There is no clear consensus in the current guidelines published by major international anaesthetic associations on what is the most appropriate time for a patient to stop chewing gum. This open-label balanced-group randomised controlled trial aimed to evaluate whether the chewing of sugar-free gum caused an increased volume or reduced pH of residual gastric fluid in fasting patients. For this study 212 patients undergoing elective gastroscopy were randomised into a control group who followed routine fasting instructions and an intervention group who were asked to chew gum while fasting. Residual gastric fluid was aspirated under direct vision via a gastroscope under anaesthesia. The primary outcome was the incidence of a gastric residual volume >50 ml in participants who chewed gum compared with a control group. Secondary outcomes were variability in the overall gastric volume distribution and gastric pH distribution between the two groups. Nine out of 110 (8.2%) in the chewing gum group and six out of 102 (5.9%) in the control group had a residual gastric fluid volume >50 ml: incidence rate ratio 1.39 (95% confidence intervals (CI) 0.51–3.77; P = 0.60). However, only one patient (in the control group) had a residual gastric volume >73 ml. There was no statistically significant difference in gastric volume distribution between groups, odds ratio 1.60 (95% CI 0.99–2.58; P = 0.054) or in the distribution of gastric pH measurement, odds ratio 0.90 (95% CI 0.57–1.44; P = 0.67). These results indicate that if there is an increase in the incidence of residual gastric volume >50 ml in patients who chew gum preoperatively, it is likely to be small. Moreover, the absence of any patients in our chewing gum group with a residual gastric volume >73 ml is reassuring.

A contributing factor in the development of ulcerative colitis (UC) and Crohn's disease (CD) is the disruption of innate and adaptive signaling pathways due to aberrant cytokine production. The cytokine, interleukin (IL)-1β, is highly inflammatory and its production is tightly regulated through transcriptional control and both inflammasome-dependent and inflammasome- independent proteolytic cleavage. In this study, qRT-PCR, immunohistochemistry, immunofluorescence confocal microscopy were used to (1) assess the mRNA expression of NLRP3, IL-1β, CASP1 and ASC in paired biopsies from UC and CD patient, and (2) the colonic localization and spatial relationship of NLRP3 and IL-1β in active and quiescent disease. NLRP3 and IL-1β were found to be upregulated in active UC and CD. During active disease, IL-1β was localized to the infiltrate of lamina propria immune cells, which contrasts with the near-exclusive epithelial cell layer expression during non-inflammatory conditions. In active disease, NLRP3 was consistently expressed within the neutrophils and other immune cells of the lamina propria and absent from the epithelial cell layer. The disparity in spatial localization of IL-1β and NLRP3, observed only in active UC, which is characterized by a neutrophil-dominated lamina propria cell population, implies inflammasome-independent processing of IL-1β. Consistent with other acute inflammatory conditions, these results suggest that blocking both caspase-1 and neutrophil-derived serine proteases may provide an additional therapeutic option for treating active UC.

A contributing factor in the development of ulcerative colitis (UC) and Crohn's disease (CD) is aberrant signaling of the innate immune complex known as the inflammasome. The inflammasome regulates the production of interleukin (IL)1β and drives downstream inflammatory pathways. In this study of human tissue (ethics approval: H11930), we provide evidence for the disease-specific up-regulation of NLRP6 transcript and protein in ileal CD and describe an NLRP6-expressing goblet cell (GC) located predominantly in the upper portion of the intestinal crypt.

BACKGROUND:Colonoscopy and polypectomy can prevent up to 80% of colon cancer; however, a significant adenoma miss rate still exists, particularly in the right side of the colon. OBJECTIVE:To assess whether retroflexion in the right side of the colon significantly improves the adenoma detection rate (ADR) over forward-view assessment. DESIGN:Multicenter prospective cohort study. SETTING:Three tertiary care public and 2 private hospitals. PATIENTS:A total of 1351 consecutive adult patients undergoing elective colonoscopy. INTERVENTION:Withdrawal from the cecum was performed in the forward view initially and identified polyps removed. Once the hepatic flexure was reached, the cecum was reintubated and the right side of the colon was assessed in the retroflexed view to the hepatic flexure. MAIN OUTCOME MEASUREMENTS:ADR in the retroflexed view when compared with forward-view examination of the right side of the colon. RESULTS:Retroflexion was successful in 95.9% of patients, with looping the predominant (69.6%) reason for failure. Forward-view assessment of the right side of the colon identified 642 polyps, of which 531 were adenomas yielding a polyp and ADR of 28.57% and 24.64%, respectively. Retroflexion identified a further 84 polyps of which 75 were adenomas, improving the polyp and ADR to 30.57% and 26.4%, respectively. LIMITATIONS:Observational study. CONCLUSION:Right-sided retroflexion was successful in most of our cohort with a statistically significant but small increase in ADR. Right-sided retroflexion is safe when performed by experienced endoscopists with no adverse events observed in this cohort. ( CLINICAL TRIAL REGISTRATION:Australian New Zealand Clinical Trials Registry, ACTRN12613000424707.).

The falciform (sickle-shaped) ligament is one of five ligaments that connect the liver to the under-surface of the diaphragm and to the anterior abdominal wall. It passes in an antero-posterior plane and is the embryonic remnant of the ligamentum teres and the para-umbilical veins wrapped within two layers of peritoneum. It may contain a variable amount of extra-peritoneal fat and represents a potential space. In infants, falciform ligament inflammation or necrosis can occur as a complication of omphalitis. In adults, a falciform ligament abscess is a rare complication of instrumentation during laparoscopic surgery. The ligament can also become canalized in patients with portal hypertension creating engorged veins which radiate from the umbilicus (caput medusae). Another rare complication is inflammation of the falciform ligament associated with acute cholecystitis. In the patient illustrated below, abdominal pain appeared to be caused by necrosis of the falciform ligament, perhaps related to mild cholecystitis or ischemia. A male, aged 88, was transferred to our hospital with a 2-week history of increasing pain in the right upper quadrant of his abdomen. On arrival, he was noted to be febrile (37.8°C) and hypotensive and required admission to an Intensive Care Unit. Blood tests revealed an elevated white cell count (24x109/l) and C-reactive protein (179 mg/l) and minor changes in liver function tests. An abdominal computed tomography (CT) scan showed dilated intrahepatic ducts and a thickened gallbladder wall with multiple stones (Figure 1). Endoscopic sphincterotomy was performed at the time of endoscopic retrograde cholangiopancreatography but only two very small stones were removed from the bile duct. Although his blood tests appeared to improve, he continued to have pain in the right upper quadrant with clinical features of localized peritonitis. Magnetic resonance cholangiopancreatography (MRCP) confirmed effective decompression of the biliary system but a fluid tract with subacute hemorrhage was seen extending from the portahepatis to the anterior abdomen (Figure 2). Review of the initial CT scan identified a fluid collection with no interval change in size compared to MRCP (Figure 1, arrow). At laparotomy, the falciform ligament was found to be necrotic with possible involvement of the posterior rectus sheath. The falciform ligament was excised and a cholecystectomy was performed although the gallbladder did not appear to be inflamed. Histology of the falciform ligament showed large areas of hemorrhagic necrosis with no evidence of abscess formation. Unfortunately, he died 7 days after surgery because of pulmonary complications. Contributed by

Accurate and timely prediction of sudden cardiac death (SCD) is a necessary prerequisite for effective prevention and therapy. Although the largest number of SCD events occurs in patients without overt heart disease, there are currently no tests that are of proven predictive value in this population. Efforts in risk stratification for SCD have focused primarily on predicting SCD in patients with known structural heart disease. Despite the ubiquity of tests that have been purported to predict SCD vulnerability in such patients, there is little consensus on which test, in addition to the left ventricular ejection fraction, should be used to determine which patients will benefit from an implantable cardioverter defibrillator. On July 20 and 21, 2006, a group of experts representing clinical cardiology, cardiac electrophysiology, biostatistics, economics, and health policy were joined by representatives of the US Food and Drug administration, Centers for Medicare Services, Agency for Health Research and Quality, the Heart Rhythm Society, and the device and pharmaceutical industry for a round table meeting to review current data on strategies of risk stratification for SCD, to explore methods to translate these strategies into practice and policy, and to identify areas that need to be addressed by future research studies. The meeting was organized by the Duke Center for the Prevention of SCD at the Duke Clinical Research Institute and was funded by industry participants. This article summarizes the presentations and discussions that occurred at that meeting.

We have studied the response of erosive or ulcerative esophagitis to treatment with omeprazole and its subsequent relapse on cessation of therapy in 196 patients. In the first phase of the study omeprazole (20 or 40 mg daily) was compared with placebo in 64 patients. After 4 wk there was endoscopic healing in 81% (25 of 31) of omeprazole-treated patients and in only 6% (2 of 32) of placebo-treated patients. Endoscopic healing of esophagitis was accompanied by symptom relief and histologic healing of ulceration. In the second (dose finding) phase a further 132 patients were randomized to omeprazole (20 or 40 mg daily) and endoscopic healing was assessed. In patients with the mildest grade of ulcerative esophagitis (grade 2), healing occurred at 4 wk in 87% receiving 20 mg and in 97% receiving 40 mg. In patients with grade 3 esophagitis, 67% (20 mg) and 88% (40 mg) were healed. Less than half the patients with grade 4 esophagitis (Barrett's ulcers or confluent ulceration) healed with either 20 mg (48%) or 40 mg (44%). Regression analysis in the 164 omeprazole-treated patients showed no evidence that healing was influenced by factors other than severity of esophagitis at entry and omeprazole dose. In phase 3 of the study the rate of endoscopic relapse was determined in 107 endoscopically healed patients after stopping omeprazole. Erosive or ulcerative esophagitis recurred in 88 of 107 (82%) by 6 mo. Neither initial dose, grade of esophagitis, nor smoking was shown to influence relapse rate. Omeprazole is a highly effective treatment for peptic esophagitis. The 40-mg/day dosage produces endoscopic healing slightly more quickly than the 20-mg/day dosage, and the initial endoscopic gradings are of prognostic value. Relapse occurs rapidly when treatment is stopped.