Simulation-based Assessment to Reliably Identify Key Resident Performance Attributes.

BACKGROUND: Obtaining reliable and valid information on resident performance is critical to patient safety and training program improvement. The goals were to characterize important anesthesia resident performance gaps that are not typically evaluated, and to further validate scores from a multiscenario simulation-based assessment. METHODS: Seven high-fidelity scenarios reflecting core anesthesiology skills were administered to 51 first-year residents (CA-1s) and 16 third-year residents (CA-3s) from three residency programs. Twenty trained attending anesthesiologists rated resident performances using a seven-point behaviorally anchored rating scale for five domains: (1) formulate a clear plan, (2) modify the plan under changing conditions, (3) communicate effectively, (4) identify performance improvement opportunities, and (5) recognize limits. A second rater assessed 10% of encounters. Scores and variances for each domain, each scenario, and the total were compared. Low domain ratings (1, 2) were examined in detail. RESULTS: Interrater agreement was 0.76; reliability of the seven-scenario assessment was r = 0.70. CA-3s had a significantly higher average total score (4.9 ± 1.1 vs. 4.6 ± 1.1, P = 0.01, effect size = 0.33). CA-3s significantly outscored CA-1s for five of seven scenarios and domains 1, 2, and 3. CA-1s had a significantly higher proportion of worrisome ratings than CA-3s (chi-square = 24.1, P < 0.01, effect size = 1.50). Ninety-eight percent of residents rated the simulations more educational than an average day in the operating room. CONCLUSIONS: Sensitivity of the assessment to CA-1 versus CA-3 performance differences for most scenarios and domains supports validity. No differences, by experience level, were detected for two domains associated with reflective practice. Smaller score variances for CA-3s likely reflect a training effect; however, worrisome performance scores for both CA-1s and CA-3s suggest room for improvement.

An electronic checklist improves transfer and retention of critical information at intraoperative handoff of care.

BACKGROUND: Communication failures are a significant cause of preventable medical errors, and poor-quality handoffs are associated with adverse events. We developed and implemented a simple checklist to improve communication during intraoperative transfer of patient care. METHODS: A prospective observational assessment was performed to compare relay and retention of critical patient information between the outgoing and incoming anesthesiologist before and after introduction of an electronic handoff checklist. Secondary measurements included checklist usage and clinician satisfaction. RESULTS: Sixty-nine handoffs were observed (39 with and 30 without the checklist). Significant improvements in the frequency of information relay occurred with checklist use, most notably related to administration of vasopressors and antiemetics (85% vs 44%, P = 0.008; 46% vs 15%, P = 0.015, respectively); estimated blood loss and urine output (85% vs 57%, P = 0.014; 85% vs 52%, P = 0.006, respectively); communication about potential areas of concern (92% vs 57%, P = 0.001), postoperative planning (92% vs 43%, P < 0.001), and introduction of the relieving anesthesiologist to the operating team (51% vs 3%, P < 0.001). When queried after the handoff, relieving anesthesiologists more frequently knew the antibiotic (97% vs 75%, P = 0.020), muscle relaxant (97% vs 63%, P = 0.003), and amount of fluid administered (97% vs 72%, P = 0.008) when the checklist was used. Voluntary use of the checklist occurred in 60% of the handoffs by the end of the observation period (99% control limits: 58%-75%.). Clinicians who reported using the checklist in at least two-thirds of their handoffs reported higher satisfaction with quality of communication at handoff (P = 0.003). CONCLUSIONS: An electronic checklist improved relay and retention of critical patient information and clinician communication at intraoperative handoff of care.

Malignant Hyperthermia Update.

Malignant hyperthermia (MH) is a rare but potentially lethal skeletal muscle disorder affecting calcium release channels. It is inherited in a mendelian autosomal dominant pattern with variable penetration. The initial clinical manifestations are of a hypermetabolic state with increased CO2 production, respiratory acidosis, increased temperature, and increased oxygen demands. If diagnosed late, MH progresses to multi-organ system failure and death. Current data suggest that mortality has improved to less than 5%. The gold standard for ruling out MH is the contracture test. Genetic testing is also available. MH-susceptible individuals should be clearly identified for safe administration of future anesthetics.

Dietary supplementation with uridine-5'-monophosphate (UMP), a membrane phosphatide precursor, increases acetylcholine level and release in striatum of aged rat.

The biosynthesis of brain membrane phosphatides, e.g., phosphatidylcholine (PtdCho), may utilize three circulating compounds: choline, uridine (a precursor for UTP, CTP, and CDP-choline), and a PUFA (e.g., docosahexaenoic acid); moreover, oral administration of the uridine source uridine-5'-monophosphate (UMP) can significantly increase levels of the phosphatides throughout the rodent brain. Since PtdCho can provide choline for acetylcholine (ACh) synthesis, we determined whether UMP administration also affects ACh levels in striatum and striatal extracellular fluid, in aged and young rats. Among aged animals consuming a UMP-containing diet (2.5%, w/w) for 1 or 6 weeks, baseline ACh levels in striatal dialysates rose from 73 fmol/min to 148 or 197 fmol/min (P<0.05). Consuming a lower dose (0.5%) for 1 week produced a smaller but still significant increase (from 75 to 92 fmol/min, P<0.05), and elevated striatal ACh content (by 16%; P<0.05). Dietary UMP (0.5%, 1 week) also amplified the increase in ACh caused by giving atropine (10 microM in the aCSF); atropine alone increased ACh concentrations from 81 to 386 fmol/min in control rats and from 137 to 680 fmol/min in those consuming UMP (P<0.05). Young rats eating the UMP-containing diet exhibited similar increases in basal ECF ACh (from 105 to 118 fmol/min) and in the increase produced by atropine (from 489 to 560 fmol/min; P<0.05). These data suggest that giving a uridine source may enhance some cholinergic functions, perhaps by increasing brain phosphatide levels.

Differential regulation of ER Ca2+ uptake and release rates accounts for multiple modes of Ca2+-induced Ca2+ release.

The ER is a central element in Ca(2+) signaling, both as a modulator of cytoplasmic Ca(2+) concentration ([Ca(2+)](i)) and as a locus of Ca(2+)-regulated events. During surface membrane depolarization in excitable cells, the ER may either accumulate or release net Ca(2+), but the conditions of stimulation that determine which form of net Ca(2+) transport occurs are not well understood. The direction of net ER Ca(2+) transport depends on the relative rates of Ca(2+) uptake and release via distinct pathways that are differentially regulated by Ca(2+), so we investigated these rates and their sensitivity to Ca(2+) using sympathetic neurons as model cells. The rate of Ca(2+) uptake by SERCAs (J(SERCA)), measured as the t-BuBHQ-sensitive component of the total cytoplasmic Ca(2+) flux, increased monotonically with [Ca(2+)](i). Measurement of the rate of Ca(2+) release (J(Release)) during t-BuBHQ-induced [Ca(2+)](i) transients made it possible to characterize the Ca(2+) permeability of the ER ((~)P(ER)), describing the activity of all Ca(2+)-permeable channels that contribute to passive ER Ca(2+) release, including ryanodine-sensitive Ca(2+) release channels (RyRs) that are responsible for CICR. Simulations based on experimentally determined descriptions of J(SERCA), and of Ca(2+) extrusion across the plasma membrane (J(pm)) accounted for our previous finding that during weak depolarization, the ER accumulates Ca(2+), but at a rate that is attenuated by activation of a CICR pathway operating in parallel with SERCAs to regulate net ER Ca(2+) transport. Caffeine greatly increased the [Ca(2+)] sensitivity of ((~)P(ER)), accounting for the effects of caffeine on depolarization-evoked [Ca(2+)](i) elevations and caffeine-induced [Ca(2+)](i) oscillations. Extending the rate descriptions of J(SERCA), ((~)P(ER)), and J(pm) to higher [Ca(2+)](i) levels shows how the interplay between Ca(2+) transport systems with different Ca(2+) sensitivities accounts for the different modes of CICR over different ranges of [Ca(2+)](i) during stimulation.

Dietary uridine-5'-monophosphate supplementation increases potassium-evoked dopamine release and promotes neurite outgrowth in aged rats.

Membrane phospholipids like phosphatidylcholine (PC) are required for cellular growth and repair, and specifically for synaptic function. PC synthesis is controlled by cellular levels of its precursor, cytidine-5'-diphosphate choline (CDP-choline), which is produced from cytidine triphosphate (CTP) and phosphocholine. In rat PC12 cells exogenous uridine was shown to elevate intracellular CDP-choline levels, by promoting the synthesis of uridine triphosphate (UTP), which was partly converted to CTP. In such cells uridine also enhanced the neurite outgrowth produced by nerve growth factor (NGF). The present study assessed the effect of dietary supplementation with uridine-5'-monophosphate disodium (UMP-2Na+, an additive in infant milk formulas) on striatal dopamine (DA) release in aged rats. Male Fischer 344 rats consumed either a control diet or one fortified with 2.5% UMP for 6 wk, ad libitum. In vivo microdialysis was then used to measure spontaneous and potassium (K+)-evoked DA release in the right striatum. Potassium (K+)-evoked DA release was significantly greater among UMP-treated rats, i.e., 341+/-21% of basal levels vs. 283+/-9% of basal levels in control rats (p<0.05); basal DA release was unchanged. In general, each animal's K+-evoked DA release correlated with its striatal DA content, measured postmortem. The levels of neurofilament-70 and neurofilament-M proteins, biomarkers of neurite outgrowth, increased to 182+/-25% (p<0.05) and 221+/-34% (p<0.01) of control values, respectively, with UMP consumption. Hence, UMP treatment not only enhances membrane phosphatide production but also can modulate two membrane-dependent processes, neurotransmitter release and neurite outgrowth, in vivo.