Update Course Rewind: Management of Recurrent Pancreatitis

Every ERCP carries a risk of post-ERCP pancreatitis, and with every pancreatitis attack, islet cells are lost.

PRSS1 is the most common genetic mutation in recurrent pancreatitis and is a trypsinogen activator that activates trypsin inside the pancreas.

The genetic panel at Cincinnati Children's tests 10 different genetic markers for pancreatitis (including PRSS1, CTRC, CFTR, CPA1).

Genetic factors are changing the approach to pediatric chronic pancreatitis treatment.

There is currently no medication to mitigate trypsin activation in genetic pancreatitis mutations.

In a Frey procedure (partial head pancreatectomy with pancreaticojejunostomy), the top half of the pancreas is removed to open the duct, which results in loss of islet cells.

In patients with PRSS1 mutation, draining the duct (e.g., via Frey) temporizes attacks but does not fix the problem, as the parenchyma continues to be attacked by the mutation and pancreatitis will likely recur.

There is no set number of ERCPs that defines when to escalate care; the sooner the referral for evaluation, the better.

Surgical management of the pancreas is not offered unless medical and endoscopic management have been maximized.

If the endoscopist has no further options (nothing to balloon dilate, open, or drain) and the patient continues to have pancreatitis despite stenting, there is no reason to continue ERCPs.

MRCP is the best non-invasive imaging study for the pancreas, particularly with T2 sequences.

ERCP is more therapeutic than diagnostic.

Pancreatic fluid collections should be drained once the wall is mature (4 to 6 weeks) only if the patient is symptomatic (e.g., gastric outlet obstruction or pain); asymptomatic collections will self-resolve and do not require drainage or antibiotics.