Hello,
Thanks for your question. I am an internal medicine physician and all
my sources will be from physician-written, peer reviewed resources.
What is the current therapy is for biliary dyskinesia (Sphincter of
Oddi dysfunction) or bile duct spasms?
The sphincter of Oddi (SO) is a muscular structure that encompasses
the confluence of the distal common bile duct and the pancreatic duct
as they penetrate the wall of the duodenum. The term "sphincter of
Oddi" dysfunction has been used to describe a clinical syndrome of
biliary or pancreatic obstruction related to mechanical or functional
abnormalities of the sphincter of Oddi.
I will focus solely on treatment – let me know if you want information
on diagnosis.
The goal of treating symptomatic sphincter of Oddi dysfunction (SOD)
is to reduce the impaired flow of biliary and pancreatic secretions
into the duodenum, which can be accomplished by pharmacologic,
endoscopic, and surgical approaches. Successful treatment depends upon
a secure diagnosis. A variety of other disorders, such as irritable
bowel syndrome and functional dyspepsia, can cause symptoms that may
be confused with SOD.
1) Pharmacologic treatment
Drugs that cause smooth muscle relaxation may be beneficial in
patients with SOD. Calcium channel blockers and nitrates have been
best studied, although the data are sparse.
Calcium channel blockers:
Nifedipine reduces basal SO pressure in volunteers without SOD, and
has a more profound effect in patients with SOD who have elevated
basal SO pressure (1,2). The efficacy of nifedipine in SOD was
evaluated in a placebo-controlled crossover trial that included 28
patients with recurrent biliary pain thought to be related to SOD (2).
Nifedipine (given in the maximal tolerated dose) was associated with
significant decreases in a cumulative pain score, number of pain
episodes, oral analgesic tablets consumed, and emergency room visits.
Nitrates:
Nitrates can produce relaxation of the SO in animal models and in
humans (3). A potential role for nitrates in patients with SOD was
suggested by a case report of a patient whose pain disappeared
following nitrate administration; pain resolution was associated with
a decrease in both basal and phasic SO activity. No controlled trials
of nitrate therapy in SOD have been performed.
Electroacupuncture:
A potential therapeutic role for electroacupuncture was suggested in a
pilot study in which an acupoint on the right lateral tibia was
stimulated, resulting in a significant decrease in basal pressure,
amplitude, duration, and frequency of phasic contractions (4). All
changes reverted to baseline upon discontinuation of stimulation. The
clinical relevance of these observations remains to be determined.
2) Endoscopic therapy
The biliary or pancreatic segment of the sphincter of Oddi can be
severed using electrocautery during endoscopic retrograde
cholangiopancreatography (ERCP). It should be performed by an
experienced, capable endoscopist who has demonstrated good outcomes by
sufficient patient follow-up.
Multiple studies have evaluated the benefit of endoscopic
sphincterotomy (5, 6). Although the duration of follow-up and
inclusion criteria varied, improvement or elimination of pain occurred
in approximately 30 to 60 percent of patients.
Biliary pain:
In patients with biliary pain, biliary sphincterotomy has the greatest
benefit for those who have elevated basal pressures (greater than 40
mmHg). In one study, 47 patients thought to have SOD based upon
clinical findings were randomized to sphincterotomy or sham
sphincterotomy prior to undergoing manometry; all the patients were
presumed to have biliary pain and had previously undergone
cholecystectomy (7). At one-year follow-up, biliary sphincterotomy
improved pain scores and objective parameters in significantly more
patients who had elevated basal sphincter pressures (90 versus 25
percent with sham sphincterotomy). In contrast, pain scores were
similar in patients without elevated pressures, regardless of
treatment.
Botulinum toxin injection:
Endoscopic injection of botulinum toxin for biliary sphincter of Oddi
dysfunction has been used successfully by some groups to determine if
a symptomatic response might predict a successful outcome to
subsequent sphincterotomy (8). The influence of botulinum toxin on the
pancreatic segment of the SO is unknown. Whether this material could
be injected successfully into the pancreatic segment without a
preceding biliary sphincterotomy is also not known.
3) Surgery
Biliary and pancreatic sphincterotomy can also be accomplished by a
transduodenal surgical approach. It is difficult to sever the
transampullary septum during conventional endoscopic sphincterotomy
without risking duodenal perforation. As a result, endoscopic
sphincterotomy may not completely relieve pancreatic duct obstruction.
Surgery may reduce the chance of recurrent stenosis due to scarring.
Improvement in biliary pain and recurrent pancreatitis have been
demonstrated in approximately 50 to 60 percent of patients treated by
surgical sphincterotomy (10). However, surgical sphincterotomy and
septoplasty for pancreatitis may be associated with worse outcomes
than for recurrent biliary pain (10).
Despite these potential advantages, endoscopic therapy is less
invasive, has similar outcomes, and is the preferred approach at most
centers with experience in this technique.
Please use the answer clarification to ask any questions before rating
this answer. I will be happy to explain any issue.
Thanks,
Kevin, M.D.
Search strategy:
No internet search engine was used in this answer. All sources are
from objective, physician-written, peer-reviewed resources.
Bibliography:
1) Guelrud, M, Mendoza, S, Rossiter, G, et al. Effect of nifedipine on
sphincter of Oddi motor activity: Studies in healthy volunteers and
patients with biliary dyskinesia. Gastroenterology 1988; 95:1050.
2) Khuroo, MS, Zargar, SA, Yattoo, GN. Efficacy of nifedipine therapy
in patients with sphincter of Oddi dysfunction: A prospective double-
blind randomized, placebo-controlled cross over trial. Br J Clin
Pharmacol 1992; 33:477.
3) Brandstatter, G, Schinzel, S, Wurzer, H. Influence of spasmolytic
analgesics on motility of sphincter of Oddi. Dig Dis Sci 1996; 41:1814.
4) Bar-Meir, S, Halpern, Z, Bardan, E. Nitrate therapy in a patient
with papillary dysfunction. Am J Gastroenterol 1983; 78:94.
5) Riemann, JF, Lux, G, Forster, P, Altendorf, A. Long-term results
after endoscopic papillotomy. Endoscopy 1983; 15 Suppl 1:165.
6) Meshkinpour, H, Mollot, M. Sphincter of Oddi dysfunction and
unexplained abdominal pain: Clinical and manometric study. Dig Dis Sci
1992; 37:257.
7) Geenen, JE, Hogan, WJ, Dodds, WJ, et al. The efficacy of endoscopic
sphincterotomy after cholecystectomy in patients with sphincter-of-
Oddi dysfunction. N Engl J Med 1989; 320:82.
8) Wehrmann, T, Seifert, H, Seipp, M, et al. Endoscopic injection of
botulinum toxin for biliary sphincter of Oddi dysfunction. Endoscopy
1998; 30:702.
9) Hogan, W. Treatment of sphincter of Oddi dysfunction. UptoDate,
2002.
10) Nussbaum, MS, Warner, BW, Sax, HC, Fischer, JE. Transduodenal
sphincteroplasty and transampullary septotomy for primary sphincter of
Oddi dysfunction. Am J Surg 1989; 157:38. |
Clarification of Answer by
kevinmd-ga
on
05 Dec 2002 08:17 PST
Hello,
Here is some clarification for the questions you had.
How do you diagnose sphincter of oddi dysfunction (SOD)?
The diagnosis of sphincter of oddi dysfunction (SOD) is established by
sphincter of oddi (SO) manometry, which is performed during ERCP
(endoscopic retrograde cholangiopancreatography – I’m sure you are
familiar with this). Several less invasive methods have also been
evaluated for establishing the diagnosis, but none has proven to be
consistently reliable in controlled clinical trials.
Biliary SOD
The presence of biliary SOD has been based upon a variety of
parameters, including dilation of the common bile duct, provocation
tests, and hepatobiliary scintigraphy.
Dilation of the common bile duct: Otherwise unexplained dilation of
the common bile duct on ultrasound is associated with SOD and may
predict a favorable response to sphincterotomy in patients with other
clinical evidence of biliary obstruction (eg, pain, abnormal liver
function tests). However, because many reasons can cause dilation,
this criteria alone is insufficient evidence for establishing the
diagnosis of SOD.
Provocation tests: To increase the specificity of common bile duct
diameter measurement for determining SOD, several provocation tests
have been developed that use either a fatty meal (fatty meal
ultrasonography) or cholecystokinin to increase bile flow. In patients
who have normal SO function, the bile duct diameter remains constant
or decreases following stimulation; an increase of more than 2 mm is
considered to be pathologic.
Hepatobiliary scintigraphy: Hepatobiliary scintigraphy using
technetium-99m labeled dyes can provide a standardized,
semiquantitative assessment of delayed biliary drainage in patients
whose gallbladder is absent. However, scintigraphy may be falsely
positive in patients who have extrahepatic biliary obstruction from a
variety of causes, or falsely negative in patients who have SO
dyskinesia in whom obstruction to bile flow may be intermittent.
Pancreatic SOD
Tests of SOD involving the pancreatic segment of the SO have focused
on pancreatic outflow obstruction due to SO stenosis.
Provocation tests: Provocation tests for evaluating pancreatic SOD are
based upon a similar principle as provocation tests for biliary SOD.
An increase in pancreatic duct diameter following secretin stimulation
of more than 1.5 mm (assessed by transabdominal ultrasound or CT)
lasting for more than 30 minutes is considered to be pathologic.
Sphincter of Oddi manometry: Sphincter of Oddi manometry remains the
gold standard for diagnosis of SOD. The most common method involves
retrograde intubation of the sphincter of Oddi with a
pressure-transducing manometry catheter during ERCP. Basal pressure
and phasic wave contractions are routinely recorded from the common
bile duct and pancreatic duct segments of the sphincter of Oddi; the
mechanical and electrical activity are similar between the two
segments.
Can you differentiate the symptoms between SOD, functional dyspepsia,
and irritable bowel?
As you can understand, these three disease entities have overlapping
symptoms. Based symptoms alone, it would be difficult to accurately
differentiate between the diseases. Here is a list of symptoms for
each disorder.
SOD:
Can present as gall bladder pain or pancreatitis.
1) gall bladder pain - episodic attacks of abdominal pain, which is
most often located in the right upper abdomen just under the margin of
the ribs but can also be felt in the back and right shoulder. Other
associated symptoms include nausea, vomiting, and intolerance to fatty
foods.
2) pancreatits - epigastric, often radiates to the back, is
occasionally associated with nausea and vomiting, and may be relieved
by sitting upright or leaning forward. The pain is often worse 15 to
30 minutes after eating. Early in the course of chronic pancreatitis,
the pain may occur in discrete attacks; as the condition progresses,
the pain tends to become more continuous.
Dyspepsia:
Dyspepsia is defined as pain or discomfort centered in the upper
abdomen (mainly in or around the midline as opposed to the right or
left hypochondrium). Discomfort is a negative feeling that the patient
does not interpret as pain, which can be characterized by or
associated with fullness, early satiety, bloating, or nausea.
Dyspepsia can be intermittent or continuous, and may or may not be
related to meals.
Irritable bowel syndrome (IBS):
Abdominal pain in IBS is usually described as a crampy sensation with
variable intensity and periodic exacerbations. The pain is generally
located in the lower abdomen, often on the left side; however, the
location and character of the pain can vary widely. The severity of
the pain may range from mildly annoying to debilitating. Several
factors, such as emotional stress and eating, may exacerbate the pain,
while defecation often provides some relief. By definition, patients
with IBS complain of altered bowel habits. Upper gastrointestinal
symptoms, including gastroesophageal reflux, dysphagia, early satiety,
intermittent dyspepsia, nausea, and non-cardiac chest pain, are common
in patients with IBS. Patients with IBS also frequently complain of
abdominal bloating and increased gas production in the form of
flatulence or belching.
I hope that this information helps. I will be happy to further
discuss the diagnosis and treatment of the above disorders in separate
questions. The efficacy of the various diagnostic methods used in SOD
have also been studied and I can research this in a separate question.
Thanks,
Kevin, M.D.
Search strategy:
No internet search engine was used in this answer. All sources are
from objective, physician-written, peer-reviewed resources.
Bibliography:
Chun et al. Clinical manifestations and diagnosis of irritable bowel
syndrome. UptoDate, 2002.
Hogan et al. Clinical manifestations and diagnosis of sphincter of
Oddi dysfunction. UptoDate, 2002.
Freedman et al. Clinical manifestations and diagnosis of chronic
pancreatitis. UptoDate, 2002.
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