This consensus statement presents a comprehensive and evidence-based set of guidelines for the care of postoperative nausea and vomiting (PONV) in both adult and pediatric populations. The guidelines are established by an international panel of experts under the auspices of the American Society of Enhanced Recovery and Society for Ambulatory Anesthesia based on a comprehensive search and review of literature up to September 2019. The guidelines provide recommendation on identifying high-risk patients, managing baseline PONV risks, choices for prophylaxis, and rescue treatment of PONV as well as recommendations for the institutional implementation of a PONV protocol. In addition, the current guidelines focus on the evidence for newer drugs (eg, second-generation 5-hydroxytryptamine 3 [5-HT3] receptor antagonists, neurokinin 1 (NK1) receptor antagonists, and dopamine antagonists), discussion regarding the use of general multimodal PONV prophylaxis, and PONV management as part of enhanced recovery pathways. This set of guidelines have been endorsed by 23 professional societies and organizations from different disciplines (Appendix 1). What Other Guidelines Are Available on This Topic? Guidelines currently available include the 3 iterations of the consensus guideline we previously published, which was last updated 6 years ago 1–3 ; a guideline published by American Society of Health System Pharmacists in 1999 4 ; a brief discussion on PONV management as part of a comprehensive postoperative care guidelines 5 ; focused guidelines published by the Society of Obstetricians and Gynecologists of Canada, 6 the Association of Paediatric Anaesthetists of Great Britain & Ireland 7 and the Association of Perianesthesia Nursing 8 ; and several guidelines published in other languages. 9–12 Why Was This Guideline Developed? The current guideline was developed to provide perioperative practitioners with a comprehensive and up-to-date, evidence-based guidance on the risk stratification, prevention, and treatment of PONV in both adults and children. The guideline also provides guidance on the management of PONV within enhanced recovery pathways. How Does This Guideline Differ From Existing Guidelines? The previous consensus guideline was published 6 years ago with a literature search updated to October 2011. Several guidelines, which have been published since, are either limited to a specific populations 7 or do not address all aspects of PONV management. 13 The current guideline was developed based on a systematic review of the literature published up through September 2019. This includes recent studies of newer pharmacological agents such as the second-generation 5-hydroxytryptamine 3 (5-HT3) receptor antagonists, a dopamine antagonist, neurokinin 1 (NK1) receptor antagonists as well as several novel combination therapies. In addition, it also contains an evidence-based discussion on the management of PONV in enhanced recovery pathways. We have also discussed the implementation of a general multimodal PONV prophylaxis in all at-risk surgical patients based on the consensus of the expert panel.

BACKGROUNDDespite growing evidence that bariatric/metabolic surgery powerfully improves type 2 diabetes (T2D), existing diabetes treatment algorithms do not include surgical options. AIMThe 2nd Diabetes Surgery Summit (DSS-II), an international consensus conference, was convened in collaboration with leading diabetes organizations to develop global guidelines to inform clinicians and policymakers about benefits and limitations of metabolic surgery for T2D. METHODSA multidisciplinary group of 48 international clinicians/scholars (75% nonsurgeons), including representatives of leading diabetes organizations, participated in DSS-II. After evidence appraisal (MEDLINE [1 January 2005-30 September 2015]), three rounds of Delphi-like questionnaires were used to measure consensus for 32 data-based conclusions. These drafts were presented at the combined DSS-II and 3rd World Congress on Interventional Therapies for Type 2 Diabetes (London, U.K., 28-30 September 2015), where they were open to public comment by other professionals and amended face-to-face by the Expert Committee. RESULTSGiven its role in metabolic regulation, the gastrointestinal tract constitutes a meaningful target to manage T2D. Numerous randomized clinical trials, albeit mostly short/midterm, demonstrate that metabolic surgery achieves excellent glycemic control and reduces cardiovascular risk factors. On the basis of such evidence, metabolic surgery should be recommended to treat T2D in patients with class III obesity (BMI ‡40 kg/m 2 ) and in those with class II obesity (BMI 35.0-39.9 kg/m 2 ) when hyperglycemia is inadequately controlled by lifestyle and optimal medical therapy. Surgery should also be considered for patients with T2D and BMI 30.0-34.9 kg/m 2 if hyperglycemia is inadequately controlled despite optimal treatment with either oral or injectable medications. These BMI thresholds should be reduced by 2.5 kg/m 2 for Asian patients. CONCLUSIONSAlthough additional studies are needed to further demonstrate long-term benefits, there is sufficient clinical and mechanistic evidence to support inclusion of metabolic surgery among antidiabetes interventions for people with T2D and obesity. To date, the DSS-II guidelines have been formally endorsed by 45 worldwide medical and scientific societies. Health care regulators should introduce appropriate reimbursement policies.

Dendritic cells (DCs) that orchestrate mucosal immunity have been studied in mice. Here we characterize human gut DC populations, and define their relationship to previously studied human and mouse DCs. CD103+Sirpα− DCs were related to human blood CD141+ and to mouse intestinal CD103+CD11b− DCs and expressed markers of cross-presenting DCs. CD103+Sirpα+ DCs aligned with human blood CD1c+ DCs and mouse intestinal CD103+CD11b+ DCs and supported regulatory T cell induction. Both CD103+ DC subsets induced TH17 cells, while CD103−Sirpα+ DCs induced TH1 cells. Comparative transcriptomics revealed conserved transcriptional programs among CD103+ DC subsets and uncovered a selective role for Bcl-6 and Blimp-1 in CD103+Sirpα− and intestinal CD103+CD11b+ DC specification, respectively. These results highlight evolutionarily conserved and divergent programming of intestinal DCs.

Objective The biological mechanisms linking obesity to insulin resistance have not been fully elucidated. We have shown that insulin resistance/glucose intolerance in diet-induced obese mice is related to a shift in the ratio of pro- and anti-inflammatory T cells in adipose tissue. We sought to test the hypothesis that the balance of T-cell phenotypes would be similarly related to insulin resistance in human obesity. Approach and Results Healthy overweight/obese human subjects underwent adipose-tissue biopsies and quantification of insulin-mediated-glucose disposal by the modified insulin-suppression test. T-cell subsets were quantitated by flow cytometry in visceral (VAT) and subcutaneous adipose tissue (SAT). Results showed that CD4 and CD8 T-cells infiltrate both depots, with pro-inflammatory T-helper (Th)-1, Th17 and CD8 T-cells significantly more frequent in VAT as compared with SAT. T-cell profiles in SAT and VAT correlated significantly with one another and with peripheral blood. Th1 frequency in SAT and VAT correlated directly, whereas Th2 frequency in VAT correlated inversely with plasma hsCRP concentrations. Th1 in SAT correlated with plasma interleukin-6. Th2 in both depots and peripheral blood was inversely associated with systemic insulin resistance. Relative expression of associated cytokines, measured by rtPCR, reflected flow cytometry results. Most notably, adipose tissue expression of interleukin-10 was inversely associated with insulin resistance. Conclusion CD4 and CD8 T-cells populate human adipose tissue and the relative frequency of Th1 and Th2 is highly associated with systemic inflammation and insulin resistance. These findings point to the adaptive immune system as a potential mediator between obesity and insulin resistance/inflammation. Identification of antigenic stimuli in adipose tissue may yield novel targets for treatment of obesity-associated metabolic disease.

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