Assessment of postoperative nausea and vomiting after bariatric surgery using a validated questionnaire

BACKGROUND: Postoperative nausea and vomiting (PONV) is known to occur after bariatric surgery, with over two thirds of patients affected. However, variability exists in how to objectively measure PONV. OBJECTIVES: The goals of the present study were to use a validated, patient-centered scoring tool, the Rhodes Index of Nausea, Vomiting, and Retching to measure the severity of PONV after bariatric surgery, to directly compare PONV between patients who underwent laparoscopic sleeve gastrectomy (LSG) and laparoscopic Roux-en-Y gastric bypass (LRYGB), and to identify risk factors for the development of PONV after bariatric surgery. SETTING: Barnes-Jewish Hospital/Washington University School of Medicine, St. Louis, Missouri, United States of America. METHODS: The Washington University Weight Loss Surgery team prospectively surveyed patients from January 1, 2017 to December 1, 2018 at the following 6 different timepoints: postoperative day (POD) 0, POD 1, POD 2, POD 3 to 4, the first postoperative outpatient visit (POV 1: POD 5-25), and the second postoperative visit (POV 2: POD 25-50). At each timepoint, a cumulative Rhodes score was calculated from the sum of 8 questions. The American Society for Metabolic and Bariatric Surgery Accreditation and Quality Improvement Program database was used to collect patient demographic characteristics and perioperative clinical data. RESULTS: A total of 274 patients met study criteria and completed 605 Rhodes questionnaires. Two hundred fifty Rhodes questionnaires were completed by patients after SG and 355 were completed by patients after LRYGB. Total Rhodes scores are statistically higher in LSG patients compared with patients who underwent LRYGB (LSG = 5.45 ± 6.27; LRYGB = 3.08 ± 4.19, P = .0002). Additionally, at the earlier timepoints, scores were higher among patients who underwent LSG than those who had undergone LRYGB as follows: POD 0 (LSG = 6.96 ± 6.50; LRYGB = 2.89 ± 2.90, P = .0115), POD 1 (LSG = 8.20 ± 6.76; LRYGB = 2.88 ± 3.44, P \u3c .0001), and POD 2 (LSG = 4.05 ± 4.88; LRYGB = 2.06 ± 3.43, P = .05). On subset analysis, examining patients who either underwent an LSG or LRYGB, both procedures had a statistically significant PONV peak emerge on POV 2. Last, overall Rhodes scores were statistically higher in female patients compared with male patients (female: 4.43 ± 5.46; male: 2.35 ± 3.90, P = .021). Although the magnitude of the difference varied somewhat across POD time intervals, the difference was most pronounced at POV 2. CONCLUSIONS: This is the largest study using a validated nausea and vomiting questionnaire to objectively measure PONV after bariatric surgery. The factors found to be most associated with increased PONV were LSG and female sex. Ultimately, these data can help bariatric surgery programs, including Washington University Weight Loss Surgery, identify patients who may require more intensive treatment of PONV, particularly POD 0 to 2, and help to identify patients that continue to struggle with PONV in the later surgical recovery phase

Progressive induction of left ventricular pressure overload in a large animal model elicits myocardial remodeling and a unique matrix signature

ObjectivePatients with severe left ventricular pressure overload secondary to aortic stenosis can present with signs and symptoms of heart failure despite normal left ventricular ejection fraction. This process occurs, at least in part, as a result of left ventricular pressure overload–induced extracellular matrix remodeling that promulgates increased left ventricular stiffness and impaired diastolic function. However, the determinants that drive extracellular matrix remodeling in this form of left ventricular pressure overload remain to be fully defined.MethodsLeft ventricular pressure overload was induced in mature pigs (n = 15) by progressive ascending aortic cuff inflation (once per week for 4 weeks), whereby left ventricular mass, left ventricular ejection fraction, and regional myocardial stiffness (rKm) were compared with referent controls (n = 12). Determinants of extracellular matrix remodeling were assessed by measuring levels of mRNA expression for fibrillar collagens, matrix metalloproteinases, and tissue inhibitors of matrix metalloproteinase 1 and 4.ResultsWith left ventricular pressure overload, left ventricular mass and rKm increased by 2- and 3-fold, respectively, compared with control, with no change in left ventricular ejection fraction. Left ventricular myocardial collagen increased approximately 2-fold, which was accompanied by reduced solubility (ie, increased cross-linking) with left ventricular pressure overload, but mRNA expression for fibrillar collagen and matrix metalloproteinases remained relatively unchanged. In contrast, a robust increase in mRNA expression for tissue inhibitors of matrix metalloproteinase-1 and 4 occurred with left ventricular pressure overload.ConclusionsIn a progressive model of left ventricular pressure overload, which recapitulates the phenotype of aortic stenosis, increased extracellular matrix accumulation and subsequently increased myocardial stiffness were not due to increased fibrillar collagen expression but rather to determinants of post-translational control that included increased collagen stability (thereby resistant to matrix metalloproteinase degradation) and increased endogenous matrix metalloproteinase inhibition. Targeting these extracellular matrix post-translational events with left ventricular pressure overload may hold both diagnostic and therapeutic relevance

Effects of diet versus gastric bypass on metabolic function in diabetes

BackgroundSome studies have suggested that in people with type 2 diabetes, Roux-en-Y gastric bypass has therapeutic effects on metabolic function that are independent of weight loss.MethodsWe evaluated metabolic regulators of glucose homeostasis before and after matched (approximately 18%) weight loss induced by gastric bypass (surgery group) or diet alone (diet group) in 22 patients with obesity and diabetes. The primary outcome was the change in hepatic insulin sensitivity, assessed by infusion of insulin at low rates (stages 1 and 2 of a 3-stage hyperinsulinemic euglycemic pancreatic clamp). Secondary outcomes were changes in muscle insulin sensitivity, beta-cell function, and 24-hour plasma glucose and insulin profiles.ResultsWeight loss was associated with increases in mean suppression of glucose production from baseline, by 7.04 μmol per kilogram of fat-free mass per minute (95% confidence interval [CI], 4.74 to 9.33) in the diet group and by 7.02 μmol per kilogram of fat-free mass per minute (95% CI, 3.21 to 10.84) in the surgery group during clamp stage 1, and by 5.39 (95% CI, 2.44 to 8.34) and 5.37 (95% CI, 2.41 to 8.33) μmol per kilogram of fat-free mass per minute in the two groups, respectively, during clamp stage 2; there were no significant differences between the groups. Weight loss was associated with increased insulin-stimulated glucose disposal, from 30.5±15.9 to 61.6±13.0 μmol per kilogram of fat-free mass per minute in the diet group and from 29.4±12.6 to 54.5±10.4 μmol per kilogram of fat-free mass per minute in the surgery group; there was no significant difference between the groups. Weight loss increased beta-cell function (insulin secretion relative to insulin sensitivity) by 1.83 units (95% CI, 1.22 to 2.44) in the diet group and by 1.11 units (95% CI, 0.08 to 2.15) in the surgery group, with no significant difference between the groups, and it decreased the areas under the curve for 24-hour plasma glucose and insulin levels in both groups, with no significant difference between the groups. No major complications occurred in either group.ConclusionsIn this study involving patients with obesity and type 2 diabetes, the metabolic benefits of gastric bypass surgery and diet were similar and were apparently related to weight loss itself, with no evident clinically important effects independent of weight loss. (Funded by the National Institutes of Health and others; ClinicalTrials.gov number, NCT02207777.)

Steatosis drives monocyte-derived macrophage accumulation in human metabolic dysfunction-associated fatty liver disease

BACKGROUND & AIMS: Metabolic dysfunction-associated fatty liver disease (MAFLD) is a common complication of obesity with a hallmark feature of hepatic steatosis. Recent data from animal models of MAFLD have demonstrated substantial changes in macrophage composition in the fatty liver. In humans, the relationship between liver macrophage heterogeneity and liver steatosis is less clear. METHODS: Liver tissue from 21 participants was collected at time of bariatric surgery and analysed using flow cytometry, immunofluorescence, and H&E microscopy. Single-cell RNA sequencing was also conducted on a subset of samples (n = 3). Intrahepatic triglyceride content was assessed via MRI and tissue histology. Mouse models of hepatic steatosis were used to investigate observations made from human liver tissue. RESULTS: We observed variable degrees of liver steatosis with minimal fibrosis in our participants. Single-cell RNA sequencing revealed four macrophage clusters that exist in the human fatty liver encompassing Kupffer cells and monocyte-derived macrophages (MdMs). The genes expressed in these macrophage subsets were similar to those observed in mouse models of MAFLD. Hepatic CD14 CONCLUSIONS: The human liver in MAFLD contains macrophage subsets that align well with those that appear in mouse models of fatty liver disease. Recruited myeloid cells correlate well with the degree of liver steatosis in humans. MdMs appear to participate in lipid uptake during early stages of MALFD. IMPACT AND IMPLICATIONS: Metabolic dysfunction associated fatty liver disease (MAFLD) is extremely common; however, the early inflammatory responses that occur in human disease are not well understood. In this study, we investigated macrophage heterogeneity in human livers during early MAFLD and demonstrated that similar shifts in macrophage subsets occur in human disease that are similar to those seen in preclinical models. These findings are important as they establish a translational link between mouse and human models of disease, which is important for the development and testing of new therapeutic approaches for MAFLD