women; alcoholic pancreatitis in men. Overall mortality is ~5% but rises to 30-50% in severe necrotising pancreatitis.

Aetiology

• Gallstones (~50%): stone migrating through/impacting at ampulla of Vater
• Alcohol (~25%): typically requires >5 years of heavy drinking (>80 g/day)
• Idiopathic (~15%): many likely microlithiasis or genetic
• Other: hypertriglyceridaemia (>11.3 mmol/L), hypercalcaemia, drugs, ERCP, autoimmune pancreatitis, pancreatic tumour, trauma, viral (mumps, CMV)

Pathophysiology

Premature activation of trypsinogen to trypsin within pancreatic acinar cells triggers an autodigestive cascade. In gallstone pancreatitis, transient biliary obstruction causes pancreatic duct hypertension. In alcoholic pancreatitis, toxic metabolites (fatty acid ethyl esters) damage acinar cells. Activated enzymes digest pancreatic tissue and peripancreatic fat (saponification). The systemic inflammatory response (SIRS) can lead to multi-organ dysfunction. Severe disease causes pancreatic necrosis, which may become secondarily infected (usually by gut bacteria, typically at day 7-21).

Typical Presentation

• Severe epigastric pain radiating straight through to the back
• Sudden onset, constant, worsened by eating, partially relieved by sitting forward
• Nausea and vomiting (>80%)
• Abdominal tenderness with guarding (often less peritonism than expected given severity — "silent abdomen")

Severe Disease Features

• Shock (tachycardia, hypotension)
• Respiratory distress (ARDS, pleural effusions — especially left-sided)
• Oliguria (AKI)
• Jaundice (if choledocholithiasis/biliary obstruction)

Rare Signs

• Grey Turner's sign: flank bruising (retroperitoneal haemorrhage)
• Cullen's sign: periumbilical bruising
• Both indicate haemorrhagic pancreatitis and are late signs

Red Flags

• Persistent organ failure >48 hours (severe pancreatitis)
• Rising CRP >150 mg/L at 48 hours
• Infected necrosis (fever, rising WCC after initial improvement at day 7-21)
• Cholangitis (Charcot's triad: fever, jaundice, RUQ pain) — needs urgent ERCP

Bedside

• Observations: pulse, BP, RR, SpO₂, temperature, urine output
• ABG/VBG: PaO₂ (ARDS risk), lactate, glucose

Bloods

• Serum lipase (preferred) or amylase: >3× ULN diagnostic; lipase is more sensitive and specific (remains elevated longer)
• FBC: leucocytosis
• CRP: key prognostic marker; >150 mg/L at 48 hours predicts severe disease
• U&Es: AKI, dehydration
• LFTs: raised ALT >2× ULN suggests gallstone aetiology; raised bilirubin/ALP suggests choledocholithiasis
• Calcium: low (saponification of peripancreatic fat — prognostic)
• Triglycerides: if >11.3 mmol/L, likely cause
• Glucose: hyperglycaemia (stress response, endocrine pancreatic damage)

Imaging

• USS abdomen: within 24 hours — assess for gallstones (aetiology); dilated CBD suggests choledocholithiasis
• CT abdomen/pelvis with IV contrast: NOT needed for diagnosis if clear clinically; indicated at 72-96 hours if severe/deteriorating — assess necrosis extent (CT severity index)
• MRCP: if CBD stones suspected but USS equivocal

Special Tests

• Modified Glasgow (Imrie) score at 48 hours: ≥3/8 = severe (PANCREAS mnemonic)
• APACHE II: at admission — ≥8 predicts severe
• CT severity index (Balthazar): grades A-E + necrosis percentage
• IgG4: if autoimmune pancreatitis suspected

Non-pharmacological

• Aggressive IV fluid resuscitation: Ringer's lactate 5-10 mL/kg/hr for first 12-24 hours, guided by urine output (target >0.5 mL/kg/hr) and haemodynamic parameters
• Early enteral nutrition: oral diet as tolerated (no need to wait for pain resolution or normalisation of enzymes); NG/NJ feeding if unable to eat; avoid TPN unless EN not possible
• HDU/ICU admission: if severe pancreatitis or organ failure
• VTE prophylaxis

Pharmacological

• Analgesia: IV paracetamol 1 g QDS + IV opioid (morphine/oxycodone — titrated); patient-controlled analgesia if needed; avoid NSAIDs in severe disease (renal risk)
• Anti-emetics: ondansetron 4-8 mg IV
• Antibiotics: NOT routinely indicated for acute pancreatitis or sterile necrosis; indicated for infected necrosis (meropenem 1 g TDS) or concurrent cholangitis

Surgical/Interventional

• ERCP: within 24 hours if concurrent cholangitis; within 72 hours if persistent biliary obstruction without cholangitis; NOT routinely for gallstone pancreatitis without obstruction
• Cholecystectomy: during index admission for mild gallstone pancreatitis (PONCHO trial — reduces recurrence from 17% to 5%); or within 2 weeks for severe
• Infected pancreatic necrosis: step-up approach (PANTER trial, TENSION trial)
  1. Percutaneous catheter drainage
  2. Endoscopic transluminal necrosectomy (if walled-off necrosis)
  3. Minimally invasive surgical necrosectomy (VARD)
  4. Open necrosectomy (last resort)
• Pseudocyst drainage: if symptomatic/infected; endoscopic (EUS-guided) preferred

Referral Criteria

• ICU/HDU: organ failure, severe disease (Glasgow ≥3)
• Hepatobiliary/pancreatic surgery: complicated pancreatitis, necrosectomy
• ERCP: concurrent cholangitis, persistent biliary obstruction
• Follow-up: identify and address cause; alcohol service if alcohol-related

Mild pancreatitis (~80%): mortality <1%, resolves within 1 week. Severe pancreatitis (~20%): mortality 15-30%. Infected necrosis: mortality 30-50% (reduced to ~15% with step-up approach). Overall mortality ~5%. Recurrence: 20-30% for gallstone pancreatitis if cholecystectomy not performed. Long-term complications include pseudocyst (10-20%), pancreatic exocrine/endocrine insufficiency, and chronic pancreatitis (especially alcohol-related).

Modified Glasgow (Imrie) Score — PANCREAS Mnemonic

Key Trials