Gallstone Pancreatitis: Mechanism, Symptoms, and Treatment

Gallstone pancreatitis occurs when a gallstone migrates from the gallbladder into the common bile duct, obstructing the pancreatic duct at the ampulla of Vater. This causes premature trypsinogen activation → autodigestion of the pancreas.

Pathophysiology

1. Stone passes cystic duct → common bile duct.
2. Lodges at ampulla (shared pancreatic/biliary channel).
3. Blocks pancreatic outflow → increased ductal pressure → acinar injury → enzyme activation → inflammation.

Clinical Presentation

• Epigastric pain radiating to back (90%), nausea/vomiting.
• Fever, tachycardia, hypotension if severe (SIRS).
• Cullen's sign (periumbilical ecchymosis) or Grey Turner's sign (flank ecchymosis) in hemorrhagic pancreatitis.

Diagnosis

• Serum lipase >3× ULN (more specific than amylase).
• CT abdomen with contrast (if diagnosis uncertain or severe): necrosis, fluid collections.
• Transabdominal ultrasound: detects gallstones, biliary dilation.

Management

• Supportive: Aggressive IV hydration (RL 250–500 mL/hr), analgesia, NPO then early enteral feeding.
• ERCP with sphincterotomy: Within 24–48 hrs if cholangitis or persistent biliary obstruction; not routine for mild pancreatitis without obstruction.
• Cholecystectomy: Same admission (mild) or after resolution (moderate/severe) to prevent recurrence.
• Antibiotics: Only for infected necrosis or cholangitis—not prophylactically.

Severity Classification (Revised Atlanta)

Mild (no organ failure, no complications) → Moderate (transient organ failure <48h or local complications) → Severe (persistent organ failure >48h).