Sphincter of Oddi dysfunction and acute pancreatitis

Abstract

Fifty years ago Lium et al stated that... “Acute pancreatitis is the result of ductal obstruction in an actively secreting pancreas”. A number of mechanisms for pancreatic ductal obstruction were reviewed and the role of the sphincter of Oddi (SO) in producing “obstruction” was discussed.1 The studies by Archibald were reported and suggested a possible role of SO “spasm” in producing ductal obstruction. It was suggested that the cause of biliary pancreatitis in patients with gallstones who did not have a stone impacted at the ampulla may be secondary to SO “spasm” and oedema. Normal human SO motility has been characterised by a number of studies and normal manometric parameters have been established using standardised manometry, as has SO dysfunction. The clinical presentation of patients with SO dysfunction may be divided into two groups: biliary SO dysfunction presenting with biliary type pain; and recurrent pancreatitis.2 In 1995, the following definition of SO dysfunction was developed: “partial obstruction of the SO biliary segment giving rise to intermittent, episodic upper abdominal pain, deranged liver function tests, dilatation or delayed drainage of injected contrast from the common bile duct. Likewise, similar condition of the pancreatic segment can give rise to pancreatitis or episodic pain suggesting a pancreatic origin”.3 The main consequence of SO dysfunction is impedance of bile and pancreatic juice flow, either through a structural stenosis or functional stenosis from hypertonia. In some instances, however, hypotonia as a result of dyskinesia may also occur and reflect SO dysfunction. The term SO dysfunction includes structural stenosis of the SO and functional stenosis secondary to hypertonia.4 It also encompasses dysmotility which may lead to intermittent or transient impedance of bile or pancreatic juice flow. The frequency of SO dysfunction in the community is not known. It is also uncertain whether …