Hi minigal-ga, and thanks for your question. My condolences on your
ongoing abdominal problems.
As usual, this is no substitute for medical advice and direct
evaluation, which it sound as though you're receiving. I have divided
the answer below into subsections to make reading and finding
Background and Anatomy
You may be familiar with it already, but a quick overview of the
anatomy of the gallbladder is helpful in understanding the types of
problems that can arise. Here's an open view of the gallbladder, the
ducts, and a portion of the duodenum (the first part of the small
A nice overview of gallbladder disease with links to diagrams and more
definitions can be found at the General Surgery Practice of New
As you imply, a gallbladder (GB) ejection fraction of 16% is
abnormally low. A normal range is 35-75%. I just saw a patient with
a similar story just yesterday. One maneuver that can help shed some
light on things, which was probably attempted, is the administration
of cholecystokinin (CCK), a chemical which is normally excreted by the
duodenum in response to ingestion of fatty foods, causes rhythmic
contraction and emptying of the gallbladder. This is often used
during the "ejection fraction" portion of the HIDA scan.
In the absence of obstructing gallstones, a low ejection fraction can
mean either that the gallbladder is not sufficiently responsive to CCK
or that the outlet of the gallbladder is obstructed by something other
than a stone. Unfortunately, the CCK challenge lacks convincing
sensitivity or specificity for functional gallbladder disease.
As you can see from the anatomy diagram at the link above in the first
section, after the gallbladder is removed, the liver will excrete bile
into the left and right hepatic bile ducts, which join to form the
common hepatic duct. After removal of the gallbladder, a small stump
of the cystic duct remains, and the hepatic duct continues on past it
to the common bile duct. The common bile duct then joins up with the
pancreatic duct and the joined duct empties into the duodenum through
the Ampulla of Vater. A portion of the common bile duct and the
pancreatic duct lie within the wall of the duodenum and are surrounded
by a muscular layer of tissue. This circumferential muscular layer is
the Sphincter of Oddi. There are other muscular sphincters in this
region, but are not important for this discussion.
So, if the Spincter of Oddi fails to relax or some portion of the
draining duct system becomes narrowed, then the liver tries to excrete
bile into the duodenum and fails, sometimes causing dilitation of the
common bile duct and reflux of bile back into the liver in severe
cases. The symptoms associated with this vary widely and can mimic
biliary colic. It can come on suddenly as you describe. The Piccinni
et al. paper below gives a nice summary of the usual clinical
"The classic patient suffering from biliary dyskinesia is frequently a
female between 20 and 50 years of age with a history of recurrent
Abdominal pain is the most common presenting symptom of patients with
SOD. The pain is usually epigastric or right upper quadrant, may be
disabling, and lasts for 30 minutes to several hours. In some
patients, the pain is continuous with episodic exacerbations. It may
radiate to the back or shoulder and be accompanied by nausea and
vomiting. The pain may begin several years after a cholecystectomy and
be similar in character to the pain leading to the operation.
Alternatively, patients may have continual pain that is not relieved
by a cholecystectomy. Jaundice, fever, and chills are rarely
Clarification of term "SOD"
SOD is now taken to refer to either functional SO dyskinesia or SO
stenosis. The introductory portion of the Piccinni, et al., paper
below states the situation well:
"Based on the underlying pathogenetic mechanism, 2 types of sphincter
dysfunction have been recently proposed: SO dyskinesia and SO
stenosis.[10,11] SO dyskinesia refers to a primary motor abnormality
of the SO, which may result in a hypotonic or a hypertonic sphincter.
In contrast, SO stenosis refers to a structural alteration of the
sphincter, in which there is a narrowing of part or the whole
sphincter, probably due to an inflammatory process from pancreatitis
or injury from gallstone migration through the papilla with subsequent
fibrosis. Because it is often difficult to distinguish patients with
SO dyskinesia from those with stenosis, the term SOD has been used to
include both groups of patients."
Sub-Types of SOD
As you describe, you presumably have Type III SOD based on the
Milwaukee classification scheme - the most controversial and difficult
to diagnose and treat of the three subtypes of SOD. A very recent
review article looked at the current state of SOD diagnosis and
management and sheds some light on the current state of thinking about
this subgroup of patients.
With regard to Type III SOD, the authors state:
"Most controversial are patients who have pain with no additional
criteria and are labeled as SOD Type III. In this group, demonstrable
SO ?dysfunction? and response to sphincterotomy occur in only a
minority of patients. As SO manometry and subsequent sphincterotomy
carry substantial morbidity, this approach is controversial as it is
based upon the possibly faulty premise that these patients have a
problem localized to the biliary sphincter of Oddi. These observations
also suggest that alternative explanations concerning the
pathophysiology and management of pain should be considered.
One possibility is that the origin of pain resides in the duodenum
rather than or in addition to the biliary tree. For example, Desautels
et al demonstrated that patients diagnosed to have SOD Type III
exhibited duodenal-specific visceral hyperalgesia and that duodenal
distension reproduced symptoms in all but 1 of the 11 patients
studied. This observation is consistent with the concept of
visceral hyperalgesia in functional gastrointestinal disorders, which
has emerged as a potentially important factor associated with the
development and perpetuation of GI symptoms in affected patients.4 In
this regard, several possible scenarios have been considered in some
patients with both acalculous and postcholecystectomy biliary pain
The first is that patients with SOD appear to have a higher than
expected prevalence of IBS 40 and that SOD may occur as part of a more
generalized functional disorder of the gut. Indeed, other studies have
found that an abnormal SO response to CCK is much more often found in
patients with SOD Type II and concomitant IBS. Selective treatment
of the SO cannot be expected to provide symptom resolution in such
patients and may account for the high failure rate of sphincterotomy
in many patients with SOD Type III."
Wald, A. Functional Biliary-Type Pain: Update and Controversies.
Journal of Clinical Gastroenterology, Volume 39(4) Supplement 3,
May/June 2005, pp S217-S222.
This article is not available free online, but you can request a
reprint directly from the author at this address:
As ERCP is associated with some morbidity (side effects), there is a
move in some camps to perform MRCP (Magnetic Resonance
Cholangiopancreatography). The advantage of MRCP is that it is
noninvasive, like an MRI. The disadvantage is that it is not
therapeutic. During ERCP, various procedures can be performed, such
as myotomy to incise the Sphincter of Oddi, etc. MRCP is sometimes
criticized because if a clinician is thinking that if MRCP is
positive, then the patient will need to have ERCP to fix the problem.
The flip side of this argument is that if the MRCP is negative, then
the patient may be spared an invasive procedure.
The authors of the paper below give their take on MRCP with regards to SOD:
"Magnetic resonance cholangiopancreatography (MRCP) is a newly
developed imaging technique for evaluating the biliary tree. The
accuracy of MRCP and the correlation with ERCP have been demonstrated
in a variety of biliary and pancreatic diseases. Its major advantage
is that it does not require endoscopy, contrast injection, or
radiation and it is complication-free.
Lee et al  demonstrated that the sensitivity, specificity, and
accuracy in distinguishing malignant from benign lesions were 81%,
92%, and 87%, respectively, for MRCP and 71%, 92%, and 83%,
respectively, for ERCP.
MRCP has shown great accuracy in detecting biliary tract
dilatation. Stimulation with secretin has been reported to improve
MRCP image quality. Secretin acts as an endogenous contrast agent that
allows visualization of the ducts, not only in the basal status but
also during a physiologic stimulation, and improves the visualization
of normal-size pancreatic ducts, anatomic variants, and early ductal
changes that are not usually revealed by conventional MRCP. Although
MRCP has numerous advantages, some limitations must be noted, such as
artefacts occasionally noted in the presence of metal clips. The major
limitation compared with ERCP is obviously its inability to offer
therapeutic options,[36,37] but it is fast and reliable in evaluating
the biliary extrahepatic and pancreatic ducts and offers a diagnostic
value equivalent to that of ERCP."
Piccinni G. Angrisano A. Testini M. Bonomo GM. Diagnosing and treating
Sphincter of Oddi dysfunction: a critical literature review and
reevaluation. Journal of Clinical Gastroenterology. 38(4):350-9, 2004
Again, this article is not available for free online, but you can
request a reprint of the article from Dr. Piccinni at either of these
ERCP provides the option to perform SO manometry to measure the
pressures within the SO. Here are some numbers on how well patients
with each subtype do, based on manometry results, after SO myotomy
[from Puccinni et al.]:
"Pain relief after ES [Endoscopic Sphincterotomy aka Sphincter of Oddi
Myotomy - SOM] is 90 to 95% for type I patients. In type II SOD
patients, the relief rates are 85% in those with abnormal SOM and 35%
in patients with normal SOM. In type III patients, relief rates are 55
to 60% with abnormal SOM and <20% with normal SOM.[74,75]"
Other theories on Type III SOD
I have come across multiple sources who cite the finding that
Inflammatory Bowel Syndrome is more common in patients with Type III
SOD and that this subtype may actually be a variant of IBS. This
would explain why these patients have poor resolution of symptoms
after sphincterotomy and why 10/11 patients had reproduction of their
symptoms with distention of the duodenum. A small subset of patients
do benefit from sphincterotomy, so being in the Type III subgroup
would not completely exclude you from consideration for this
procedure. Because this is a controversial area, each individual GI
physician will likely have an opinion and standard that they practice.
Each patient requires individual evaluation. The first line of
therapy is conservative, and includes agents with utility in chronic
pain such as tricyclic antidepressants.
As you can see from the anatomy in the first section, the pancreatic
duct and common bile duct are connected, allowing for the possibility
of a gallstone making it's way from the bile system into the
pancreatic portion of the duct system. This leads to gallstone
The NIH page on pancreatitis is a good overview:
This page summarizes the symptoms of chronic pancreatitis:
"Most people with chronic pancreatitis have abdominal pain, although
some people have no pain at all. The pain may get worse when eating or
drinking, spread to the back, or become constant and disabling. In
certain cases, abdominal pain goes away as the condition advances,
probably because the pancreas is no longer making digestive enzymes.
Other symptoms include nausea, vomiting, weight loss, and fatty
People with chronic disease often lose weight, even when their
appetite and eating habits are normal. The weight loss occurs because
the body does not secrete enough pancreatic enzymes to break down
food, so nutrients are not absorbed normally. Poor digestion leads to
excretion of fat, protein, and sugar into the stool. If the
insulin-producing cells of the pancreas (islet cells) have been
damaged, diabetes may also develop at this stage."
eMedicine.com is an excellent free resource. Here is their page on
chronic pancreatitis, which describes the pathophysiology, diagnosis,
and treatment of this disorder and is well worth reading.
Of interest, this article outlines the means by which chronic
pancreatitis can be diagnosed in an early stage. These are all
invasive methods, but ERCP is one of these:
"Determination in pancreatic juice: This test generally is performed
in conjunction with an endoscopic retrograde cholangiopancreatography
(ERCP). The pancreatic duct is freely cannulated, an exogenous
secretagogue is administered as above, and the pancreatic juice then
is aspirated out of the duct as it is produced. The output of
pancreatic bicarbonate, protease, amylase, and lipase are measured.
This test is gaining popularity because most patients undergo ERCP at
some point in their evaluation."
ERCP may be able to kill two birds with one stone, so to speak.
UCLA has an excellent page describing SOD, including the three sub-types:
Here is a nice review article available for free on SOD, including
diagnosis and treatment of all subtypes.
I hope this information was useful. Best of luck with the diagnosis
and treatment of your symptoms. Please feel free to request any