Relationship between patient safety indicator events and hospital location for inpatient hysterectomy.

BACKGROUND: Previous studies suggest surgical quality outcomes are similar between rural and urban hospitals, but data about gynecology in rural hospitals is sparse. METHODS: This was a retrospective cohort study utilizing the National Inpatient Sample database from the Agency of Healthcare Research and Quality. Patients who underwent benign hysterectomy for non-prolapse indications between 2012-2016 were identified using ICD-9 and 10 codes. Patients were stratified into rural or urban non-teaching groups; urban teaching hospitals were the referent group. The primary outcome was the rate of patient safety indicator (PSI) events. PSI events were identified using ICD-9 and 10 codes. Statistical analysis was performed using analysis of variance and uni- and multivariate Poisson regressions. RESULTS: 154,810 patients met all inclusion criteria. The cumulative rate of PSI events was 11.9% at rural hospitals, 13.9% at urban non-teaching hospitals and 16.9% at urban teaching hospitals, P<0.001. The most common PSI events were postoperative metabolic derangement, hemorrhage, and accidental puncture. The rate of transfusion was highest in urban teaching hospitals (6.7%) and similar for rural (5.1%) and urban non-teaching hospitals (5.5%), P<0.001. The rate of genitourinary tract injury was between 1.4-1.6%, and similar across sites, P=0.89. After adjusting for confounders, the risk of PSI events was similar across locations. The risk of transfusion was lower at rural hospitals (aRR=0.84, 95% CI: 0.74-0.94). CONCLUSIONS: Hysterectomy performed at rural hospitals, typically thought of as having low surgical volume compared to urban hospitals, is associated with similar risk of PSI events and lower risk of transfusion.

Intercellular contact and cargo transfer between Müller glia and to microglia precede apoptotic cell clearance in the developing retina.

To clarify our understanding of glial phagocytosis in retinal development, we used real-time imaging of larval zebrafish to provide cell-type specific resolution of this process. We show that radial Müller glia frequently participate in microglial phagocytosis while also completing a subset of phagocytic events. Müller glia actively engage with dying cells through initial target cell contact and phagocytic cup formation, after which an exchange of the dying cell from Müller glia to microglia often takes place. In addition, we find evidence that Müller glia cellular material, possibly from the initial Müller cell phagocytic cup, is internalized into microglial compartments. Previously undescribed Müller cell behaviors were seen, including cargo splitting, wrestling for targets and lateral passing of cargo to neighbors. Collectively, our work provides new insight into glial functions and intercellular interactions, which will allow future work to understand these behaviors on a molecular level.

Faculty Decision Making in Ad Hoc Entrustment of Pediatric Critical Care Fellows: A National Case-Based Survey.

Phenomenon: Ad hoc entrustment decisions reflect a clinical supervisor's estimation of the amount of supervision a trainee needs to successfully complete a task in the moment. These decisions have important consequences for patient safety, trainee learning, and preparation for independent practice. Determinants of these decisions have previously been described but have not been well described for acute care contexts such as critical care and emergency medicine. The ad hoc entrustment of trainees caring for vulnerable patient populations is a high-stakes decision that may differ from other contexts. Critically ill patients and children are vulnerable patient populations, making the ad hoc entrustment of a pediatric critical care medicine (PCCM) fellow a particularly high-stakes decision. This study sought to characterize how ad hoc entrustment decisions are made for PCCM fellows through faculty ratings of vignettes. The authors investigated how acuity, relationship, training level, and task interact to influence ad hoc entrustment decisions. Approach: A survey containing 16 vignettes that varied by four traits (acuity, relationship, training level, and task) was distributed to U.S. faculty of pediatric critical care fellowships in 2020. Respondents determined an entrustment level for each case and provided demographic data. Entrustment ratings were dichotomized by "high entrustment" versus "low entrustment" (direct supervision or observation only). The authors used logistic regression to evaluate the individual and interactive effects of the four traits on dichotomized entrustment ratings. Findings: One hundred seventy-eight respondents from 30 institutions completed the survey (44% institutional response rate). Acuity, relationship, and task all significantly influenced the entrustment level selected but did not interact. Faculty most frequently selected "direct supervision" as the entrustment level for vignettes, including for 24% of vignettes describing fellows in their final year of training. Faculty rated the majority of vignettes (61%) as "low entrustment." There was no relationship between faculty or institutional demographics and the entrustment level selected. Insights: As has been found in summative entrustment for pediatrics, internal medicine, and surgery trainees, PCCM fellows often rated at or below the "direct supervision" level of ad hoc entrustment. This may relate to declining opportunities to practice procedures, a culture of low trust propensity among the specialty, and/or variation in interpretation of entrustment scales.

Intercellular contact and cargo transfer between Müller glia and to microglia precede apoptotic cell clearance in the developing retina.

To clarify our understanding of glial phagocytosis in retinal development, we used real time imaging of larval zebrafish to provide cell-type specific resolution of this process. We show that radial Müller glia frequently participate in microglial phagocytosis while also completing a subset of phagocytic events. Müller glia (MG) actively engage with dying cells through initial target cell contact and phagocytic cup formation after which an exchange of the dying cell from MG to microglia often takes place. Additionally, we find evidence that Müller glia cellular material, possibly from the initial Müller cell's phagocytic cup, is internalized into microglial compartments. Previously undescribed Müller cell behaviors were seen, including cargo splitting, wrestling for targets, lateral passing of cargo to neighbors, and engulfment of what is possibly synaptic puncta. Collectively, our work provides new insight into glial functions and intercellular interactions, which will allow future work to understand these behaviors on a molecular level.

Generating Widespread and Scalable Retinal Lesions in Adult Zebrafish by Intraocular Injection of Ouabain.

Zebrafish regenerate functional retinal neurons after injury. Regeneration takes place following photic, chemical, mechanical, surgical, or cryogenic lesions, as well as after lesions that selectively target specific neuronal cell populations. An advantage of chemical retinal lesion for studying the process of regeneration is that the lesion is topographically widespread. This results in the loss of visual function as well as a regenerative response that engages nearly all stem cells (Müller glia). Such lesions can therefore be used to further our understanding of the process and mechanisms underlying re-establishment of neuronal wiring patterns, retinal function, and visually mediated behaviors. Widespread chemical lesions also permit the quantitative analysis of gene expression throughout the retina during the period of initial damage and over the duration of regeneration, as well as the study of growth and targeting of axons of regenerated retinal ganglion cells. The neurotoxic Na+/K+ ATPase inhibitor ouabain specifically offers a further advantage over other types of chemical lesions in that it is scalable; the extent of damage can be targeted to include only inner retinal neurons, or all retinal neurons, simply by adjusting the intraocular concentration of ouabain that is used. Here we describe the procedure through which these "selective" vs. "extensive" retinal lesions can be generated.

PCNA Staining of Retinal Cryosections to Assess Microglial/Macrophage Proliferation.

Detection of the protein PCNA (proliferating cell nuclear antigen) is used to identify cells in the S phase of the cell cycle to indicate cellular proliferation. Here we describe our method to detect PCNA expression by microglia and macrophages in retinal cryosections. We have used this procedure with zebrafish tissue, but this procedure could be applied to cryosections from any organism. Retinal cryosections are subjected to a heat-mediated antigen retrieval step in Citrate Buffer, then immunostained with antibodies to label PCNA and microglia/macrophages, and counterstained for cell nuclei. After fluorescent microscopy, the number of total and PCNA+ microglia/macrophages can be quantified and normalized to compare across samples and groups.

Assessing Rewiring of the Retinal Circuitry by Electroretinogram (ERG) After Inner Retinal Lesion in Adult Zebrafish.

Adult zebrafish respond to retinal injury with a regenerative response that replaces damaged neurons with Müller glia-derived regenerated neurons. The regenerated neurons are functional, appear to make appropriate synaptic connections, and support visually mediated reflexes and more complex behaviors. Curiously, the electrophysiology of damaged, regenerating, and regenerated zebrafish retina has only recently been examined. In our previous work, we demonstrated that electroretinogram (ERG) recordings of damaged zebrafish retina correlate with the extent of the inflicted damage and that the regenerated retina at 80 days post-injury exhibited ERG waveforms consistent with functional visual processing. In this paper we describe the procedure for obtaining and analyzing ERG recordings from adult zebrafish previously subjected to widespread lesions that destroy inner retinal neurons and engage a regenerative response that restores retinal function, in particular the synaptic connections between photoreceptor axon terminals and the dendritic trees of retinal bipolar neurons.

The Neural Basis for Biased Behavioral Responses Evoked by Galvanic Vestibular Stimulation in Primates.

Noninvasive electrical stimulation of the vestibular system in humans has become an increasingly popular tool with a broad range of research and clinical applications. However, common assumptions regarding the neural mechanisms that underlie the activation of central vestibular pathways through such stimulation, known as galvanic vestibular stimulation (GVS), have not been directly tested. Here, we show that GVS is encoded by VIIIth nerve vestibular afferents with nonlinear dynamics that differ markedly from those predicted by current models. GVS produced asymmetric activation of both semicircular canal and otolith afferents to the onset versus offset and cathode versus anode of applied current, that in turn produced asymmetric eye movement responses in three awake-behaving male monkeys. Additionally, using computational methods, we demonstrate that the experimentally observed nonlinear neural response dynamics lead to an unexpected directional bias in the net population response when the information from both vestibular nerves is centrally integrated. Together our findings reveal the neural basis by which GVS activates the vestibular system, establish that neural response dynamics differ markedly from current predictions, and advance our mechanistic understanding of how asymmetric activation of the peripheral vestibular system alters vestibular function. We suggest that such nonlinear encoding is a general feature of neural processing that will be common across different noninvasive electrical stimulation approaches.SIGNIFICANCE STATEMENT Here, we show that the application of noninvasive electrical currents to the vestibular system (GVS) induces more complex responses than commonly assumed. We recorded vestibular afferent activity in macaque monkeys exposed to GVS using a setup analogous to human studies. GVS evoked notable asymmetries in irregular afferent responses to cathodal versus anodal currents. We developed a nonlinear model explaining these GVS-evoked afferent responses. Our model predicts that GVS induces directional biases in centrally integrated head motion signals and establishes electrical stimuli that recreate physiologically plausible sensations of motion. Altogether, our findings provide new insights into how GVS activates the vestibular system, which will be vital to advancing new clinical and biomedical applications.

Altered integration of excitatory inputs onto the basal dendrites of layer 5 pyramidal neurons in a mouse model of Fragile X syndrome.

Layer 5 (L5) pyramidal neurons receive predictive and sensory inputs in a compartmentalized manner at their apical and basal dendrites, respectively. To uncover how integration of sensory inputs is affected in autism spectrum disorders (ASD), we used two-photon glutamate uncaging to activate spines in the basal dendrites of L5 pyramidal neurons from a mouse model of Fragile X syndrome (FXS), the most common genetic cause of ASD. While subthreshold excitatory inputs integrate linearly in wild-type animals, surprisingly those with FXS summate sublinearly, contradicting what would be expected of sensory hypersensitivity classically associated with ASD. We next investigated the mechanism underlying this sublinearity by performing knockdown of the regulatory ß4 subunit of BK channels, which rescued the synaptic integration, a result that was corroborated with numerical simulations. Taken together, these findings suggest that there is a differential impairment in the integration of feedforward sensory and feedback predictive inputs in L5 pyramidal neurons in FXS and potentially other forms of ASD, as a result of specifically localized subcellular channelopathies. These results challenge the traditional view that FXS and other ASD are characterized by sensory hypersensitivity, proposing instead a hyposensitivity of sensory inputs and hypersensitivity of predictive inputs onto cortical neurons.

Dipstick urinalysis does not predict post-urodynamic study morbidity.

INTRODUCTION AND HYPOTHESIS: Pre-procedure urinalysis may add unnecessary cost and inconvenience for patients undergoing urodynamics. The hypothesis of this study was that urinalysis would perform poorly when predicting complications following urodynamics. METHODS: Case-control study of women aged 18-89 undergoing urodynamics from 01 January2008 to 31 December 2017 at two tertiary medical centers. Data collected included patient demographics, past medical history, lower urinary tract symptoms, urodynamics indication, urodynamics results, urinalysis result, antibiotic administration, and adverse events within 30 days. Wilcoxon rank-sum test was used to compare those with and without an adverse event. Logistic regression was performed using statistically significant variables on pairwise analysis. RESULTS: A total of 601 patients met the criteria; 11 of these experienced an adverse event, of which all were a urinary tract infection. There were no differences in the frequency of adverse events based on any urinalysis result, regardless of whether the patient received antibiotics. On pairwise analysis, variables associated with a higher frequency of adverse events were higher parity (3.5 (2-5) vs 2 (2, 3), p=0.038) and complaint of suprapubic pain (1 (9.1%) vs 4 (0.7%), p=0.002). On logistic regression, significant variables included increasing age (adjusted odds ratio [aOR] 1.03 per year (95% CI 1.03-4.06); p=0.002), any prolapse (aOR 6.45 (95% CI 3.60-11.54); p<0.001), pelvic organ prolapse as the indication for urodynamics (aOR 7.27 (95% CI 2.60-20.36); p<0.001), and a diagnosis of stress urinary incontinence (4.98 (95% CI 1.95-12.67); p<0.001). CONCLUSION: The frequency of adverse events after urodynamics is low, and urinalysis in asymptomatic patients does not seem to be useful in predicting morbidity.

Securin Regulates the Spatiotemporal Dynamics of Separase.

Separase is a key regulator of the metaphase to anaphase transition with multiple functions. Separase cleaves cohesin to allow chromosome segregation and localizes to vesicles to promote exocytosis in mid-anaphase. The anaphase promoting complex/cyclosome (APC/C) activates separase by ubiquitinating its inhibitory chaperone, securin, triggering its degradation. How this pathway controls the exocytic function of separase has not been investigated. During meiosis I, securin is degraded over several minutes, while separase rapidly relocalizes from kinetochore structures at the spindle and cortex to sites of action on chromosomes and vesicles at anaphase onset. The loss of cohesin coincides with the relocalization of separase to the chromosome midbivalent at anaphase onset. APC/C depletion prevents separase relocalization, while securin depletion causes precocious separase relocalization. Expression of non-degradable securin inhibits chromosome segregation, exocytosis, and separase localization to vesicles but not to the anaphase spindle. We conclude that APC/C mediated securin degradation controls separase localization. This spatiotemporal regulation will impact the effective local concentration of separase for more precise targeting of substrates in anaphase.

Dynamic functional and structural remodeling during retinal regeneration in zebrafish.

Introduction: Zebrafish regenerate their retinas following damage, resulting in restoration of visual function. Here we evaluate recovery of retinal function through qualitative and quantitative analysis of the electroretinogram (ERG) over time following retinal damage, in correlation to histological features of regenerated retinal tissue. Methods: Retinas of adult zebrafish were lesioned by intravitreal injection of 10 µM (extensive lesion; destroys all neurons) or 2 µM (selective lesion; spares photoreceptors) ouabain. Unlesioned contralateral retinas served as controls. Function of retinal circuitry was analyzed at selected timepoints using ERG recordings from live zebrafish, and whole eyes were processed for histological analyses immediately thereafter. Results: Qualitative and quantitative assessment of waveforms during retinal regeneration revealed dynamic changes that were heterogeneous on an individual level within each sampling time, but still followed common waveform recovery patterns on a per-fish and population-level basis. Early in the regeneration period (13-30 days post injury; DPI), for both lesion types, b-waves were essentially not detected, and unmasked increased apparent amplitudes, implicit times, and half-widths of a-waves (vs. controls). In control recordings, d-waves were not obviously detected, but apparent d-waves (OFF-bipolar responses) from regenerating retinas of several fish became prominent by 30DPI and dominated the post-photoreceptor response (PPR). Beyond 45DPI, b-waves became detectable, and the ratio of apparent d- to b-wave contributions progressively shifted with most, but not all, fish displaying a b-wave dominated PPR. At the latest timepoints (extensive, 90DPI; selective, 80DPI), recordings with measurable b-waves approached a normal waveform (implicit times and half-widths), but amplitudes were not restored to control levels. Histological analyses of the retinas from which ERGs were recorded showed that as regeneration progressed, PKCa + ON-bipolar terminals and parvalbumin + amacrine cell processes became more stereotypically positioned within the deep sublaminae of the INL over recovery time after each lesion type, consistent with the shift in PPR seen in the ERG recordings. Discussion: Taken together, these data suggest that photoreceptor-OFF-bipolar component/connectivity may functionally recover and mature earlier during regeneration compared to the photoreceptor-ON-bipolar component, though the timeframe in which such recovery happens is heterogeneous on a per-fish basis. Collectively our studies suggest gradual restoration of ON-bipolar functional circuitry during retinal regeneration.

Does gabapentin impact response to anticholinergics for overactive bladder?

INTRODUCTION AND HYPOTHESIS: It is unknown whether gabapentin modulates the therapeutic effect of anticholinergics (AC) in patients with overactive bladder. We hypothesized that pre-existing gabapentin use would improve response rates in these patients. METHODS: Female patients treated with AC between 2010-2018 were identified. Data were collected on gabapentin use, indication, dose and duration of use as well as demographic and clinical characteristics. Patients were stratified by those that only took AC and those that took both AC and gabapentin ("combination therapy"). Response was determined through chart review. Descriptive statistics were expressed as medians and interquartile ranges (IQR). Pairwise analysis was performed using Wilcoxon rank-sum. Multivariable logistic regression was used to identify independent variables predicting response. A subgroup analysis was performed in patients with chronic pain disorders. RESULTS: Seven hundred fifty-six subjects met all criteria; 16.5% (n = 125) were on combination therapy. Those taking gabapentin were more likely to have chronic (49.6% vs. 22.5%, p < 0.001) or neuropathic pain (25.6% vs. 9.4%, p < 0.001) and to use narcotics (41.6% vs. 15.5%, p < 0.001). Patients taking combination therapy were not more likely to improve compared to patients taking AC alone (41.6% vs. 47.7%, p = 0.211), which persisted after adjusting for confounders (aOR = 1.02, 95% CI: 0.63-1.65). In the 182 patients with chronic pain, those receiving combination therapy were more likely to respond than those taking AC alone (35.2% vs. 21.9%, p = 0.0015), although this did not persist after adjusting for confounders (aOR = 1.15, 95% CI: 0.70-1.90). CONCLUSIONS: Pre-existing gabapentin use does not seem to influence response to AC in patients with overactive bladder.

Compensatory engulfment and Müller glia reactivity in the absence of microglia.

Microglia are known for important phagocytic functions in the vertebrate retina. Reports also suggest that Müller glia have phagocytic capacity, though the relative levels and contexts in which this occurs remain to be thoroughly examined. Here, we investigate Müller glial engulfment of dying cells in the developing zebrafish retina in the presence and absence of microglia, using a genetic mutant in which microglia do not develop. We show that in normal conditions clearance of dying cells is dominated by microglia; however, Müller glia do have a limited clearance role. In retinas lacking intact microglial populations, we found a striking increase in the engulfment load assumed by the Müller glia, which displayed prominent cellular compartments containing apoptotic cells, several of which localized with the early phagosome/endosome marker Rab5. Consistent with increased engulfment, lysosomal staining was also increased in Müller glia in the absence of microglia. Increased engulfment load led to evidence of Müller glia reactivity including upregulation of gfap but did not trigger cell cycle re-entry by differentiated Müller glia. Our work provides important insight into the phagocytic capacity of Müller glia and the ability for compensatory functions and downstream effects. Therefore, effects of microglial deficiency or depletion on other glial cell types should be well-considered in experimental manipulations, in neurodegenerative disease, and in therapeutic approaches that target microglia. Our findings further justify future work to understand differential mechanisms and contexts of phagocytosis by glial cells in the central nervous system, and the significance of these mechanisms in health and disease.

Selective activation of BK channels in small-headed dendritic spines suppresses excitatory postsynaptic potentials.

Dendritic spines are the main receptacles of excitatory information in the brain. Their particular morphology, with a small head connected to the dendrite by a slender neck, has inspired theoretical and experimental work to understand how these structural features affect the processing, storage and integration of synaptic inputs in pyramidal neurons (PNs). The activation of glutamate receptors in spines triggers a large voltage change as well as calcium signals at the spine head. Thus, voltage-gated and calcium-activated potassium channels located in the spine head likely play a key role in synaptic transmission. Here we study the presence and function of large conductance calcium-activated potassium (BK) channels in spines from layer 5 PNs. We found that BK channels are localized to dendrites and spines regardless of their size, but their activity can only be detected in spines with small head volumes (≤0.09 µm3 ), which reduces the amplitude of two-photon uncaging excitatory postsynaptic potentials recorded at the soma. In addition, we found that calcium signals in spines with small head volumes are significantly larger than those observed in spines with larger head volumes. In accordance with our experimental data, numerical simulations predict that synaptic inputs impinging onto spines with small head volumes generate voltage responses and calcium signals within the spine head itself that are significantly larger than those observed in spines with larger head volumes, which are sufficient to activate spine BK channels. These results show that BK channels are selectively activated in small-headed spines, suggesting a new level of dendritic spine-mediated regulation of synaptic processing, integration and plasticity in cortical PNs. KEY POINTS: BK channels are expressed in the visual cortex and layer 5 pyramidal neuron somata, dendrites and spines regardless of their size. BK channels are selectively activated in small-headed spines (≤0.09 µm3 ), which reduces the amplitude of two-photon (2P) uncaging excitatory postsynaptic potentials (EPSPs) recorded at the soma. Two-photon imaging revealed that intracellular calcium responses in the head of 2P-activated spines are significantly larger in small-headed spines (≤0.09 µm3 ) than in spines with larger head volumes. In accordance with our experimental data, numerical simulations showed that synaptic inputs impinging onto spines with small head volumes (≤0.09 µm3 ) generate voltage responses and calcium signals within the spine head itself that are significantly larger than those observed in spines with larger head volumes, sufficient to activate spine BK channels and suppress EPSPs.

Modulation of retinoid-X-receptors differentially regulates expression of apolipoprotein genes apoc1 and apoeb by zebrafish microglia.

Transcriptome analyses performed in both human and zebrafish indicate strong expression of Apoe and Apoc1 by microglia. Apoe expression by microglia is well appreciated, but Apoc1 expression has not been well-examined. PPAR/RXR and LXR/RXR receptors appear to regulate expression of the apolipoprotein gene cluster in macrophages, but a similar role in microglia in vivo has not been studied. Here, we characterized microglial expression of apoc1 in the zebrafish central nervous system (CNS) in situ and demonstrate that in the CNS, apoc1 expression is unique to microglia. We then examined the effects of PPAR/RXR and LXR/RXR modulation on microglial expression of apoc1 and apoeb during early CNS development using a pharmacological approach. Changes in apoc1 and apoeb transcripts in response to pharmacological modulation were quantified by RT-qPCR in whole heads, and in individual microglia using hybridization chain reaction (HCR) in situ hybridization. We found that expression of apoc1 and apoeb by microglia were differentially regulated by LXR/RXR and PPAR/RXR modulating compounds, respectively, during development. Our results also suggest RXR receptors could be involved in endogenous induction of apoc1 expression by microglia. Collectively, our work supports the use of zebrafish to better understand regulation and function of these apolipoproteins in the CNS.

Evidence of regional specializations in regenerated zebrafish retina.

Adult zebrafish are capable of functional retinal regeneration following damage. A goal of vision science is to stimulate or permit a similar process in mammals to treat human retinal disease and trauma. Ideally such a process would reconstitute the stereotyped, two-dimensional topographic patterns and regional specializations of specific cell types, functionally important for representation of the visual field. An example in humans is the cone-rich fovea, essential for high-acuity color vision. Stereotyped, global topographic patterns of specific retinal cell types are also found in zebrafish, particularly for cone types expressing the tandemly-replicated lws (long wavelength-sensitive) and rh2 (middle wavelength-sensitive) opsins. Here we examine whether regionally specialized patterns of LWS1 and LWS2 cones are restored in regenerated retinas in zebrafish. Adult transgenic zebrafish carrying fluorescent reporters for lws1 and lws2 were subjected to retinal lesions that destroy all neurons but spare glia, via intraocular injection of the neurotoxin ouabain. Regenerated and contralateral control retinas were mounted whole or sectioned, and imaged. Overall spatial patterns of lws1 vs. lws2 opsin-expressing cones in regenerated retinas were remarkably similar to those of control retinas, with LWS1 cones in ventral/peripheral regions, and LWS2 cones in dorsal/central regions. However, LWS2 cones occupied a smaller fraction of regenerated retina, and several cones co-expressed the lws1 and lws2 reporters in regenerated retinas. Local patterns of regenerated LWS1 cones showed modest reductions in regularity. These results suggest that some of the regional patterning information, or the source of such signals, for LWS cone subtypes may be retained by undamaged cell types (Müller glia or RPE) and re-deployed during regeneration.

Taking the Pulse on Pediatric Simulation: A National Survey of Pediatric Residency Programs' Simulation Practices and Challenges.

OBJECTIVES: There is abundant literature on simulation use in individual pediatric residency programs but limited overall data on simulation in US pediatric residency programs. This study sought to determine how US pediatric residency programs use simulation for teaching and assessment and the challenges programs face in their use of simulation. METHODS: The Association of Pediatric Program Director's Healthcare Simulation in Pediatrics Learning Community members developed a 15-multipart question survey on the use of simulation in US pediatric residency programs using best practices in survey design. The survey was distributed electronically to US pediatric residency program directors. Qualitative questions were analyzed by content analysis and quantitative questions using descriptive statistics. RESULTS: The survey response rate was 21%; respondents were disproportionately from large academic medical centers. Qualitative analysis found that respondents use simulation to teach pediatric residents in the areas of urgent/emergent situations, procedures, and communication, and common challenges to simulation implementation are time, physical resources, expertise, competing priorities, logistics, and buy-in. Quantitative analysis demonstrated that, although respondents are largely confident that their simulation programs improve resident preparedness and competence, few objectively evaluate their simulation programs. CONCLUSIONS: Pediatric residency programs use simulation for similar purposes and face similar challenges. By collaborating, the resources of the national pediatric simulation community can be leveraged to collect evidence for best practices for simulation use in pediatric residency training.

Simulation-Based Curricula for Enhanced Retention of Pediatric Resuscitation Skills: A Randomized Controlled Study.

INTRODUCTION: Resuscitation skills decay as early as 4 months after course acquisition. Gaps in research remain regarding ideal educational modalities, timing, and frequency of curricula required to optimize skills retention. Our objective was to evaluate the impact on retention of resuscitation skills 8 months after the Pediatric Advanced Life Support (PALS) course when reinforced by an adjunct simulation-based curriculum 4 months after PALS certification. We hypothesized there would be improved retention in the intervention group. METHODS: This is a partial, double-blind, randomized controlled study. First-year pediatric residents were randomized to an intervention or control group. The intervention group participated in a simulation-based curriculum grounded in principles of deliberate practice and debriefing. The control group received no intervention. T-tests were used to compare mean percent scores (M) from simulation-based assessments and multiple-choice tests immediately following the PALS course and after 8 months. RESULTS: Intervention group (n = 12) had overall improved retention of resuscitation skills at 8 months when compared with the control group (n = 12) (mean, 0.57 ± 0.05 vs 0.52 ± 0.06; P = 0.037). No significant difference existed between individual skills stations. The intervention group had greater retention of cognitive knowledge (mean, 0.78 ± 0.09 vs 0.68 ± 0.14; P = 0.049). Residents performed 61% of assessment items correctly immediately following the PALS course. CONCLUSIONS: Resuscitation skills acquisition from the PALS course and retention are suboptimal. These findings support the use of simulation-based curricula as course adjuncts to extend retention beyond 4 months.

Obesity Is Not an Independent Predictor of Necrotizing Soft Tissue Infection Outcomes.

Background: Necrotizing soft tissue infections (NSTIs) are a group of rapidly progressive infections of the skin and its underlying tissue. These infections result in substantial morbidity and mortality. The focus of this study was to determine if obesity is associated with a worsened clinical outcome or prolonged hospital course for patients with NSTIs. Patients and Methods: We conducted a retrospective chart review of patients with NSTI presenting to a single tertiary hospital. Fat content, measured with body mass index (BMI) and abdominal fat thicknesses, including subcutaneous and visceral fat, were compared against primary and secondary outcomes of NSTIs. Results: We found that women had a higher mortality rate compared with men (27% vs. 15% mortality). Women also had an increased subcutaneous abdominal fat thickness (55.7 vs. 36.9 mm, p = 0.028). However, no measurements of fat, BMI, subcutaneous fat, or visceral fat differed between survivors and mortalities of NSTIs. In fact, with the exception of a higher BMI in those who developed acute kidney injury (AKI, p = 0.034), we found no correlation between increases in fat measurement and secondary outcome, including propensity to develop sepsis during hospitalization, length of hospital stay, length of intensive care stay, or antibiotic usage. Multivariable logistic regression analysis was conducted, and we found no statistically significant differences in primary or secondary outcomes. Conclusion: Women appear to have a higher mortality in NSTI, although the reasons for this are unclear. Obesity, as measured by BMI, subcutaneous, and visceral fat thicknesses, does not appear to be an independent risk factor.