Recurrent Acute Pancreatitis

Recurrent acute pancreatitis is two or more separate episodes of acute pancreatitis with full resolution of symptoms between attacks. The aim of workup is to find and remove the cause to prevent progression to chronic pancreatitis.

About 20% of patients with a first attack have a recurrence, and about 35% of those progress to chronic disease. Causes are gallstones and microlithiasis, alcohol, hypertriglyceridaemia (triglycerides over 11.3 mmol/L), pancreas divisum, sphincter of Oddi dysfunction, hypercalcaemia, drugs, genetic variants (PRSS1, SPINK1, CFTR, CTRC), autoimmune pancreatitis and duct obstructing tumours such as intraductal papillary mucinous neoplasm. About 10% to 30% remain idiopathic.

Pathophysiology.

Premature intrapancreatic trypsin activation, duct obstruction and impaired bicarbonate secretion lead to acinar injury. Repeated injury activates stellate cells and drives fibrosis.

Epigastric pain radiating to the back with nausea and vomiting, lasting hours to days and resolving between attacks. Fat intolerance and diabetes appear if chronic disease develops.

Red flags.

• Organ failure or hypotension.
• Fever with jaundice.
• Weight loss between attacks.
• Age over 50 years with a first unexplained attack.

Confirm each attack with lipase over 3 times the upper limit. Between attacks check liver tests, fasting triglycerides, calcium, IgG4 and alcohol history. Transabdominal ultrasound looks for stones and sludge. Magnetic resonance cholangiopancreatography with secretin and endoscopic ultrasound look for microlithiasis, divisum, duct anomalies and small tumours. Offer genetic counselling and testing when the family history is positive or onset is before 35 years.

Differential diagnosis.

• Biliary colic or choledocholithiasis.
• Chronic pancreatitis with acute flares.
• Peptic ulcer disease.
• Mesenteric ischaemia.
• Sphincter of Oddi dysfunction.

Treat the cause. Perform cholecystectomy after gallstone pancreatitis (in the same admission for mild disease, and when the collections have resolved or after 6 weeks for severe disease). Stop alcohol and tobacco, withdraw implicated drugs, correct calcium, and treat duct obstruction endoscopically. For each attack give fluids, analgesia and early oral feeding.

• Ringer lactate: bolus of 10 mL/kg IV if hypovolaemic, then 1.5 mL/kg/h IV for 24 to 48 hours; maximum 3 mL/kg/h; monitor urine output, respiratory rate and oxygen saturation (94% to 98%); reduce in heart failure or renal impairment.
• Paracetamol: 1 g IV or orally every 6 hours; maximum 4 g daily (3 g daily if weight under 50 kg or chronic liver disease); monitor liver tests.
• Morphine for severe pain: 2.5 to 5 mg IV every 4 hours as needed for the duration of the attack; titrate; monitor sedation and respiratory rate; reduce the dose by half in renal impairment and in older adults.
• Fenofibrate (hypertriglyceridaemia): 145 mg orally once daily long term; maximum 145 mg daily; monitor triglycerides, liver tests and creatine kinase; use 48 mg daily when creatinine clearance is 30 to 59 mL/min and avoid if under 30 mL/min.
• Insulin infusion (triglycerides over 11.3 mmol/L with pancreatitis): 0.1 to 0.2 units/kg/h IV, with glucose as needed, until triglycerides are under 5.6 mmol/L (usually 24 to 72 hours); maximum 0.3 units/kg/h; monitor glucose hourly and potassium; reduce if glucose is under 4 mmol/L.

Monitoring. Triglycerides, glucose and weight at 3 months and yearly; faecal elastase and imaging if attacks continue.

Referral and escalation. Pancreatic endoscopy, hepatobiliary surgery and genetics for idiopathic or familial cases; critical care for organ failure.

Special groups. Pregnancy with severe hypertriglyceridaemia needs plasmapheresis considered and specialist obstetric care.