Sphincter of Oddi function and dysfunction: Classification of SO dysfunction
Two classification systems for SO dysfunction have been developed for patients with biliary type pain. One system involves a ‘clinical’ classification based on endoscopic retrograde pancreato- cholangiography (ERCP) and liver function test abnormalities and the other, SO manometry.
The clinical classification system stratifies patients into three groups (types 1, 2 and 3), depending on the likelihood that SO dysfunction is present. Type 1 patients have all three abnormalities: a dilated common bile duct (12 mm) on ERCP; delayed drainage of contrast for the common bile duct (45 mins); and, on two occasions in association with pain episodes, abnormal alkaline phosphatase (AP) or abnormal ratio of alanine aminotransferase to aspartate aminotransferase (twice the upper limit of normal) on liver function testing. Type 2 patients have one or two abnormalities, and type 3 patients experience pain with none of the above abnormalities. It is thought that SO dysfunction is present in all type 1 patients, approximately 50% to 60% of type 2 patients and fewer than 10% of type 3 patients. Type 3 patients are believed to be the patients most likely to have irritable bowel syndrome.
Manometry is able to describe patients as ‘normal’ or ‘abnormal’. Normal manometric values have been determined from studies of healthy volunteers (Table 1), and abnormal values calculated as three standard deviations from the mean of normal values (Table 2). Patients with abnormal manometric values can be further classified into two subgroups of SO dysfunction. The first classification of abnormal manometry, SO stenosis, is represented by an elevated basal pressure (40 mmHg). SO stenosis defines a manometric abnormality and not necessarily a fixed structural lesion. A good example of this is seen in patients with superimposed phasic activity on an elevated basal pressure diagnostic of SO stenosis. The other manometric abnormality is known as SO dyskinesia and broadly suggests an incoordinate sphincter. The manometric abnormalities include excessive retrograde propagation of phasic waves (50%); an elevated basal pressure (40 mmHg) that relaxes with CCK or other smooth muscle relaxants (eg, buscopan), which is often termed SO spasm; gigantic phasic wave amplitudes (300 mmHg above the baseline); high frequency of phasic waves (seven/min), which is often termed tachyoddia; and finally, a paradoxical response to CCK. A paradoxical response to CCK is defined as no change or an increase in phasic activity. SO spasm has also been used to describe patients with an intermittently raised basal pressure.
Both classification systems have strengths and weaknesses. Bile duct dilation following cholecystectomy has been suggested to be a common finding, but in a well conducted prospective study, bile duct dilation was usually found to be less than 1 mm five years after cholecystectomy. Delayed biliary drainage observed in one study was found to be a common finding in asymptomatic subjects following chole- cystectomy and, thus, not a specific abnormality in patients with suspected SO dysfunction. This study has been methodolgically criticized for assessing biliary drainage in the prone position and for using a type of contrast that differed from that used in other studies. Assessment of contrast drainage at ERCP for up to 45 mins is very labour intensive and rarely performed for the full 45 mins. The same criticism can be made about manometry; it probably uses even more resources and requires significant technical expertise to be undertaken. As well, manometry is invasive and carries the risk of pancreatitis.
With the clinical classification, type 2 patients are poorly delineated as normal or abnormal. The effects of endoscopic sphincterotomy have been studied in type 2 patients, and manometry performed before sphincterotomy. The only reliable predictor of response to the therapy, and presumably indicative of the correct diagnosis, was manometri- cally proven SO stenosis (ie, an elevated basal pressure). A further criticism of this system is that type 3 patients are not all normal. In one study, 28% of type 3 patients were found to have manometrically proven SO stenosis. Another smaller study found that 55% of type 3 patients had an elevated SO basal pressure. Response to sphincterotomy for type 3 patients, based on the manometric finding of an elevated basal pressure, has found differences in improvement compared with type 2 patients, and also the duration of improvement, suggesting that the clinical classification may provide additional information over manometry alone. One study showed that type 1 patients appear to respond to sphincterotomy, even in the absence of manomet- ric abnormalities, leading to the suggestion that manometry in type 1 patients may be misleading.
Overall, manometry is a more reliable system for correctly diagnosing and classifying patients. Manometry can also more often reliably predict response to therapy, accepting that the ERCP findings of a dilated duct and delayed drainage of contrast, as well as transient liver enzyme abnormalities, may provide additional information when deciding on an appropriate therapy.
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A similar clinical classification system for pancreatic SO dysfunction has been proposed, but includes patients without pancreatitis and only ‘pancreatic’ pain. This condition of ‘pancreatic’ pain without pancreatitis is poorly defined. Manometry is clearly the superior way of classifying patients with pancreatic SO dysfunction.