Informed Consent in Pediatric Anesthesia: A Narrative Review.

Informed consent for pediatric anesthesia challenges practitioners to navigate complex ethical, medical, and legal ambiguities. A patient's status as a minor does not negate the importance of his or her participation in the decision-making process but, rather, necessitates a nuanced evaluation of age and development to involve the patient to an appropriate extent. Given the complexities involved with pediatric informed consent in anesthesia practice and research, it is important to understand the experience of key stakeholders involved. For this review, we searched Medline, the Cochrane database, PROSPERO, and Clinicaltrials.gov for studies involving pediatric anesthesia informed consent. Inclusion and exclusion criteria were designed to select for studies that included issues related to informed consent as primary outcomes. The following data were extracted from included studies: title, authors, date of publication, study type, intervention, data collection method, participant type (ie, parent, pediatric patient, anesthesia provider), number of participants, pediatric patient age range, and primary outcome measures. Twenty-two articles were included for final review: studies of informed consent in pediatric anesthesia span many aspects of informed consent. Parental understanding has been studied most often (7/22 studies), followed by parental preferences (5/22 studies) and provider-related outcomes (5/22 studies) such as time spent interacting with patients, subjective reporting on amount of training related to informed consent, and provider satisfaction with the informed consent process. Outcomes pertaining to pediatric patients themselves constitute the smallest number of studies, including child anxiety (1/22), child understanding (1/22), and child refusal (1/22). Among the parties involved, parents have been most frequently identified as the subjects of these studies (2719/3805 subjects across all included studies, or 71% of all subjects). Pediatric patients are the least frequently involved subjects of studies that investigate informed consent in pediatric anesthesia (493/3805, or 13% of all subjects). Anesthesia providers and investigators have been study subjects (593/3805, or 16% of all subjects) for a range of topics including time spent interacting with patient, nature of informed consent conversation in relation to trainee status, satisfaction with informed consent process, and priorities for informed consent content. The aim of the present narrative review is to summarize the work that has been done on informed consent for pediatric anesthesia.

$1.8 Million and counting: how volatile agent education has decreased our spending $1000 per day.

STUDY OBJECTIVE: Volatile anesthetic agents comprise a substantial portion of every hospital's pharmacy budget. Challenged with an initiative to lower anesthetic drug expenditures, we developed an education-based intervention focused on reducing volatile anesthetic costs while preserving access to all available volatile anesthetics. When postintervention evaluation demonstrated a dramatic year-over-year reduction in volatile agent acquisition costs, we undertook a retrospective analysis of volatile anesthetic purchasing data using time series analysis to determine the impact of our educational initiative. DESIGN/SETTING: We obtained detailed volatile anesthetic purchasing data from the Central Supply of Wake Forest Baptist Health from 2007 to 2014 and integrated these data with the time course of our educational intervention. PATIENTS: Aggregate volatile anesthetic purchasing data were analyzed for 7 consecutive fiscal years. INTERVENTION: The educational initiative emphasized tissue partition coefficients of volatile anesthetics in adipose tissue and muscle and their impact on case management. MEASUREMENTS: We used an interrupted time series analysis of monthly cost per unit data using autoregressive integrated moving average modeling, with the monthly cost per unit being the amount spent per bottle of anesthetic agent per month. MAIN RESULTS: The cost per unit decreased significantly after the intervention (t=-6.73, P<.001). The autoregressive integrated moving average model predicted that the average cost per unit decreased $48 after the intervention, with 95% confidence interval of $34 to $62. As evident from the data, the purchasing of desflurane and sevoflurane decreased, whereas that of isoflurane increased. CONCLUSIONS: An educational initiative focused solely on the selection of volatile anesthetic agent per case significantly reduced volatile anesthetic expense at a tertiary medical center. This approach appears promising for application in other hospitals in the rapidly evolving, value-added health care environment. We were able to accomplish this with instruction on tissue partition coefficients and each agent's individual cost per MAC-hour delivered.

PKCgamma knockout mouse lenses are more susceptible to oxidative stress damage.

Cataracts, or lens opacities, are the leading cause of blindness worldwide. Cataracts increase with age and environmental insults, e.g. oxidative stress. Lens homeostasis depends on functional gap junctions. Knockout or missense mutations of lens gap junction proteins, Cx46 or Cx50, result in cataractogenesis in mice. We have previously demonstrated that protein kinase Cgamma (PKCgamma) regulates gap junctions in the lens epithelium and cortex. In the current study, we further determined whether PKCgamma control of gap junctions protects the lens from cataractogenesis induced by oxidative stress in vitro, using PKCgamma knockout and control mice as our models. The results demonstrate that PKCgamma knockout lenses are normal at 2 days post-natal when compared to control. However, cell damage, but not obvious cataract, was observed in the lenses of 6-week-old PKCgamma knockout mice, suggesting that the deletion of PKCgamma causes lenses to be more susceptible to damage. Furthermore, in vitro incubation or lens oxidative stress treatment by H(2)O(2) significantly induced lens opacification (cataract) in the PKCgamma knockout mice when compared to controls. Biochemical and structural results also demonstrated that H(2)O(2) activation of endogenous PKCgamma resulted in phosphorylation of Cx50 and subsequent inhibition of gap junctions in the lenses of control mice, but not in the knockout. Deletion of PKCgamma altered the arrangement of gap junctions on the cortical fiber cell surface, and completely abolished the inhibitory effect of H(2)O(2) on lens gap junctions. Data suggest that activation of PKCgamma is an important mechanism regulating the closure of the communicating pathway mediated by gap junction channels in lens fiber cells. The absence of this regulatory mechanism in the PKCgamma knockout mice may cause those lenses to have increased susceptibility to oxidative damage.

Differential phosphorylation of connexin46 and connexin50 by H2O2 activation of protein kinase Cgamma.

PURPOSE: Fiber cell gap junction proteins connexin 46 (Cx46) and connexin 50 (Cx50) play distinct roles in the avascular lens. The purpose of this study was to determine how protein kinase Cgamma (PKCgamma) differentially regulates phosphorylation of Cx46 and Cx50 in oxidatively stressed lenses. METHODS: Sprague Dawley rats (six week old) were used in the experiments. PKCgamma enzyme activity was analyzed by use of the PepTag assay kit. Phosphorylation of caveolin-1, Cx46, and Cx50 was determined by immunoblotting. Lipid rafts were isolated by continuous sucrose gradient centrifugation. Lipid raft-localization of PKCgamma, Cx46, or Cx50 was demonstrated by immunoblotting. Association of caveolin-1 with PKCgamma, Cx46, or Cx50 was revealed by co-immunoprecipitation. RESULTS: H2O2 (100 microM) stimulated PKCgammaactivation in rat whole lens. Activated PKCgamma was recruited into caveolin-1 (Cav-1) containing lipid rafts and this activation enhanced the coimmunoprecipitation of Cav-1, Cx46, and Cx50 with PKCgamma. Both Cx50 and Cx46 were associated with Cav-1 in lipid rafts. H2O2 significantly induced threonine (Thr) phosphorylation of Cx46 and Cx50, and serine (Ser) phosphorylation of Cx50. However, There was only a small stimulation of Cx46 phosphorylation at Ser by H2O2, as Cx46 was already phosphorylated. CONCLUSIONS: Activation of PKCgamma by H2O2 stimulated differential Ser phosphorylation of Cx50 versus Cx46, within lipid rafts. This suggests that Cx50 and Cx46 may have different functions in lens.