TextbookSurgeryAcute Pancreatitis

Acute Pancreatitis

Acute pancreatitis is acute inflammation of the pancreas, most commonly caused by gallstones (50%) and alcohol (25%). Severity ranges from mild self-limiting to severe necrotising disease with high mortality.

MRCSPLAB 1UKMLA0 questions

Key Facts

Gallstones (~50%) and alcohol (~25%) account for ~75% of cases — mnemonic GET SMASHED for causes Diagnosis: Requires 2 of 3 — (1) characteristic pain, (2) amylase/lipase >3× ULN, (3) imaging findings Lipase is more specific and remains elevated longer than amylase Modified Glasgow (Imrie) criteria: ≥3 within 48 hours predicts severe pancreatitis (PaO₂, Age, Neutrophils, Calcium, Renal, Enzymes, Albumin, Sugar) Management: Aggressive IV fluid resuscitation (goal-directed), analgesia, nutritional support (enteral preferred) ERCP within 72 hours if cholangitis or persistent biliary obstruction complicates gallstone pancreatitis Necrotising pancreatitis: ~20-30% of cases; infected necrosis requires intervention (step-up approach — percutaneous drainage → necrosectomy) Cholecystectomy should be performed during the same admission or within 2 weeks for gallstone pancreatitis (UK guideline)

Overview

Key Facts

Acute pancreatitis has a wide spectrum of severity. Early aggressive fluid resuscitation and identification of aetiology are the cornerstones of management.

Epidemiology

Incidence ~30-40 per 100,000/year in UK. Increasing incidence due to rising rates of gallstones and alcohol consumption. Male predominance for alcohol-related cases. Overall mortality ~5%; severe necrotising pancreatitis mortality ~15-30%.

Aetiology

GET SMASHED:

  • Gallstones (~50%)
  • Ethanol (~25%)
  • Trauma, Steroids, Mumps, Autoimmune, Scorpion stings, Hyperlipidaemia/Hypothermia/Hypercalcaemia, ERCP, Drugs (azathioprine, valproate, mesalazine)
  • Idiopathic ~10-20%

Pathophysiology

  • Premature intrapancreatic activation of trypsinogen → trypsin → autodigestion of pancreatic tissue
  • Release of inflammatory mediators → local and systemic inflammatory response
  • Severe cases: Pancreatic necrosis, peripancreatic fluid collections, organ failure (lung, kidney, cardiovascular)
  • Fat necrosis → hypocalcaemia (calcium saponification)

Clinical Presentation

Classic Presentation

  • Epigastric pain radiating straight through to the back
  • Constant, severe, worsened by lying flat, relieved by sitting forward
  • Nausea and vomiting
  • Abdominal tenderness with guarding

Examination Findings

  • Epigastric tenderness ± generalised peritonism
  • Reduced bowel sounds (paralytic ileus)
  • Tachycardia, hypotension, fever (in severe cases)
  • Grey Turner's sign: Flank bruising (retroperitoneal haemorrhage) — rare, late sign
  • Cullen's sign: Periumbilical bruising — rare, late sign

Red Flags (Severe Pancreatitis)

  • Persistent organ failure >48 hours (Revised Atlanta Classification: Severe)
  • CRP >150 at 48 hours
  • Modified Glasgow score ≥3
  • Evidence of pancreatic necrosis on CT
  • Respiratory failure (ARDS)
  • Shock requiring vasopressors

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Perforated peptic ulcerSudden onset, peritonism, free air on CXRErect CXR, CT
Acute cholecystitisRUQ pain, Murphy's positive, normal amylaseUS, LFTs
Mesenteric ischaemiaPain out of proportion, AF, raised lactateCT angiography
Ruptured AAASudden back/abdominal pain, pulsatile mass, hypotensionCT angiography
MI (inferior)Epigastric pain, ECG changesECG, troponin
Bowel obstructionColicky pain, vomiting, distensionAXR, CT

Diagnosis / Investigation

Bedside

  • Observations: NEWS2
  • ABG/VBG: PaO₂, lactate, glucose, calcium
  • ECG: Exclude MI

Bloods

  • Amylase/lipase: >3× ULN diagnostic (lipase preferred — more specific and sustained)
  • FBC, CRP: WCC, CRP >150 at 48h suggests severe
  • U&Es: Renal function, dehydration
  • LFTs: ALT >3× ULN suggests gallstone aetiology
  • Calcium: May be low (fat saponification — poor prognostic sign)
  • Glucose: May be elevated (endocrine dysfunction)
  • Triglycerides: If >10 mmol/L, consider as cause
  • G&S/crossmatch: If haemorrhagic pancreatitis suspected

Imaging

  • US abdomen: First-line — assess for gallstones, CBD dilatation
  • CT abdomen with IV contrast: At 72-96 hours if severe (assess necrosis — Balthazar score); or earlier if diagnostic uncertainty
  • MRCP: If CBD stones suspected and not seen on US

Management

Initial Management

  • Aggressive IV fluid resuscitation: Goal-directed (Ringer's lactate preferred); target UO >0.5 mL/kg/hr
  • Analgesia: IV paracetamol + opioids (morphine or PCA); avoid NSAIDs (renal risk)
  • NBM initially → early enteral nutrition (within 24-48 hours via NG/NJ tube if not tolerating orally) — reduces infection and mortality vs TPN
  • VTE prophylaxis: LMWH
  • Catheter: Monitor urine output
  • Avoid prophylactic antibiotics — only if confirmed/suspected infected necrosis

Specific Management

Gallstone pancreatitis:

  • ERCP within 72 hours if concurrent cholangitis or persistent biliary obstruction
  • Cholecystectomy during same admission or within 2 weeks (reduces recurrence)

Necrotising pancreatitis:

  • If infected necrosis (gas in necrosis on CT, positive FNA culture, clinical deterioration):
    • Step-up approach (PANTER trial): Percutaneous/endoscopic drainage → video-assisted retroperitoneal debridement (VARD) or endoscopic necrosectomy if drainage insufficient
    • Antibiotics: Meropenem 1g IV TDS or piperacillin-tazobactam

Referral Criteria

  • All acute pancreatitis — surgical/gastroenterology team
  • Severe pancreatitis — HDU/ICU for organ support
  • Necrotising pancreatitis with infection — specialist hepatobiliary/pancreatic unit

Prognosis

  • Mild (no organ failure): Mortality <1%; most resolve within 1 week
  • Moderate (transient organ failure <48h): Mortality ~5%
  • Severe (persistent organ failure >48h): Mortality ~15-30%
  • Infected necrosis: Mortality ~20-30% (doubles compared to sterile necrosis)
  • Gallstone pancreatitis recurrence: ~30-50% without cholecystectomy
  • Long-term: Risk of chronic pancreatitis (~10% after severe episode), diabetes, exocrine insufficiency

Other Relevant Information

Modified Glasgow (Imrie) Score

CriterionThreshold
PaO₂<8 kPa
Age>55 years
Neutrophils (WCC)>15 × 10⁹/L
Calcium<2 mmol/L
Renal function (urea)>16 mmol/L
Enzymes (LDH/AST)LDH >600 / AST >200
Albumin<32 g/L
Sugar (glucose)>10 mmol/L
≥3 = severe pancreatitis

Revised Atlanta Classification (2012)

SeverityDefinition
MildNo organ failure, no local complications
ModerateTransient organ failure (<48h) or local complications
SeverePersistent organ failure (>48h)