Joint Advisory Group on Gastrointestinal Endoscopy (JAG) framework for managing underperformance in gastrointestinal endoscopy.

Underperformance can be defined as performance which persistently falls below a desired minimum standard considered acceptable for patient care. Within gastrointestinal endoscopy, underperformance may be multifactorial, related to an individual's knowledge, skills, attitudes, health or external factors. If left unchecked, underperformance has the potential to impact on care and ultimately patient safety. Managing underperformance should be a key attribute of high-quality endoscopy service, as recognised in the Joint Advisory Group on Gastrointestinal Endoscopy (JAG) accreditation process. However, it is recognised that not all services have robust mechanisms to do this. This article provides the JAG position on managing underperformance in endoscopy, defined through a practical framework. This follows a stepwise process of detecting underperformance, verification, identification of additional causative factors, providing support and reassessment. Detection and verification of issues may require use of multiple evidence sources, including performance data, feedback and appraisal reports. Where technical underperformance is identified, this should be risk stratified by potential risk to patient safety. Support should be tailored to each individual case based on the type of underperformance detected, any causative factors with an action plan developed. Support may include coaching, mentoring, training and upskilling. Wider support from the medical director's office or external services may also be required. Monitoring and reassessment is a crucial part of the overall process.

Endoscopy training in the UK pre-COVID-19 environment: a multidisciplinary survey of endoscopy training and the experience of reciprocal feedback.

OBJECTIVE: Training in gastrointestinal endoscopy in the UK occurs predominantly in a real world one-to-one trainer to trainee interaction. Previous surveys have shown surgical and gastroenterology trainees have had mixed experiences of supervision and training, and no surveys have explored specifically the role of trainee to trainer feedback. This study aimed to explore the experience of training and of providing trainer feedback for all disciplines of endoscopy trainees. DESIGN/METHOD: An online survey designed in collaboration with Joint Advisory Committee training committee and trainee representatives was distributed from January 2020 but was interrupted by the COVID-19 pandemic and hence terminated early. RESULTS: There were 129 responses, including trainees from all disciplines and regions, of which 86/129 (66.7%) rated the culture in their endoscopy units favourably-either good or excellent. 65/129 (50.4%) trainees reported having one or more training lists allocated per week, with 41/129 (31.8%) reporting only ad hoc lists. 100/129 (77.5%) respondents were given feedback and 97/129 (75.2%) were provided with learning points from the list. 65/129 (50.4%) respondents reported their trainer completed a direct observation of procedure or direct observation of polypectomies. 73/129 (56.6%) respondents reported that they felt able to give feedback to their trainer, with 88/129 (68.2%) feeling they could do this accurately. Barriers to trainer feedback cited included time constraints, lack of anonymity and concerns about affecting the trainer-trainee relationship. CONCLUSION: Overall, the training environment has improved since previous surveys. There are still issues around interdisciplinary differences with some surgical trainees finding the training environment less welcoming, and trainee perceptions of hierarchical barriers and trainer responsiveness to feedback limiting the accuracy of their feedback.

Training pathway for small bowel capsule endoscopy in the UK.

The demand for small bowel (SB) capsule endoscopy (CE) is increasing in the UK. However, there remains a wide variation in the number of CE procedures performed in different centres. Across the UK there is a lack of a clear training pathway or certification process. A standardised national Joint Advisory Group (JAG) on Gastrointestinal Endoscopy approved a 1-year training and accreditation programme accessible to all professional groups that may wish to train in SB CE. Structured training is delivered using JAG-accredited CE courses and an electronic learning module. Prior to setting a knowledge-based assessment, a minimum of 50 SB CE cases are recommended to be read in tandem with a trainer at a local centre, with proficiency documented using Direct Observation of Procedural Skill (DOPS) assessments.

Training in general internal medicine: what do trainees want and what can we deliver?

General internal medicine (GIM) training, usually as part of a dual accreditation programme, is increasingly challenging to deliver as a result of increased numbers of acute admissions, changes to consultant input into medical 'on call' and the reduction in the numbers of units taking unselected medical patients. GIM has become synonymous with acute medical take, reducing the scope of programmes to deliver a true general medical experience. The role of the 'medical registrar' is reported to be increasingly unpopular with trainees. Differing models of the delivery of training are in place. We have carried out a two-stage questionnaire in order to determine the views of both trainees and trainers on different models of training and their deliverability. The first stage defined the key areas of concern for trainees and the second focused on these areas and the ability of local education providers to deliver an expanded GIM programme. Our data suggest that trainees would value a face-to-face annual review of competence progression (ARCP) for GIM, separate from their specialty ARCP, and would support more structured blocks of GIM training in order to allow later specialty-focused training. However, -significant concerns were raised about the ability of many units to deliver such training beyond the acute medical 'take'.

Cyclooxygenase 2, p53, beta-catenin, and APC protein expression in gastric adenomatous polyps.

Gastric adenomatous polyps are rare findings in upper gastrointestinal endoscopy; however, they are associated strongly with malignant transformation. Few series describe the oncogenic characteristics of gastric adenomas. In the present study, we immunohisto-chemically assessed the expression of cyclooxygenase (COX)-2, beta-catenin, p53, and adenomatous polyposis coli (APC) in paraffin-embedded specimens of 14 gastric adenomas. Control samples of normal gastric tissue and gastric adenocarcinoma also were analyzed. Of the adenomas, 7 demonstrated overexpression of COX-2, and all demonstrated nuclear p53 accumulation. Accumulation of beta-catenin in the nucleus and cytoplasm was detected in 38% (3/8) of specimens. Loss of APC staining was observed in 50% (4/8). Similar alterations in oncoprotein expression were seen in gastric cancers but not in normal control sections. Gastric adenomas display alterations in the expression of COX-2, beta-catenin, and APC similar to those seen in adenocarcinomas; however, accumulation of p53 was significantly more common in adenomas than in cancers.

The effect of ascorbic acid on Helicobacter pylori induced cyclooxygenase 2 expression and prostaglandin E2 production by gastric epithelial cells in vitro.

BACKGROUND: Cyclooxygenase 2 (COX-2) is induced by the presence of Helicobacter pylori (H. pylori) on the gastric mucosa as part of the inflammatory response; this results in the synthesis of prostaglandins that amplify the local inflammatory response. The presence of H. pylori inhibits the secretion of ascorbate into the gastric lumen. Interestingly, ascorbate inhibits the growth of H. pylori and low dietary levels are associated with an increased risk of gastric adenocarcinoma. We therefore investigated the effect of ascorbate on H. pylori mediated COX-2 induction and prostaglandin production in vitro. METHODS: H. pylori was cocultured with gastric epithelial cells in the presence of ascorbate at physiological concentrations. The expression of COX-2 was assessed by Western blotting and prostaglandin E(2) (PGE(2)) was assessed by ELISA. RESULTS: Ascorbate inhibited gastric cell PGE(2) synthesis but not in COX-2 expression in response to H. pylori. In the absence of the organism, ascorbate also reduced PGE(2) expression in cells that constitutively express COX-2, again with no reduction of COX-2 protein expression. CONCLUSIONS: Physiological concentrations of ascorbate inhibit PGE(2) but not COX-2 expression in response to H. pylori in gastric epithelial cells.

Induction of cyclooxygenase 2 by Escherichia coli but not Helicobacter pylori lipopolysaccharide in gastric epithelial cells in vitro.

BACKGROUND: Cyclooxygenase 2 (COX-2) is an inducible enzyme that plays a key role in the synthesis of prostaglandins in response to inflammatory stimuli. It is expressed in the gastric mucosa as part of the response to infection with Helicobacter pylori. The specific interaction between H. pylori and the gastric epithelium that results in COX-2 expression has not been identified. METHODS: In order to investigate the hypothesis that lipopolysaccharide (LPS) from H. pylori plays a role in the induction of cyclooxygenase 2 in the stomach, gastric cell lines MKN-7 and MKN-45 were incubated with LPS from either H. pylori NCTC 11637 or Escherichia coli 055:B5. Incubation of cells with live H. pylori NCTC 11637 was also carried out as a positive control. Cells were then analysed for COX-2 protein and mRNA and prostaglandin E2 synthesis. RESULTS: Cyclooxygenase 2 protein and mRNA expression was induced by E. coli LPS and live H. pylori, but not by H. pylori LPS. Prostaglandin E2 synthesis increased in a dose-dependent manner in both cell lines with E. coli but not H. pylori LPS. CONCLUSIONS: H. pylori LPS is of low biological activity when compared with E. coli LPS in its ability to induce the expression of cyclooxygenase 2 and synthesis of prostaglandin E2. This may provide one mechanism by which H. pylori minimizes the inflammatory response in the gastric mucosa, allowing chronic infection.