Anorectal dysfunction is the focus of diagnostic investigations for faecal incontinence. However, severity of incontinence and anorectal investigation results can be discordant. The aim of this study was to define the relationships between anorectal investigation results and incontinence severity to determine which measures, if any, were predictive of incontinence severity. Patients presenting for investigation of faecal incontinence completed a symptom questionnaire, anorectal manometry, rectal sensation, pudendal nerve terminal motor latency, and endoanal ultrasound. Bivariate analyses were conducted between the Jorge-Wexner score and investigation results. Subgroup analyses were performed for gender and symptom subtypes (urge, passive, mixed). A multiple regression analysis was performed. Five hundred and thirty-eight patients were included. There were weak correlations between the Jorge-Wexner score and maximal squeeze pressure [r = − 0.24, 95%CI(− 0.31, − 0.16), p < 0.001], and resting pressure [r = − 0.18, (95%CI(− 0.26, − 0.10), p < 0.001]. In men only, there were significant associations between the Jorge-Wexner score and endoanal sonography [IAS defects: t(113) = − 2.26, p = 0.03, d = 0.58, 95%CI(− 4.38, − 0.29)] and rectal sensation (MTV: rs = − 0.24, 95%CI(− 0.41, − 0.06), p = 0.01). No substantial differences were observed in the urge/passive/mixed subgroup analyses. Multiple regression analysis included three variables: age (β = 0.02, p = 0.17), maximal resting pressure (β = − 0.01, p = 0.28), and maximal squeeze pressure (β = − 0.01, p < 0.01). The variance in the Jorge-Wexner score accounted for by this model was < 10%, (R2 = 0.07, p = < 0.01, adjusted R2 = 0.06). Anorectal investigations cannot predict the severity of faecal incontinence. This may be due to limitations of diagnostic modalities, the heterogeneity of anorectal dysfunction in these patients, or contributing factors which are extrinsic to the anorectum.

PROBLEM:A retrospective audit of surveillance for Barrett's oesophagus 1996-2001 identified the need to improve adherence to guidelines for the endoscopic surveillance of patients with Barrett's oesophagus.DESIGN:Prospective audit of the effect of disseminating guidelines in 2002. Prospective audit of the effect of introducing local guidelines and Barrett's oesophagus surveillance officers, 2003-2005.SETTING:Two general hospitals in Australia, 2002-5. All adult patients diagnosed with Barrett's oesophagus were included.KEY MEASURES FOR IMPROVEMENT:Proportions of patients in a Barrett's oesophagus surveillance programme who had appropriate time intervals between follow-up endoscopies and who had appropriate numbers of biopsies collected at endoscopy.STRATEGIES FOR CHANGE:Local guidelines were laid down. Surveillance coordinators for Barrett's oesophagus were introduced to manage the process according to a clinical protocol designed for each patient.EFFECTS OF CHANGE:Disseminating guidelines had little effect on practice. Six months after surveillance coordinators were introduced, adherence to the planned surveillance interval increased from 17% to 92% and the number of endoscopies at which sufficient biopsies were collected increased from 45% to 83%. These changes have been maintained.LESSONS LEARNT:Disseminating guidelines and results of an audit on endoscopic surveillance in Barrett's oesophagus had no effect on practice. Introducing coordinators who proactively managed the process greatly improved adherence to guidelines.

The squeeze pressure in the anal canal reflects the contribution of the external anal sphincter and is normally assessed manometrically by asking patients to contract their anal muscles. However, this is an artificial situation as normally the external sphincter contracts to retain rectal content. Some patients with normal anal sphincter anatomy and innervation record low squeeze pressures suggesting that the concept of voluntary squeeze is foreign. The aim of this study was to examine whether squeezing to retain a balloon mimics the physiology of defaecation more accurately.Patients undergoing routine anorectal manometry testing had in addition the inflation of a balloon catheter to the volume of the first and sustained sensation to simulate a faecal bolus within the rectum. The patient was asked to retain it when the balloon was subjected to gentle traction, thus contracting their anal sphincter to prevent passage of the balloon. Squeeze pressure was measured in response to voluntary contraction, the pressure generated to retain the balloon, then voluntary contraction again.Eighteen women and 2 men were tested. The median maximal squeeze pressures with the routine assessment was 131.0cmH(2)O. This increased to 210.0cmH(2)O when the patients attempted to retain the balloon and fell to 165.4cmH(2)O when patients were reassessed with voluntary squeeze postintervention. 15 of the patients improved their squeeze pressures with traction on the balloon.External anal sphincter contraction is difficult for some patients to perform on request. With traction on a balloon catheter anal squeeze pressures improved in most patients. This indicates that many patients perform maximal anal squeeze pressures better once that muscle group has been tested in a more normal physiological function. This simple technique could improve the accuracy of anorectal manometry results and evaluation in a larger popluation of symptomatic patients is warranted.

BACKGROUND:Faecal incontinence commonly affects women, principally because of childbirth. Our aims were to determine the functional effect of childbirth on the pressures generated by the anal sphincter and to determine the patterns of injury to the sphincter. METHODS:Anal manometry was performed in 53 primiparous women prenatally, in 50 women at a median of 5 weeks postnatally, and repeated in 26 women at a median of 6 months postnatally. In addition, anal ultrasound was performed postnatally. Pelvic floor symptoms were assessed. The mode of delivery was examined to determine what variables affected anal function. RESULTS:Squeeze pressure was significantly reduced (P < 0.001) 6 weeks postnatally (mean, 170.4 cm H2O; standard deviation (s), 56) compared with the prenatal value (mean, 225.6 cm H2O; s, 58). This occurred in symptomatic and asymptomatic women and in women with a normal anal ultrasound. Resting pressure was significantly reduced at 6 weeks (P < 0.001; prenatal mean, 91.6 cm H2O; s, 25; postnatal mean, 80.Ocm H2O; s, 21). Delivery method (vaginal or caesarean) was the only factor significant for the reduced squeeze pressure (r=53.377; standard error, 13.973; P < 0.001). Sphincter defects (41%) were common but did not influence anal sphincter function. CONCLUSION:Anal function was significantly affected by vaginal delivery with short-duration follow-up. This occurred with and without evidence of an anal sphincter injury. The importance of a sphincter injury is questioned.

Increasing evidence suggests that motility disorders of the sphincter of Oddi may lead to episodes of recurrent pancreatitis in a small proportion of patients with the diagnosis of idiopathic recurrent pancreatitis. Over 10 years, 35 patients have been identified and treated for this condition. The aim of the study was to assess symptomatic outcome in these patients. Following the exclusion of common causes of pancreatitis the patients underwent sphincter of Oddi manometry. Patients with manometric abnormalities and three with normal manometric findings underwent treatment. Twenty-six patients with persistent symptoms underwent total division of the sphincter via open sphincteroplasty and septectomy. Patients were followed up according to symptoms and classed as having a cure, mild symptoms or no change. At a median follow-up of 24 (range 9-105) months, 15 of the 26 patients were cured, eight had only mild symptoms and three remained unchanged. In the majority of patients with a good clinical outcome, manometry had demonstrated sphincter of Oddi stenosis. Total division of the sphincter of Oddi is associated with good symptomatic outcome in patients with recurrent episodes of pancreatitis and documented sphincter of Oddi stenosis.