This is a repository copy of Effectiveness of a national quality improvement programme to improve survival after emergency abdominal surgery (EPOCH) : a stepped-wedge cluster-randomised trial. Effectiveness of a national quality improvement programme to improve survival after emergency abdominal surgery (EPOCH) : a stepped-wedge cluster-randomised trial. The Lancet. ISSN 0140-6736 https://doi.org/10.1016/S0140-6736(18)32521-2 eprints@whiterose.ac.uk https://eprints.whiterose.ac.uk/ ReuseThis article is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs (CC BY-NC-ND) licence. This licence only allows you to download this work and share it with others as long as you credit the authors, but you can't change the article in any way or use it commercially. More information and the full terms of the licence here: https://creativecommons.org/licenses/ Implications of all the available evidenceDespite the success of some smaller projects, there was no survival benefit from a national quality improvement programme to implement a care pathway for patients undergoing emergency abdominal surgery. To succeed, large national quality improvement programmes need to allow for differences between hospitals and ensure teams have both the time and resources needed to improve patient care.

Loop ileostomy is an effective procedure to protect downstream intestinal anastomoses. Ileostomy reversal surgery is often performed within 12 months of formation but is associated with substantial morbidity due to severe post-surgical complications. Distal ileum is deprived of enteral nutrition and rendered inactive, often becoming atrophied and fibrotic. This study aimed to investigate the microbial and morphological changes that occur in the defunctioned ileum following loop ileostomy-mediated fecal stream diversion. Functional and defunctioned ileal resection tissue was obtained at the time of loop-ileostomy closure. Intrapatient comparisons, including histological assessment of morphology and epithelial cell proliferation, were performed on paired samples using the functional limb as control. Mucosal-associated microflora was quantified via determination of 16S rRNA gene copy number using qPCR analysis. DGGE with Sanger sequencing and qPCR methods profiled microflora to genus and phylum level, respectively. Reduced villous height and proliferation confirmed atrophy of the defunctioned ileum. DGGE analysis revealed that the microflora within defunctioned ileum is less diverse and convergence between defunctioned microbiota profiles was observed. Candidate Genera, notably Clostridia and Streptococcus, reduced in relative terms in defunctioned ileum. We conclude that Ileostomy-associated nutrient deprivation results in dysbiosis and impaired intestinal renewal in the defunctioned ileum. Altered host-microbial interactions at the mucosal surface likely contribute to the deterioration in homeostasis and thus may underpin numerous postoperative complications. Strategies to sustain the microflora before reanastomosis should be investigated.

Chronic venous ulcers are an example of abnormal wound healing showing chronic inflammation which together with the underlying vascular pathology results in delayed healing. Prostaglandins are among the most important mediators of inflammation. They have proinflammatory effects, predominantly by affecting the vasculature. Cyclooxygenase (COX) is the rate-limiting enzyme in prostanoid synthesis. It is present in two isoforms: COX-1 (constitutive cyclooxygenase) which is produced in the body to maintain normal haemostatic functions, and COX-2 (inducible cyclooxygenase), which is induced during inflammation in response to cytokines. Using immunoenzymatic labelling and western blot analysis, this study has shown that both COX-1 and COX-2 were up-regulated in chronic venous leg ulcers by comparison with normal human skin. De novo appearance of COX-2 in chronic venous ulcers was demonstrated, which is not seen in normal human skin. The main cellular sources of both COX isoforms are macrophages and endothelial cells. COX-2 is also produced by mast cells and fibroblasts. A COX radioimmunoassay showed up-regulation of COX activity in chronic venous ulcers compared with normal skin (p<0.05). Up-regulation of COX-1 in chronic venous leg ulcers could produce prostacyclin, which contributes to angiogenesis. Thus, inhibition of COX-1 by non-steroidal anti-inflammatory drugs (NSAIDs) could increase the local ischaemia and hypoxia associated with chronic venous ulcers. On the other hand, up-regulation of COX-2 is most likely responsible for the persistent inflammation in chronic venous leg ulcers. COX-2 selective inhibitors could therefore be effective in the treatment of chronic venous ulcers.

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Objective: Current treatment of venous leg ulcers (VLU) includes four-layer bandaging, appropriate superficial venous surgery and leg elevation. The aims of this study were to: investigate a device designed to measure leg elevation; assess how long patients elevate; and to assess the effect of elevation on ulcer healing, femoral vein velocity (FVV) and popliteal vein cross-sectional area (PVCSA), and venous pressure. Patients and methods: A datalogger and accelerometer were manufactured to measure leg elevation. The device was validated in eight control subjects; elevation was measured in 24 patients with VLU. Ulcers were traced over six weeks in 29 patients and elevation measured to correlate healing with elevation. Ten patients and 10 controls underwent duplex measurement of FVV and PVCSA to measure flow in relation to posture; nine patients underwent measurement of venous pressure with postural changes. Non-parametric statistical analysis was used. Results: The datalogger accurately recorded all episodes of elevation. Median (range) elevation time was 53 (0–350) mins/24 h; correlation between ulcer healing and elevation was poor at 0.103 ( P=0.616, Spearman); change in posture from sitting to supine produced a significant increase in median (range) FVV from 11 (7–24) to 34 (22–66) in VLU ( P=0.005) and 15 (12–34) to 38 (16–69) in controls ( P=0.005, Wilcoxon). Change in posture from supine to 25 degrees elevation produced no change in FVV in either group ( P=0.173 in VLU, P=0.327 in controls, Wilcoxon). In VLU, sitting PVCSA was 1.07 (0.51–1.45) cm2. Supine position significantly reduced the area to 0.46 (0.27–1.01) cm2 ( P=0.005, Wilcoxon). On elevation to 25°, PVCSA was further reduced to 0.28 (0.07–0.63) cm2 ( P=0.058, Wilcoxon). In controls, sitting PVCSA was 0.79 (0.31–1.56) cm2, supine was reduced to 0.46 (0.27–1.09) cm2 ( P=0.047, Wilcoxon) and on elevation was reduced to 0.23 (0.10–0.44) cm2 ( P=0.005, Wilcoxon). Venous pressure standing was 99 (73–116) mmHg, reduced to 76 (53–113) mmHg on sitting ( P=0.084), and further reduced to 23 (7–36) mmHg supine ( P=0.008, Wilcoxon). Conclusions: Leg elevation in patients with VLU is poor but can be accurately measured. Elevation in the presence of compression may not improve ulcer healing. Postural changes of the leg can produce an increase in deep venous flow and a reduction in venous pressure.