Use of Evidence-Based Vital Signs in Pediatric Early Warning Score to Predict Clinical Deterioration on Acute Care Units.

The pediatric early warning score (PEWS) is a tool used to predict clinical deterioration. Referenced vital sign parameters are based on expert opinion but heart rate and respiratory rate percentiles in hospitalized children have been published. This retrospective case-control study of unplanned intensive care unit (ICU) transfers compares evidence-based vital signs (EBVS) effect on PEWS sensitivity and specificity, determines the impact of age categories on PEWS deterioration prediction, and evaluates whether EBVS PEWS is associated with need for invasive ICU supports. EBVS PEWS improved sensitivity (43%-71% vs 30%-63%) for unplanned transfers with slightly decreased specificity (88%-98% vs 93%-99%). Logistic regression analysis and odds ratios (ORs) demonstrated EBVS PEWS was associated with increased risk for ICU-specific supports (OR = 1.16, 95% confidence interval [CI] = 1.0-1.34, P = .0498). Evidence-based vital signs can improve PEWS sensitivity to identify unplanned ICU transfers and identify patients requiring ICU-specific interventions.

Measurement of Ambulatory Medication Errors in Children: A Scoping Review.

BACKGROUND AND OBJECTIVES: Children use most medications in the ambulatory setting where errors are infrequently intercepted. There is currently no established measure set for ambulatory pediatric medication errors. We have sought to identify the range of existing measures of ambulatory pediatric medication errors, describe the data sources for error measurement, and describe their reliability. METHODS: We performed a scoping review of the literature published since 1986 using PubMed, CINAHL, PsycINFO, Web of Science, Embase, and Cochrane and of grey literature. Studies were included if they measured ambulatory, including home, medication errors in children 0 to 26 years. Measures were grouped by phase of the medication use pathway and thematically by measure type. RESULTS: We included 138 published studies and 4 studies from the grey literature and identified 21 measures of medication errors along the medication use pathway. Most measures addressed errors in medication prescribing (n = 6), and administration at home (n = 4), often using prescription-level data and observation, respectively. Measures assessing errors at multiple phases of the medication use pathway (n = 3) frequently used error reporting databases and prospective measurement through direct in-home observation. We identified few measures of dispensing and monitoring errors. Only 31 studies used measurement methods that included an assessment of reliability. CONCLUSIONS: Although most available, reliable measures are too resource and time-intensive to assess errors at the health system or population level, we were able to identify some measures that may be adopted for continuous measurement and quality improvement.

Effect of Patient and Family Centered I-PASS on adverse event rates in hospitalized children with complex chronic conditions.

BACKGROUND: Children with complex chronic conditions (CCCs) are at risk for adverse events (AEs) during hospitalizations. OBJECTIVE: We compared the effect of Patient and Family Centered (PFC)I-PASS on AE rates in children with and without CCCs. DESIGNS, SETTINGS, AND PARTICIPANTS: Patients were drawn from the PFCI-PASS study, which included 3106 hospitalized children from seven North American pediatric hospitals between December 2014 and January 2017. MAIN OUTCOME AND MEASURES: An effect modification analysis did not show difference in the intervention on children with and without CCCs (RRR 0.81, 95% CI [0.59-1.10]; p = .2). RESULTS: In multivariable analysis, the adjusted incidence rate ratiofor AEs in children with CCCs was 0.5 (95% CI = 0.3-0.9, p = .01) with PFC I-PASS exposure; there was no statistically significant change in AEs for children without CCCs [IRR 0.6 (95% CI = 0.3-1.2; p = .1)].

A Pediatric Resident Safety Council: A Framework for Developing Quality and Safety Leadership.

Quality improvement (QI) and patient safety are essential to the practice of medicine. Specific training in these fields has become a requirement in graduate medical education, although there is great variation in how residency programs choose to approach trainee education in QI and patient safety. Residents have a unique vantage point into the operations of a health care system and can guide the development of system improvement initiatives. In this report, we (1) describe the context that led to the creation of a pediatric resident safety council (PRSC) in its current structure, (2) identify the organizational features implemented to best meet the objectives of this council, and (3) describe the local and institutional impact of the PRSC. A PRSC is a useful model to build resident engagement in safe and high-quality patient care within a residency program and health care system. A PRSC encourages the professional development of future pediatric safety leaders and facilitates experiential training in patient safety and QI science.

Adipocyte lipid chaperone AP2 is a secreted adipokine regulating hepatic glucose production.

Proper control of hepatic glucose production is central to whole-body glucose homeostasis, and its disruption plays a major role in diabetes. Here, we demonstrate that although established as an intracellular lipid chaperone, aP2 is in fact actively secreted from adipocytes to control liver glucose metabolism. Secretion of aP2 from adipocytes is regulated by fasting- and lipolysis-related signals, and circulating aP2 levels are markedly elevated in mouse and human obesity. Recombinant aP2 stimulates glucose production and gluconeogenic activity in primary hepatocytes in vitro and in lean mice in vivo. In contrast, neutralization of secreted aP2 reduces glucose production and corrects the diabetic phenotype of obese mice. Hyperinsulinemic-euglycemic and pancreatic clamp studies upon aP2 administration or neutralization demonstrated actions of aP2 in liver. We conclude that aP2 is an adipokine linking adipocytes to hepatic glucose production and that neutralizing secreted aP2 may represent an effective therapeutic strategy against diabetes.

Gq/11-mediated signaling and hypertrophy in mice with cardiac-specific transgenic expression of regulator of G-protein signaling 2.

Cardiac hypertrophy is a well-established risk factor for cardiovascular morbidity and mortality. Activation of G(q/11)-mediated signaling is required for pressure overload-induced cardiomyocyte (CM) hypertrophy to develop. We previously showed that among Regulators of G protein Signaling, RGS2 selectively inhibits G(q/11) signaling and its hypertrophic effects in isolated CM. In this study, we generated transgenic mice with CM-specific, conditional RGS2 expression (dTG) to investigate whether RGS2 overexpression can be used to attenuate G(q/11)-mediated signaling and hypertrophy in vivo. Transverse aortic constriction (TAC) induced a comparable rise in ventricular mass and ANF expression and corresponding hemodynamic changes in dTG compared to wild types (WT), regardless of the TAC duration (1-8 wks) and timing of RGS2 expression (from birth or adulthood). Inhibition of endothelin-1-induced G(q/11)-mediated phospholipase C ß activity in ventricles and atrial appendages indicated functionality of transgenic RGS2. However, the inhibitory effect of transgenic RGS2 on G(q/11)-mediated PLCß activation differed between ventricles and atria: (i) in sham-operated dTG mice the magnitude of the inhibitory effect was less pronounced in ventricles than in atria, and (ii) after TAC, negative regulation of G(q/11) signaling was absent in ventricles but fully preserved in atria. Neither difference could be explained by differences in expression levels, including marked RGS2 downregulation after TAC in left ventricle and atrium. Counter-regulatory changes in other G(q/11)-regulating RGS proteins (RGS4, RGS5, RGS6) and random insertion were also excluded as potential causes. Taken together, despite ample evidence for a role of RGS2 in negatively regulating G(q/11) signaling and hypertrophy in CM, CM-specific RGS2 overexpression in transgenic mice in vivo did not lead to attenuate ventricular G(q/11)-mediated signaling and hypertrophy in response to pressure overload. Furthermore, our study suggests chamber-specific differences in the regulation of RGS2 functionality and potential future utility of the new transgenic model in mitigating G(q/11) signaling in the atria in vivo.