'Case of the month': a novel way to learn from endoscopy-related patient safety incidents.

Patient safety incidents (PSIs) are unintended or unexpected incidents which can or do lead to patient harm. The Joint Advisory Group on Gastrointestinal Endoscopy (JAG) acknowledges that PSIs should be reviewed by endoscopy services and learning shared among staff. It is recognised that more could be done to promote shared learning as outlined by the JAG 'Improving Safety and Reducing Error in Endoscopy' strategy. The 'Case of the month' series aims to provide a broad selection of cases and subsequent learning that can be shared among services and their workforce. This review focuses on five case vignettes that highlight a variety of PSIs in endoscopy. A structured approach, based on incident analysis methodology, is applied to each case to categorise PSIs and develop learning points. Learning is directed toward the individual, team and healthcare organisation. A selection of methods to disseminate learning at local, regional and national levels are also described.

Diagnostic accuracy of whole-body MRI versus standard imaging pathways for metastatic disease in newly diagnosed colorectal cancer: the prospective Streamline C trial.

BACKGROUND: Whole-body MRI (WB-MRI) could be an alternative to multimodality staging of colorectal cancer, but its diagnostic accuracy, effect on staging times, number of tests needed, cost, and effect on treatment decisions are unknown. We aimed to prospectively compare the diagnostic accuracy and efficiency of WB-MRI-based staging pathways with standard pathways in colorectal cancer. METHODS: The Streamline C trial was a prospective, multicentre trial done in 16 hospitals in England. Eligible patients were 18 years or older, with newly diagnosed colorectal cancer. Exclusion criteria were severe systemic disease, pregnancy, contraindications to MRI, or polyp cancer. Patients underwent WB-MRI, the result of which was withheld until standard staging investigations were complete and the first treatment decision made. The multidisciplinary team recorded its treatment decision based on standard investigations, then on the WB-MRI staging pathway (WB-MRI plus additional tests generated), and finally on all tests. The primary outcome was difference in per-patient sensitivity for metastases between standard and WB-MRI staging pathways against a consensus reference standard at 12 months, in the per-protocol population. Secondary outcomes were difference in per-patient specificity for metastatic disease detection between standard and WB-MRI staging pathways, differences in treatment decisions, staging efficiency (time taken, test number, and costs), and per-organ sensitivity and specificity for metastases and per-patient agreement for local T and N stage. This trial is registered with the International Standard Randomised Controlled Trial registry, number ISRCTN43958015, and is complete. FINDINGS: Between March 26, 2013, and Aug 19, 2016, 1020 patients were screened for eligibility. 370 patients were recruited, 299 of whom completed the trial; 68 (23%) had metastasis at baseline. Pathway sensitivity was 67% (95% CI 56 to 78) for WB-MRI and 63% (51 to 74) for standard pathways, a difference in sensitivity of 4% (-5 to 13, p=0·51). No adverse events related to imaging were reported. Specificity did not differ between WB-MRI (95% [95% CI 92-97]) and standard pathways (93% [90-96], p=0·48). Agreement with the multidisciplinary team's final treatment decision was 96% for WB-MRI and 95% for the standard pathway. Time to complete staging was shorter for WB-MRI (median, 8 days [IQR 6-9]) than for the standard pathway (13 days [11-15]); a 5-day (3-7) difference. WB-MRI required fewer tests (median, one [95% CI 1 to 1]) than did standard pathways (two [2 to 2]), a difference of one (1 to 1). Mean per-patient staging costs were £216 (95% CI 211-221) for WB-MRI and £285 (260-310) for standard pathways. INTERPRETATION: WB-MRI staging pathways have similar accuracy to standard pathways and reduce the number of tests needed, staging time, and cost. FUNDING: UK National Institute for Health Research.

An unusual cause of intestinal failure.

A 62-year-old man presented to the emergency department with 5 weeks of worsening lower abdominal pain associated with watery diarrhoea, vomiting and 10% loss of body weight. He had recently experienced night blindness. There was no history of foreign travel. His past medical history included hypertension, sickle cell trait and type 2 diabetes well controlled on metformin. He had not been prescribed any recent steroids and denied significant alcohol intake. On examination, he had a tachycardia at 110 bpm and was afebrile and normotensive. He was malnourished with pedal pitting oedema extending to both knees. His abdomen was soft but distended and diffusely tender. Blood tests showed a serum albumin of 12 g/L. Stool samples were negative. HIV testing was negative, and immunoglobulin levels were normal. CT of the abdomen showed thickened, hyperenhancing jejunal loops with diffuse mesenteric inflammatory fat stranding and enlarged mesenteric lymph nodes. Colonoscopy was unremarkable. Enteroscopy showed granular oedematous mucosa and extensive, deep ulcerations. Jejunal biopsies were obtained. Microscopy samples were negative for tuberculosis (TB) culture. Histology revealed inflamed and ulcerated small bowel mucosa with plump endothelial cells with the appearance below. There were no granulomata (figures 1 and 2). Figure 1Endoscopic examination of the jejunum. Figure 2Plump endothelial cells seen on microscopy. QUESTION: What is the differential diagnosis?

Dedicated Barrett's surveillance sessions managed by trained endoscopists improve dysplasia detection rate.

Background and study aim Barrett's esophagus (BE)-associated dysplasia is an important marker for risk of progression to esophageal adenocarcinoma (EAC) and an indication for endoscopic therapy. However, BE surveillance technique is variable. The aim of this study was to assess the effect of dedicated BE surveillance lists on dysplasia detection rate (DDR). Patients and methods This was a prospective study of patients undergoing BE surveillance at two hospitals - community (UHL) and upper gastrointestinal center (GSTT). Four endoscopists (Group A) were trained in Prague classification, Seattle protocol biopsy technique, and lesion detection prior to performing BE surveillance endoscopies at both sites, with dedicated time slots or lists. The DDR was then compared with historical data from 47 different endoscopists at GSTT and 24 at UHL (Group B) who had undertaken Barrett's surveillance over the preceding 5-year period. Results A total of 729 patients with BE underwent surveillance endoscopy between 2007 and 2012. There was no significant difference in patient age, sex, or length of BE between the two groups. There was a significant difference in detection rate of confirmed indefinite or low grade dysplasia and high grade dysplasia (HGD)/EAC between the two groups: 18 % (26 /142) Group A vs. 8 % (45/587) in Group B (P  < 0.001). Documentation of Prague criteria and adherence to the Seattle protocol was significantly higher in Group A. Conclusion This study demonstrated that a group of trained endoscopists undertaking Barrett's surveillance on dedicated lists had significantly higher DDR than a nonspecialist cohort. These findings support the introduction of dedicated Barrett's surveillance lists.

Anaemia investigation in practice: inappropriate, cost inefficient with a risk of missing gastrointestinal cancer. Can we improve?

Iron-deficiency anaemia (IDA) is often inappropriately investigated. This study aimed to improve referrals, estimate cost implications and determine effectiveness of referral criteria for diagnosing cancer. Patients referred for investigation of anaemia were studied. IDA was defined as haemoglobin < 12.5 g/dl (M) and < 11.5 g/dl (F), with ferritin <15 ng/l (if normal erythrocyte sedimentation rate) or mean corpuscular volume <76 fl. After referral form redesign/trust education, data were recollected. Sixty-six of 118 referred patients had non-IDA with annual cost of inappropriate referrals pounds 176,840. The haematology database identified 37 patients (30 F) with uninvestigated IDA (lost revenue pounds 120,254). After changes, 43/103 referred patients had non-IDA (p < 0.05), with an annual saving of pounds 72,600. Fourteen of 112 patients with IDA had cancer versus 4/109 non-IDA (p < 0.025), overall prevalence 8.1%. Many referrals for anaemia investigation are inappropriate and a 35% reduction was achieved. The sensitivity and negative predictive value of the referral criteria for diagnosing gastrointestinal cancer were 77.8% and 96.3% respectively.

Selective white cell apheresis reduces relapse rates in patients with IBD at significant risk of clinical relapse.

BACKGROUND: We assessed whether selective granulocyte and monocyte/macrophage adsorption apheresis maintained clinical remission in asymptomatic inflammatory bowel disease (IBD) patients at significant risk of clinical relapse. METHODS: Sixty asymptomatic patients (age 18-70 years) with IBD (in clinical remission) with fecal calprotectin over 250 microg/g (which defines those at risk of clinical relapse with >80% specificity and sensitivity) were recruited for this open-label, prospective, randomized, controlled study. Twenty-nine underwent selective leukocytapheresis, undergoing 5, once weekly, out-patient sessions. Thirty-one had unchanged maintenance treatment and acted as controls. Follow-up for a clinical relapse was 6 months. The secondary outcome variable was the time to relapse. RESULTS: The number of patients who remained in clinical remission at 6 months was significantly lower in controls (32.3%) than in the apheresis (72.4%) group (P = 0.0023, Fisher's exact test). The time to first relapse was significantly earlier in the control group (99 +/- 73 days) as compared with the apheresis group (161 +/- 44 days) (log-rank test; P = 0.0004). Mild and transient headache was reported by 16 of the 29 (55%) for up to 3 hours, but no serious side effects were observed. CONCLUSIONS: This study represents a new approach to the treatment of IBD by targeting a group of asymptomatic patients for treatment who are at significant risk of relapse based on high fecal calprotectin concentrations. Selective leukocytapheresis significantly reduced the number of, and increased the time to, clinical relapse in these patients without serious side effects.

Helicobacter hypothesis for idiopathic parkinsonism: before and beyond.

We challenge the concept of idiopathic parkinsonism (IP) as inevitably progressive neurodegeneration, proposing a natural history of sequential microbial insults with predisposing host response. Proof-of-principle that infection can contribute to IP was provided by case studies and a placebo-controlled efficacy study of Helicobacter eradication. "Malignant" IP appears converted to "benign", but marked deterioration accompanies failure. Similar benefit on brady/hypokinesia from eradicating "low-density" infection favors autoimmunity. Although a minority of UK probands are urea breath test positive for Helicobacter, the predicted probability of having the parkinsonian label depends on the serum H. pylori antibody profile, with clinically relevant gradients between this "discriminant index" and disease burden and progression. In IP, H. pylori antibodies discriminate for persistently abnormal bowel function, and specific abnormal duodenal enterocyte mitochondrial morphology is described in relation to H. pylori infection. Slow intestinal transit manifests as constipation from the prodrome. Diarrhea may flag secondary small-intestinal bacterial overgrowth. This, coupled with genetically determined intense inflammatory response, might explain evolution from brady/hypokinetic to rigidity-predominant parkinsonism.

Sequence changes in predicted promoter elements of STK11/LKB1 are unlikely to contribute to Peutz-Jeghers syndrome.

BACKGROUND: Germline mutations or large-scale deletions in the coding region and splice sites of STK11/LKB1 do not account for all cases of Peutz-Jeghers syndrome (PJS). It is conceivable that, on the basis of data from other diseases, inherited variation in promoter elements of STK11/LKB1 may cause PJS. RESULTS: Phylogenetic foot printing and transcription factor binding site prediction of sequence 5' to the coding sequence of STK11/LKB1 was performed to identify non-coding sequences of DNA indicative of regulatory elements. A series of 33 PJS cases in whom no mutation in STK11/LKB1 could be identified were screened for sequence changes in the putative promoter defined by nucleotides -1090 to -1472. Two novel sequence changes were identified, but were found to be present in healthy individuals. CONCLUSION: These findings indicate that promoter sequence changes are unlikely to contribute to PJS.

Diagnostic value of Doppler assessment of the hepatic and portal vessels and ultrasound of the spleen in liver disease.

OBJECTIVES: To investigate the clinical utility and the intra-observer and inter-observer variability of Doppler ultrasound assessment of the hepatic and portal vessels along with measurement of spleen size in the diagnosis of chronic liver disease and cirrhosis. METHODS AND MATERIALS: Ultrasound measurements of portal vein diameter (PVD), portal vein velocity (PVV), hepatic arterial resistance index (HARI), hepatic vein profile (HVP), and spleen size were obtained in 49 controls and 45 patients with liver disease (23 with primary biliary cirrhosis, 22 with hepatitis C) by two experienced observers, who each performed three blinded measurements of each variable. Control values were derived from normal hospital workers. Percutaneous liver biopsies in 41 of the patients showed cirrhosis (14 patients), moderate/severe fibrosis (13 patients), and early disease (14 patients). RESULTS: Seventy-one percent of cirrhotic patients had splenomegaly (> 13.6 cm). The spleen size was significantly larger in cirrhotics (16.0 cm) than in non-cirrhotics (13.0 cm, P < 0.009) and healthy controls (10.7 cm, P < 0.00005), and was the only independent predictor of cirrhosis, with a threshold of 15 cm predicting cirrhosis with a specificity of 98%, positive predictive value of 93%, sensitivity of 57% and negative predictive value of 80%. HVP was abnormal in 76.9% of cirrhotics, 57.7% of non-cirrhotics and 2.1% of controls (P < 0.04). However, the mean PVV, PVD and HARI were no different between controls and patients or between cirrhotic and non-cirrhotic liver disease. There was significant inter-observer variability for PVV, but intra-observer and inter-observer variability was acceptable for the other measurements. CONCLUSIONS: Splenomegaly size and abnormal HVP are useful predictors of chronic liver disease and cirrhosis, and both can be measured reliably and reproducibly. However, Doppler measurements of PVV, PVD and HARI are not useful in distinguishing patients with chronic liver disease from normal controls.

Immunohistochemical differences in the portal tract and acinar infiltrates between primary biliary cirrhosis and autoimmune cholangitis.

BACKGROUND: Antimitochondrial antibody-negative primary biliary cirrhosis, or autoimmune cholangitis, may be indistinguishable clinically and histologically from antimitochondrial antibody-positive primary biliary cirrhosis. AIMS: We aimed to compare the phenotypic markers of the portal and acinar infiltrates in autoimmune cholangitis and antimitochondrial antibody-positive primary biliary cirrhosis. PATIENTS AND METHODS: Formalin-fixed, paraffin-embedded liver sections were identified from 32 patients with a clinical and histological diagnosis of primary biliary cirrhosis. Thirteen were antimitochondrial antibody-negative (autoimmune cholangitis group) and 19 were antimitochondrial antibody-positive. The groups were well matched for age, histological stage, liver biochemistry and drug treatment. Immunohistochemical staining was performed using monoclonal antibodies against CD3 (pan T cell), CD8 (cytotoxic), CD45RO (memory), CD45RA (naive), CD68 (macrophages) and against the secreted form of eosinophilic cationic protein (EG2). RESULTS: In autoimmune cholangitis, both portal and acinar CD3 cell counts were significantly higher than in antimitochondrial antibody-positive primary biliary cirrhosis (median portal count 421 vs 257 cells/graticule, P< 0.03; median acinar count 18 vs 9 cells/graticule, P< 0.02). There were no differences between the groups in portal or lobular CD8, CD45RO, CD45RA, CD68 or EG2. Of the total group (antimitochondrial antibody positives and negatives), there were significantly more CD45RA cells in early (stage 1) compared with cirrhotic (stage 4) disease (median 19.3 vs 14 cells/graticule, P< 0.03). EG2 staining was found in eight of the 32 sections overall, but not in the patients with stage 1 disease (P< 0.04). CONCLUSION: CD3 counts are higher in autoimmune cholangitis than in antimitochondrial antibody-positive primary biliary cirrhosis in both portal and acinar areas. However, there are no significant differences in memory/naïve T-cell subsets between both conditions and, in both, loss of naive T lymphocytes and secretion of eosinophilic cationic protein occur with disease progression. This implies that the effector pathways of bile duct destruction are similar in autoimmune cholangitis and primary biliary cirrhosis.