The sphincter of Oddi is a fibromuscular band that surrounds the terminal
portion of the common bile duct, pancreatic duct, and common canal as they pass
through the wall of the duodenum. We speak of '' Oddi dysfunction, when the
leakage of bile and pancreatic juice is hindered for functional reasons of
spasticity of the muscular structures of the apparatus.
Notions of anatomy of the sphincter apparatus
In fact these two ducts, the pancreatic and the biliary, discharge together in a
funnel-like structure which is called the `` ampulla of Vater '', and which, in
essence, constitutes a common channel. This partly explains the genesis of
biliary pancreatitis, in which the biliary sludge and the stop of the biliary
tract discharge, due to an increase in upstream pressure, is the cause of
pancreatitis and the same happens when with invasive maneuvers of cannulation of
the biliary tract main pressure is generated in the excretory path with
consequent risk of developing dangerous post-ERCP pancreatitis
To anatomically describe the structure, the smooth muscle fibers in the
sphincter are arranged both circularly and longitudinally. Although the
choledochus sphincter was identified in 1681 by Francis Glisson, it was later
named after Ruggero Oddi who published his morphological observations on the
sphincter in 1887 while he was a medical student at the University of Perugia in
Italy.
The sphincter of Oddi is made up of three contiguous segments:
• the choledochus sphincter surrounding the distal common bile duct
• the pancreatic sphincter along the Wirsung duct
• the ampullary sphincter that surrounds the common canal.
Some manometric studies have shown that the length of the physiological sphincter is about 8-10 mm, shorter than that of the anatomical sphincter.
Normal functions of the sphincter of Oddi
There are three main unions:
a) regulate the flow of bile and pancreatic juice into the duodenum during
duodenal digestion.
b) avoid the reflux of duodenal contents into the bile ducts and pancreas, which
is a risk for the consequent sepsis of the biliary tract
c) stimulate the filling of the gallbladder with hepatic bile.
All three functions appear to be related to the sphincter's ability to regulate
the pressure gradient between the duct systems and the duodenum. Mutual
contractile activity between the gallbladder and the sphincter of Oddi causes
the gallbladder to fill during the interdigestive period, which is important, as
it subsequently allows for adequate clearance of bile at the time a fatty meal
is to be digested, (e.g. . a coffee granita with messinese cream!). Otherwise,
in the event that the gallbladder is absent or not functioning, the so-called
post-cholecystectomy syndrome occurs.
The physiological control of the sphincter of Oddi appears to be multifactorial,
in the sense that the motor activity of the sphincter is coordinated with that
of the remaining gastrointestinal system and with the migrating motor complex
during fasting. The sphincter is also sensitive to multiple neurological and
hormonal stimuli and can be modulated, by means of reflex mechanisms, by other
areas of the pancreatic-biliary tree. The sphincter receives both sympathetic
and parasympathetic innervation and its activity is increased by cholinergic
stimulation.
Cholecystokinin appears to be the main hormonal regulator and causes inhibition
of the sphincter of Oddi with a reciprocal effect (for example, contraction) on
the gallbladder. The physiological role of other GI hormones, such as gastrin
and secretin, is less clear.
Sphincter of Oddi (SOD) dysfunction refers to a clinical condition characterized
by a benign, non-stone-induced obstruction of the flow of bile or pancreatic
juice, which occurs at the pancreatic-biliary junction. In clinical terms, the
extent is not well defined and has been the subject of considerable controversy.
Patients with suspected SOD generally present with unexplained abdominal pain
and sometimes with increased liver enzymes.
SOD can also be found in a small percentage of patients with "idiopathic"
pancreatitis. When the cause of the patient's symptoms is thought to be at the
level of the sphincter of Oddi, the term "sphincter of Oddi dysfunction" is
preferred over any other terminology (eg, papillary stenosis, biliary dyskinesia,
postcholecystectomy syndrome). SOD is thought to be a condition in which partial
obstruction of the sphincter segment has an organic (e.g., structural) or
functional (e.g., dysmotility) basis. Consequently, patients can be divided into
those with sphincter stenosis and those with sphincter dyskinesia.
True structural stenosis of the sphincter and papillary orifice could be due to
inflammation, fibrosis, or perhaps mucosal hyperplasia. Conditions that can
contribute to the inflammatory / fibrotic process include the passage of small
stones into the common bile duct and possibly recurrent episodes of pancreatitis.
The etiology of functional SOD is unknown. It is generally difficult to
distinguish patients who have organic stenosis from those with functional
stenosis as there is almost certainly an overlap of etiologies.
An alteration in biliary motility should be considered in the three clinical
pictures listed below.
Most of the studies have addressed the SOD present in these patients. In a
situation like this, the other causes of upper abdominal pain should also be
considered as they are often easier to rule out. The differential diagnosis for
postcholecystectomy pain is quite extensive (see table on next page).
Some recent studies have highlighted the link between idiopathic pancreatitis
and SOD. These studies focused mainly on pancreatitis associated with sphincter
of Oddi (SO) manometry. SO manometry can reveal elevated baseline sphincter
pressure in 15-57% of these patients.
Episodic pain of the gallbladder type, but with negative diagnostic tests
(including ultrasound of the abdomen and ejection fraction of the gallbladder).
In patients with gallbladder in situ and biliary pain, the gallbladder is
generally the focus of evaluation. Recent studies have shown that some of these
patients may also have altered SOD and SO manometry. Optimal treatment for this
patient group requires further research.
SOD patients can be divided into two categories based on the clinical
presentation. Most have biliary abdominal pains, a small group have symptoms
that can be attributed to the pancreas. The classification system of the SOD
must take into account the different etiologies and the overlap of different
clinical presentations, therefore it is based on the clinical history,
laboratory tests and the results of diagnostic endoscopic retrograde
cholangiopancreatography (ERCP) and distinguishes patients with type pain
biliary in three groups:
Criteria
- a) Typical biliary pain
- b) Altered liver enzymes (AST and / or alkaline phosphatase with an increase greater than 2 times the norm on at least two occasions)
- c) Delayed drainage of ERCP contrast (> 45 minutes)
- d) Dilated common bile duct (> 12 mm)
- Biliary type I - brings together all the above types (a, b, c and d)
- Biliary type II - typical biliary pain (a) plus one or two between b, e and d
- Biliary type III - biliary type pain only (a)
In etiological terms, type I patients probably have a true anatomical stenosis
of the sphincter, those of type II a structural or functional narrowing, while
in those of type III the stenosis is usually functional. Some specialists have
found this classification system useful in determining which patients are most
likely to have normal SO manometry and which patients are likely to respond to
endoscopic sphincterotomy.
Most patients screened for suspected SOD have already undergone a previous
cholecystectomy. In many of them, pain after cholecystectomy has significantly
lessened, but recurrent abdominal pain recurs after surgery. Others have not
benefited from cholecystectomy, in fact they have even made it worse, probably
due to the removal of a reserve reservoir.
Recurrent bouts of pain often appear within 3-5 years of surgery. The pain
usually has similar characteristics to that before cholecystectomy; it is
typically located in the right upper quadrant of the abdomen or epigastrium,
with or without irradiation to the right shoulder, scapula or back and is
usually stable and non-colic. In most patients, pain episodes occur infrequently
at first, last several hours, and are followed by asymptomatic intervals. In
some people, the frequency and severity of attacks progress over time, and acute
intermittent episodes develop over an underlying chronic pain syndrome.
The relationship between pain episodes and meals presents some variability. A
pain attack often occurs within two to three hours of eating; many patients can
identify certain foods (fatty or spicy foods) as the trigger for the attacks.
Unfortunately, other painful episodes do not seem to have a significant
relationship with meals or the type of food. A subset of patients were sensitive
to opioid-containing drugs that cause abdominal pain exacerbation.