207 research outputs found

    Recurrent and High‐frequency Use of the Emergency Department by Pediatric Patients

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    Objectives The authors sought to describe the epidemiology of and risk factors for recurrent and high‐frequency use of the emergency department (ED) by children. Methods This was a retrospective cohort study using a database of children aged 0 to 17 years, inclusive, presenting to 22 EDs of the Pediatric Emergency Care Applied Research Network (PECARN) during 2007, with 12‐month follow‐up after each index visit. ED diagnoses for each visit were categorized as trauma, acute medical, or chronic medical conditions. Recurrent visits were defined as any repeat visit; high‐frequency use was defined as four or more recurrent visits. Generalized estimating equations (GEEs) were used to measure the strength of associations between patient and visit characteristics and recurrent ED use. Results A total of 695,188 unique children had at least one ED visit each in 2007, with 455,588 recurrent ED visits in the 12 months following the index visits. Sixty‐four percent of patients had no recurrent visits, 20% had one, 8% had two, 4% had three, and 4% had four or more recurrent visits. Acute medical diagnoses accounted for most visits regardless of the number of recurrent visits. As the number of recurrent visits per patient rose, chronic diseases were increasingly represented, with asthma being the most common ED diagnosis. Trauma‐related diagnoses were more common among patients without recurrent visits than among those with high‐frequency recurrent visits (28% vs. 9%; p < 0.001). High‐frequency recurrent visits were more often within the highest severity score classifications. In multivariable analysis, recurrent visits were associated with younger age, black or Hispanic race or ethnicity, and public health insurance. Conclusions Risk factors for recurrent ED use by children include age, race and ethnicity, and insurance status. Although asthma plays an important role in recurrent ED use, acute illnesses account for the majority of recurrent ED visits. Resumen Objetivos Describir la epidemiología y los factores de riesgo de revista e hiperfrecuentación del servicio de urgencias (SU) por parte de los pacientes pediátricos. Metodología Estudio de cohorte retrospectivo mediante una base de datos de niños entre 0 y 17 años inclusive, que acudieron a 22 SU de la Pediatric Emergency Care Applied Research Network durante 2007, con un seguimiento de 12 meses tras cada visita índice. Los diagnósticos del SU de cada visita se clasificaron como traumatológico, médico agudo o enfermedades médicas crónicas. Las revisitas se definieron como cualquier visita repetida; la hiperfrecuentación se definió como cuatro o más revisitas. Se utilizaron ecuaciones de estimación generalizada para medir la fuerza de las asociaciones entre las características al paciente y la visita y la revisita del SU. Resultados Un total de 695.188 niños tuvieron al menos una visita al SU en 2007, con 455.588 revisitas al SU en los 12 meses tras las visitas índice. Un 64% de los pacientes no tuvieron revisitas, un 20% tuvo una, un 8% tuvo dos, un 4% tuvo tres y un 4% tuvo cuatro o más revisitas. Los diagnósticos médicos agudos representan la mayoría de las visitas, con independencia del número de revisitas. A medida que el número de revisitas por paciente aumentaba, las enfermedades crónicas estaban más representadas, y el asma fue el diagnóstico más común en el SU. Los diagnósticos relacionados con lo traumatológico fueron más frecuentes entre los pacientes sin revisitas que entre aquéllos con hiperfrecuentación (28% vs. 9%; p < 0,001). La alta frecuencia de revisitas fue más frecuente en las clasificaciones de gravedad más altas. En el análisis multivariable, las revisitas se asociaron con una edad más joven, raza o etnia negra o hispana, y la tenencia de un seguro de salud público. Conclusiones Los factores de riesgo para la revisita al SU por los niños incluyen la edad, la raza o etnia, y el tipo de seguro médico. Aunque el asma juega un papel importante en la revisita al SU, las enfermedades agudas representan la mayoría de la revistas al SU.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/106853/1/acem12347.pd

    Classificação do atendimento pré-hospitalar pediátrico como instrumento para otimizar a alocação de recursos no atendimento do trauma na cidade de São Paulo, Brasil

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    PURPOSE: To evaluate the pediatric prehospital care in São Paulo, the databases from basic life support units (BLSU) and ALSU, and to propose a simple and effective method for evaluating trauma severity in children at the prehospital phase. METHODS: A single firemen headquarter coordinates all prehospital trauma care in São Paulo city. Two databases were analyzed for children from 0 to 18 years old between 1998 and 2001: one from the Basic Life Support Units (BLSU - firemen) and one from the Advanced Life Support Units (ALSU - doctor and firemen). During this period, advanced life support units provided medical reports from 604 victims, while firemen provided 12.761 reports (BLSU+ALSU). Pre-Hospital Pediatric Trauma Classification is based on physiological status, trauma mechanism and anatomic injuries suggesting high energy transfer. In order to evaluate the proposed classification, it was compared to the Glasgow Coma Score and to the Revised Trauma Score. RESULTS: There was a male predominance in both databases and the most common trauma mechanism was transport related, followed by falls. Mortality was 1.6% in basic life support units and 9.6% in ALSU. There was association among the proposed score, the Glasgow Coma Score and to the Revised Trauma Score (p<0.0001). CONCLUSION: Pre-Hospital Pediatric Trauma Classification is a simple and reliable method for assessment, triage and recruitment of pediatric trauma resources.OBJETIVO: Avaliar o atendimento pré-hospitalar de crianças e adolescentes em São Paulo, avaliar o banco de dados das Unidades de Suporte Básico (UR) e Avançado (USA) e propor um método simples e eficaz para a avaliação da gravidade do trauma pediátrico na fase pré-hospitalar. MÉTODOS: Uma única central do Corpo de Bombeiros (COBOM) coordena todo o atendimento pré-hospitalar em São Paulo. Dois bancos de dados foram analisados para crianças de 0 a 18 anos de idade, entre 1998 e 2001: um das Unidades de Suporte Básico de Vida (UR- bombeiros) e outra de Unidades de Suporte Avançado (USA - médico e bombeiros). Neste período, o Serviço de Atendimento Médico de Urgência do Estado de São Paulo (SAMU) forneceu relatórios médicos de 604 vítimas, enquanto os bombeiros forneceram relatórios de 12.761 vitimas (UR+USA). A classificação do trauma pré-hospitalar pediátrico é baseada na condição fisiológica, mecanismo de trauma e lesões anatômicas das vítimas. A classificação do trauma pré-hospitalar pediátrico foi comparada à Escala de Coma de Glasgow (GCS) e ao Escore de Trauma Revisado (RTS). RESULTADOS: Houve predominância do sexo masculino em ambos bancos de dados. O mecanismo de trauma mais freqüente foi relacionado a transporte, seguido de quedas. A mortalidade foi 1,6% nas Unidades Básicas e 9,6% no Suporte Avançado. Houve associação entre a classificação do trauma pré-hospitalar pediátrico, Escala de Coma de Glasgow (GCS) e ao Escore de Trauma Revisado (RTS) GCS e RTS (p<0,0001). CONCLUSÃO: A classificação do trauma pré-hospitalar pediátrico é um método simples e confiável para a avaliação, triagem e recrutamento de recursos para o atendimento pré-hospitalar do trauma pediátrico.Universidade Federal de São Paulo (UNIFESP) Department of SurgeryUNIFESP, Department of SurgerySciEL

    Mepolizumab Alters Regulation of Airway Type-2 Inflammation in Urban Children with Asthma by Disrupting Eosinophil Gene Expression but Enhancing Mast Cell and Epithelial Pathways

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    Rationale: Mepolizumab (anti-IL5) reduces asthma exacerbations in urban children. We previously utilized nasal transcriptomics to identify inflammatory pathways (gene co-expression modules) associated with exacerbations despite this therapy. To understand mepolizumab’s precise impact on these pathways, we assess gene co-expression and loss of correlation, “decoherence,” using differential co-expression network analyses. Methods: 290 urban children (6-17 years) with exacerbation-prone asthma and blood eosinophils ≥150/microliter were randomized (1:1) to q4 week placebo or mepolizumab injections added to guideline-based care for 52 weeks. Nasal lavage samples were collected before and during treatment for RNA-sequencing. Differential co-expression of gene networks was evaluated to assess interactions and regulatory aspects of type-2 and eosinophilic airway inflammation. Results: Mepolizumab, but not placebo, significantly reduced the overall expression of an established type-2 inflammation gene co-expression module (fold change=0.77, p=0.002) enriched for eosinophil, mast cell, and epithelial IL-13 response genes (242 genes). Mepolizumab uncoupled co-expression of genes in this pathway. During mepolizumab, but not placebo treatment, there was significant loss of correlation among eosinophil-specific genes including RNASE2 (EDN), RNASE3 (ECP), CLC, SIGLEC8, and IL5RA contrasting a reciprocal increase in correlation among mast cell-specific genes (TPSAB1, CPA3, FCER1A), T2 cytokines (IL4, IL5, and IL13), and POSTN. Conclusions: These results suggest mepolizumab disrupts the regulatory interactions of gene co-expression among airway eosinophils, mast cells and epithelium by interrupting transcription regulation in eosinophils with enhancement in mast cell and epithelial inflammation. This paradoxical effect may contribute to an incomplete reduction of asthma exacerbations and demonstrates how differential co-expression network analyses can identify targets for more precise therapies

    Towards mentoring as feminist praxis in early childhood education and care in England

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    Following our contribution to a study of mentoring in seven European countries, we explored epistemological and ontological inconsistencies within mainstream mentoring systems and their regulated practice in England. We considered how feminist mentoring praxis can unsettle conceptualisations of mentoring relationships and challenge inequity in the early education systems and the practice of teaching young children. Predominantly female, early childhood educators suffer from low status in England, and their working lives may be controlled and policed through inequitable systems. On entering the workforce, trainees encounter a reductionist policy milieu where mentoring structures and normative assessment arrangements contribute to inequity. Mentors play pivotal roles in inducting trainees into their worlds of work with young children. Mentoring relationships can determine whether trainees accept the status quo. Principles derived from feminist praxis enable mentors to practise an ‘engaged pedagogy’, co-constructing knowledge, subverting hierarchies and contesting taken-for-granted aspects of policy and practice

    Quantitative measurements of inequality in geographic accessibility to pediatric care in Oita Prefecture, Japan: Standardization with complete spatial randomness

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    <p>Abstract</p> <p>Background</p> <p>A quantitative measurement of inequality in geographic accessibility to pediatric care as well as that of mean distance or travel time is very important for priority setting to ensure fair access to pediatric facilities. However, conventional techniques for measuring inequality is inappropriate in geographic settings. Since inequality measures of access distance or travel time is strongly influenced by the background geographic distribution patterns, they cannot be directly used for regional comparisons of geographic accessibility. The objective of this study is to resolve this issue by using a standardization approach.</p> <p>Methods</p> <p>Travel times to the nearest pediatric care were calculated for all children in Oita Prefecture, Japan. Relative mean differences were considered as the inequality measure for secondary medical service areas, and were standardized with an expected value estimated from a Monte Carlo simulation based on complete spatial randomness.</p> <p>Results</p> <p>The observed mean travel times in the area considered averaged 4.50 minutes, ranging from 1.83 to 7.02 minutes. The mean of the observed inequality measure was 1.1, ranging from 0.9 to 1.3. The expected values of the inequality measure varied according to the background geographic distribution pattern of children, which ranged from 0.3 to 0.7. After standardizing the observed inequality measure with the expected one, we found that the ranks of the inequality measure were reversed for the observed areas.</p> <p>Conclusions</p> <p>Using the indicator proposed in this paper, it is possible to compare the inequality in geographic accessibility among regions. Such a comparison may facilitate priority setting in health policy and planning.</p

    Persistent activation of interlinked type 2 airway epithelial gene networks in sputum-derived cells from aeroallergen-sensitized symptomatic asthmatics

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    © 2018 The Author(s). Atopic asthma is a persistent disease characterized by intermittent wheeze and progressive loss of lung function. The disease is thought to be driven primarily by chronic aeroallergen-induced type 2-associated inflammation. However, the vast majority of atopics do not develop asthma despite ongoing aeroallergen exposure, suggesting additional mechanisms operate in conjunction with type 2 immunity to drive asthma pathogenesis. We employed RNA-Seq profiling of sputum-derived cells to identify gene networks operative at baseline in house dust mite-sensitized (HDM S ) subjects with/without wheezing history that are characteristic of the ongoing asthmatic state. The expression of type 2 effectors (IL-5, IL-13) was equivalent in both cohorts of subjects. However, in HDM S -wheezers they were associated with upregulation of two coexpression modules comprising multiple type 2- and epithelial-associated genes. The first module was interlinked by the hubs EGFR, ERBB2, CDH1 and IL-13. The second module was associated with CDHR3 and mucociliary clearance genes. Our findings provide new insight into the molecular mechanisms operative at baseline in the airway mucosa in atopic asthmatics undergoing natural aeroallergen exposure, and suggest that susceptibility to asthma amongst these subjects involves complex interactions between type 2- and epithelial-associated gene networks, which are not operative in equivalently sensitized/exposed atopic non-asthmatics

    Sickness behaviour pushed too far – the basis of the syndrome seen in severe protozoal, bacterial and viral diseases and post-trauma

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    Certain distinctive components of the severe systemic inflammatory syndrome are now well-recognized to be common to malaria, sepsis, viral infections, and post-trauma illness. While their connection with cytokines has been appreciated for some time, the constellation of changes that comprise the syndrome has simply been accepted as an empirical observation, with no theory to explain why they should coexist. New data on the effects of the main pro-inflammatory cytokines on the genetic control of sickness behaviour can be extended to provide a rationale for why this syndrome contains many of its accustomed components, such as reversible encephalopathy, gene silencing, dyserythropoiesis, seizures, coagulopathy, hypoalbuminaemia and hypertriglyceridaemia. It is thus proposed that the pattern of pathology that comprises much of the systemic inflammatory syndrome occurs when one of the usually advantageous roles of pro-inflammatory cytokines – generating sickness behaviour by moderately repressing genes (Dbp, Tef, Hlf, Per1, Per2 and Per3, and the nuclear receptor Rev-erbα) that control circadian rhythm – becomes excessive. Although reversible encephalopathy and gene silencing are severe events with potentially fatal consequences, they can be viewed as having survival advantages through lowering energy demand. In contrast, dyserythropoiesis, seizures, coagulopathy, hypoalbuminaemia and hypertriglyceridaemia may best be viewed as unfortunate consequences of extreme repression of these same genetic controls when the pro-inflammatory cytokines that cause sickness behaviour are produced excessively. As well as casting a new light on the previously unrationalized coexistence of these aspects of systemic inflammatory diseases, this concept is consistent with the case for a primary role for inflammatory cytokines in their pathogenesis across this range of diseases
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