Although it could be many things this is one worth looking at. Get in to see your doctor.
Sphincter of Oddi Dysfunction
http://www.medscape.com/viewarticle/705256
Sphincter of Oddi Dysfunction
"Doctor, it feels like my gallbladder has come back!"
The diagnosis of sphincter of Oddi dysfunction (SOD) is often considered in patients with recurrent pains after cholecystectomy. Many patients have impressive objective findings on laboratory studies or imaging (eg, abnormal liver enzymes or a dilated bile duct), and are categorized traditionally by the Milwaukee classification as SOD type I.[1-3] When an endoscopic retrograde cholangiopancreatography (ERCP) is done, these patients are often found to have small bile duct stones or fibrotic sphincter stenosis, and are treated (usually effectively) by biliary sphincterotomy.
Much more problematic are the many patients who have only 1 abnormal finding (ie, a dilated duct or elevated transaminases), or indeed none at all (SOD types II and III, respectively). These patients are very difficult to evaluate and manage effectively because there are no definitive noninvasive diagnostic tests. In addition, some physicians are skeptical of the very existence of SOD, or assume that it is a psychiatric issue, or only a small part of a broader problem of motility disturbance or visceral hypersensitivity.
Patient Evaluation
The National Institutes of Health (NIH) State-of-the-Science Conference on ERCP strongly emphasized that patients with types II and III should be managed very carefully with noninvasive approaches and avoiding ERCP, if at all possible.[4]
Patients should undergo thorough evaluation, recognizing that there are many causes for "postcholecystectomy pain" other than SOD. There may be an organic biliary problem (leak, stone, or stricture). These can be suspected on clinical grounds (type and severity of pain, fluctuating lab values), and clarified with modern imaging. Often the cholecystectomy proves to have been a vain attempt to treat pains originating from another source. Thus, it may be necessary to consider musculoskeletal problems, functional digestive disorders, atypical dyspepsia, and pancreatic diseases.
When these other causes of pain have been considered and eliminated, if necessary with trials of various treatments, it is legitimate to consider SOD.
Magnetic resonance cholangiopancreatography (MRCP), preferably with secretin infusion, is an excellent and safe way to demonstrate the biliary and pancreatic ductal systems, and should always be considered in this context. Endoscopic ultrasound may be useful if low-grade pancreatitis is suspected. Checking liver enzymes and amylase/lipase within 24 hours of any acute pain attack may also provide evidence for transient obstruction.
Attempts have been made to demonstrate sphincter abnormalities with noninvasive tests, such as morphine-prostigmin provocation tests, dynamic isotope studies, and changes in bile duct diameter on scans after stimulation with fatty meals or cholecystokinin. Although some still advocate the use of these tests, most "expert centers" have found them to be insufficiently accurate for clinical use. Trials of medical therapy, such as antidepressants, antispasmodics, and calcium channel blocking agents may be worthwhile, but are rarely effective in the long term.[3]
Diagnostic Testing
When all of these approaches are exhausted, and when the symptoms are disabling, it is reasonable to consider ERCP. The NIH conference recommended that testing should always include sphincter manometry. Some have suggested avoiding manometry because of the risks, but several studies have shown that the likelihood of ERCP provoking pancreatitis is determined by the characteristics of the patient with "suspected SOD," and that sphincter manometry does not add to the risk.[5,6] The risk for pancreatitis can be reduced considerably with the use of temporary pancreatic stenting, usually with a 3 or 4FG flapless stent that is designed to pass spontaneously within a week or two.[7]
Sphincter manometry is widely thought to be the "gold standard" for the diagnosis of SOD, but the evidence is very thin. Cohort studies of manometry-directed sphincterotomy claim improvement in only about 2 of 3 of patients.[3] However, these patients are always anxious and sometimes desperate when they reach tertiary referral centers, and the interventions have a powerful placebo effect.[2,3] The first properly sham-controlled study in 40 patients with SOD type II (now 20 years old) did show that manometry predicted the outcome of biliary sphincterotomy,[8] but a subsequent study was far less convincing.[9] There are currently no data to support the predictive value of manometry in patients with SOD type III.
Because the benefit/risk ratio of sphincterotomy is less than ideal, efforts have been made to develop and encourage the use of somewhat less invasive ERCP treatments. Attempts to use biliary sphincter dilation and/or stenting as trials of treatment have resulted in unacceptably high rates of pancreatitis.[10] However, botulinum toxin injection into the sphincter appears to have promise.[3]
The Bottom Line
"Suspected sphincter of Oddi dysfunction" is a minefield that practitioners and patients should enter with great caution.[4,11] Extensive noninvasive imaging and trials of medical therapy should always precede consideration of ERCP, which carries particular hazards in this context. More research is badly needed to reduce the burdens of unsuccessful treatments and bad complications.
Opportunities for Research
We need to know how to identify those patients, if any, who actually have sphincter dysfunction and learn how to treat them effectively, with drug therapy or sphincter ablation. There are many interlinking outstanding issues. The Rome III project has recently defined SOD purely on clinical grounds (certain patterns of pain and disability), in the absence of detectable structural disease.[12] Although not validated, this definition does provide a starting point for appropriate studies.
Whether SOD "type III" really exists can be answered only by a large sham-controlled randomized evaluation of sphincter ablation. The role of manometry could be evaluated in such a study only if the results were ignored in the (random) treatment decision. Is it then ethical to randomize patients to sphincterotomy in the presence of normal manometry? We know that biliary and pancreatic pressures are often discordant, so some may need pancreatic sphincterotomy as well. If we assume that such a study can be performed, and that it does show that there are some subjects who respond to sphincter ablation, then it is possible to explore the predictors of success and failure. It would be helpful to know whether patients are more or less likely to respond depending on the pattern of their pain before and after cholecystectomy, the reasons for surgery and its immediate impact, their psychological profiles, and evidence for other functional diseases. In the context of such a comprehensive study, it would be possible to reexamine the value of dynamic biliary imaging, or trials of intrasphincteric botulinum toxin.
There are 2 problems in pursuing such studies. The first is how to define "successful treatment," including how to measure the burden of pain-related disability and how to decide how much improvement is clinically needed to justify the risks. Standard pain scores are not applicable in the context of intermittent pain. The second major hurdle is that the procedures are expensive, and must be grant funded in a randomized study.
