Synthesizing Multiple Stakeholder Perspectives on Using Virtual Reality to Improve the Periprocedural Experience in Children and Adolescents: Survey Study.

BACKGROUND: Virtual reality (VR) technology is a powerful tool for augmenting patient experience in pediatric settings. Incorporating the needs and values of stakeholders in the design of VR apps in health care can contribute to better outcomes and meaningful experiences for patients. OBJECTIVE: We used a multiperspective approach to investigate how VR apps can be designed to improve the periprocedural experiences of children and adolescents, particularly those with severe anxiety. METHODS: This study included a focus group (n=4) and a survey (n=56) of clinicians. Semistructured interviews were conducted with children and adolescents in an immunization clinic (n=3) and perioperative setting (n=65) and with parents and carers in an immunization clinic (n=3) and perioperative setting (n=35). RESULTS: Qualitative data were examined to determine the experience and psychological needs and intervention and design strategies that may contribute to better experiences for children in three age groups (4-7, 8-11, and 12-17 years). Quantitative data were used to identify areas of priority for future VR interventions. CONCLUSIONS: We propose a set of ten design considerations for the creation of future VR experiences for pediatric patients. Enhancing patient experience may be achieved by combining multiple VR solutions through a holistic approach considering the roles of clinicians and carers and the temporality of the patient's experience. These situations require personalized solutions to fulfill the needs of pediatric patients before and during the medical procedure. In particular, communication should be placed at the center of preprocedure solutions, while emotional goals can be embedded into a procedure-focused VR app to help patients shift their focus in a meaningful way to build skills to manage their anxiety.

L-carnitine reduces susceptibility to bupivacaine-induced cardiotoxicity: an experimental study in rats.

BACKGROUND: The primary aim of this study was to evaluate the effect of acute administration of L-carnitine 100 mg·kg-1 iv on susceptibility to bupivacaine-induced cardiotoxicity in rats. METHODS: In the first of two experiments, L-carnitine 100 mg·kg-1 iv (n = 10) or saline iv (n = 10) was administered to anesthetized and mechanically ventilated Sprague-Dawley rats following which an infusion of bupivacaine 2.0 mg·kg-1·min-1 iv was given until asystole occurred. The primary outcome was the probability of survival. Secondary outcomes included times to asystole, first dysrhythmia, and to 50% reductions in heart rate (HR) and mean arterial pressure (MAP). To determine whether the same dose of L-carnitine is effective in treating established bupivacaine cardiotoxicity, we also conducted a second experiment in which bupivacaine 20 mg·kg-1 iv was infused over 20 sec. Animals (n = 10 per group) received one of four iv treatments: 30% lipid emulsion 4.0 mL·kg-1, L-carnitine 100 mg·kg-1, 30% lipid emulsion plus L-carnitine, or saline. The primary outcome was the return of spontaneous circulation (ROSC) during resuscitation. RESULTS: In the first study, L-carnitine 100 mg·kg-1 increased the probability of survival during bupivacaine infusion (hazard ratio, 12.0; 95% confidence interval, 3.5 to 41.5; P < 0.001). In L-carnitine-treated animals, the times to asystole, first dysrhythmia, and to 50% reductions in HR and MAP increased by 33% (P < 0.001), 65% (P < 0.001), 71% (P < 0.001), and 63% (P < 0.001), respectively. In the second study, no animal in the control or L-carnitine alone groups achieved ROSC when compared with the lipid emulsion groups (P < 0.01). CONCLUSION: These findings suggest that acute administration of L-carnitine 100 mg·kg-1 decreases susceptibility to bupivacaine cardiotoxicity, but is ineffective during resuscitation from bupivacaine-induced cardiac arrest.

Unusual presentation of postdural puncture headache requiring repeat epidural blood patch in a 4-year-old child.

We present the case of a 4-year-old child who required two epidural blood patches (EBPs) to treat a delayed onset postdural puncture headache (PDPH) caused by lumbar cerebrospinal fluid drain. The first EBP was unsuccessful with 0.41 ml·kg(-1) of blood injected. A second EBP with 0.76 ml·kg(-1) of blood was performed 2 days later with the complete resolution of symptoms. The volume of blood necessary for effective treatment for symptomatic cerebrospinal fluid leaks in children remains controversial, and a repeat EBP may be required for resolution of symptoms.

Major complications related to epidural analgesia in children: a 15-year audit of 3,152 epidurals.

BACKGROUND: Complications associated with epidural analgesia in children have a reported incidence of 40-90 in 10,000 epidurals. We sought to determine the incidence of major complications with the use of continuous epidural analgesia that occurred in our centre over the past 15 years and to describe the nature of these complications. METHODS: The Acute Pain Service database at a tertiary care academic pediatric hospital was reviewed retrospectively over a 15-year period. Data were categorized according to patient age (neonate, infant, child one through eight years, and child > eight years), mode of insertion of the epidural (caudal, transsacral, lumbar, thoracic), complication type, and complication severity. RESULTS: Over the 15-year period, 3,152 epidurals were performed. The use of caudal-thoracic epidurals in neonates and infants has increased since 2007. Twenty-four major complications were identified (incidence, 7.6 in 1,000 epidurals). The rate of complications in neonates was 4.2% compared with 1.4% in infants, 0.5% in children aged one through eight years, and 0.8% in children over eight years of age. The two most common complications were local skin infection and drug error. CONCLUSIONS: Our incidence of major complications and our finding that complications were more common in neonates and infants are both consistent with previously published data. The two most common types of complications are potentially preventable.

Carnitine deficiency increases susceptibility to bupivacaine-induced cardiotoxicity in rats.

BACKGROUND: Anecdotal reports suggest that carnitine deficiency increases susceptibility to bupivacaine-induced cardiotoxicity. Bupivacaine inhibits lipid-based respiration in myocardial mitochondria via inhibition of acylcarnitine exchange in rats. The authors hypothesized that carnitine deficiency increases susceptibility to bupivacaine-induced asystole in rats and that acute repletion with L-carnitine reverses this effect. METHODS: Thirty male Sprague-Dawley rats were assigned to three groups. Rats assigned to the L-carnitine-deficient and L-carnitine-replete groups received subcutaneous D-carnitine on the 10 d before the experiment to induce L-carnitine deficiency. Control rats received an equal volume of subcutaneous normal saline. The rats were anesthetized and mechanically ventilated. Bupivacaine was infused intravenously at a rate of 2.0 mg · kg⁻¹ · min⁻¹ until asystole occurred. The L-carnitine-replete group received intravenous L-carnitine 100 mg · kg⁻¹ immediately before bupivacaine infusion. At asystole, blood was sampled to measure bupivacaine concentration. The primary outcome was time to asystole. RESULTS: L-carnitine deficiency significantly decreased survival duration (P < 0.0001). Time to bupivacaine-induced asystole decreased by 22% (P < 0.05) in the L-carnitine-deficient group (847 s [787-898]) (median [interquartile range]) compared with controls (1,082 s [969-1,427]). Intravenous administration of L-carnitine completely reversed the reduction in time to asystole. At asystole, the median plasma bupivacaine concentration in the L-carnitine-deficient group was 38% (P < 0.05) less than that in control animals. Plasma bupivacaine concentration was similar in L-carnitine-replete and control animals. CONCLUSIONS: Carnitine deficiency increased sensitivity to bupivacaine-induced asystole, an effect that was reversed completely by L-carnitine repletion. This study suggests that carnitine deficiency may predispose to bupivacaine-induced cardiotoxicity. L-carnitine may have a protective role against bupivacaine cardiotoxicity.

Preparation of the Dräger Fabius GS workstation for malignant hyperthermia-susceptible patients.

PURPOSE: In order to establish guidelines for the preparation of the Dräger Fabius GS premium anesthetic workstation for malignant hyperthermia-susceptible patients, the authors evaluated the effect of the workstation's exchangeable and autoclavable components on the washout of isoflurane. METHODS: A Dräger Fabius GS workstation was primed with 1.5% isoflurane, and exchangeable components were replaced as follows: Group 1: no replacement (control); Group 2: autoclaved ventilator diaphragm and ventilator hose; Group 3: flushed ventilator diaphragm and ventilator hose; Group 4: autoclaved compact breathing system. The fresh gas flow (FGF) was set at 10 L . min(-1), and the concentration of isoflurane in the inspiratory limb of the circle breathing circuit was recorded every minute until an endpoint of 5.0 parts per million (ppm) was achieved, at which time the FGF was reduced to 3 L . min(-1). Six experiments were conducted in each of the four groups. RESULTS: The time to achieve an isoflurane concentration of 5.0 ppm decreased in the following order: Group 1 (151 +/- 17 min) > Group 3 (137 +/- 7 min) > Group 4 (122 +/- 11 min) > Group 2 (42 +/- 6 min) (P < 0.01 vs control). Isoflurane concentration increased approximately fivefold when the FGF was reduced to 3 L . min(-1). CONCLUSION: Anesthetic washout from the Dräger Fabius GS is relatively slow. Although washout was accelerated when the Dräger Fabius GS was equipped with autoclaved components, the reduction in washout time may be less than that required for this technique to be accepted into clinical practice. A dedicated vapor-free workstation may be preferable for rapid turnover between cases.

Knowledge translation and process improvement interventions increased pain assessment documentation in a large quaternary paediatric post-anaesthesia care unit.

BACKGROUND: Due to inadequate pain assessment documentation in our paediatric post-anaesthetic care unit (PACU), we were unable to monitor pain intensity, and target factors contributing to moderate and severe postoperative pain in children. The purpose of this study was to improve pain assessment documentation in PACU through a process improvement intervention and knowledge translation (KT) strategy. The study was set in a PACU within a large university affiliated paediatric hospital. Participants included PACU and Acute Pain Service nursing staff, administrative staff and anaesthesiologists. METHODS: The Plan-Do-Study-Act method of quality improvement was used. Benchmark data were obtained by chart review of 99 patient medical records prior to interventions. Data included pain assessment documentation (pain intensity score, use of validated pain intensity measure) during PACU stay. Repeat chart audit took place at 4, 5 and 6 months after the intervention. INTERVENTION: Key informant interviews were conducted to identify barriers to pain assessment documentation. A process improvement was implemented whereby the PACU flowsheets were modified to facilitate pain assessment documentation. KT strategy was implemented to increase awareness of pain assessment documentation and to provide the knowledge, skill and judgement to support this practice. The KT strategy was directed at PACU nursing staff and comprised education outreach (educational meetings for PACU nurses, discussions at daily huddles), reminders (screensavers, bedside posters, email reminders) and feedback of audit results. RESULTS: The proportion of charts that included at least one documented pain assessment was 69%. After intervention, pain assessment documentation increased to >90% at 4 and 5 months, respectively, and to 100% after 6 months. CONCLUSION: After implementing process improvement and KT interventions, pain assessment documentation improved. Additional work is needed in several key areas, specifically monitoring moderate to severe pain, in order to target factors contributing to significant postoperative pain in children.

Molecular mechanisms of diabetic cardiovascular disease.

Cardiovascular disease is a major cause of morbidity and mortality in persons with diabetes mellitus. This population represents an important target for preventive therapies aimed at reducing atherosclerosis. Recent molecular research has uncovered many of the cellular mechanisms that lead to atherosclerosis in the diabetic patient. This review, part 1 of a 2-part series, is geared toward clinicians and discusses these mechanisms as they pertain to prevention of cardiovascular disease in patients with diabetes.

Current recommendations for prevention of cardiovascular disease in patients with diabetes mellitus. Part II of II.

Patients with diabetes mellitus are at a high risk of developing cardiovascular disease, and therefore stand to benefit greatly from a preventive strategy. Recommendations regarding assessment and management of traditional risk factors are basically similar for diabetic and nondiabetic patients with several important differences. Several nontraditional risk factors also play a substantial role in the development of cardiovascular disease in diabetic patients, and need to be addressed if full preventive care is to be provided. In this second in a two-part series, we present current recommendations for reducing the risk of cardiovascular disease in the diabetic patient.

BMP-2 inhibits proliferation of human aortic smooth muscle cells via p21Cip1/Waf1.

Bone-morphogenetic proteins (BMP)-2 and -7, multifunctional members of the transforming growth factor (TGF)-beta superfamily with powerful osteoinductive effects, cause cell cycle arrest in a variety of transformed cell lines by activating signaling cascades that involve several cyclin-dependent kinase inhibitors (CDKIs). CDKIs in the cip/kip family, p21(Cip1/Waf1) and p27(Kip1), have been shown to negatively regulate the G1 cyclins and their partner cyclin-dependent kinase proteins, resulting in BMP-mediated growth arrest. Bone morphogens have also been associated with antiproliferative effects in vascular tissue by unknown mechanisms. We now show that BMP-2-mediated inhibition of platelet-derived growth factor (PDGF)-stimulated human aortic smooth muscle cell (HASMC) proliferation is accompanied by increased levels of p21 protein. Antisense oligodeoxynucleotides specific for p21 attenuate BMP-2-induced inhibition of proliferation when transfected into HASMCs, demonstrating that BMP-2 inhibits PDGF-stimulated proliferation of HASMCs through induction of p21. Whether p21-mediated induction of cell cycle arrest by BMP-2 sets the stage for osteogenic differentiation of vascular smooth muscle cells, ultimately leading to vascular mineralization, remains to be investigated.