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Emergency medicine (EM) has expanded rapidly since its inception in 1979. Workforce projections from current data demonstrate a rapid rise in the number of accredited EM residency programs and trainee positions. Based on these trends, the specialty may soon reach a point of saturation, particularly in urban areas. This could negatively impact future trainees entering the job market as well as the career plans of medical students. More time and resources should be devoted to obtaining accurate projections, assessing the distribution of emergency physicians in rural versus urban settings, and implementing central workforce planning to protect the future of graduating trainees.
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The Association of Academic Chairs of Emergency Medicine Chair Development Program (CDP) was started in 2014 to provide emergency medicine (EM) chairs and leaders who aspired to become academic chairs with EM-specific leadership training. Each class participated in a 1-year program, with five sessions taught primarily by EM leaders. Data from the first 5 years of the CDP are provided. A total of 81 participants completed the program (16% women). Twenty participants who were not chairs at entry have become EM chairs. Ratings of the CDP based on a survey of participants with a 94% response rate were very favorable. The CDP has been a popular and successful vehicle to increase leadership skills and prepare EM leaders for academic chair positions.
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Medicina de Emergencia/educación , Liderazgo , Servicio de Urgencia en Hospital/organización & administración , Femenino , Humanos , Masculino , Desarrollo de Programa , Evaluación de Programas y Proyectos de Salud , Encuestas y Cuestionarios , Estados UnidosRESUMEN
Life sometimes creates interesting confluences, and these should not be ignored. I was the Chair who sat on the other side of the desk during the job interview of the author of this remarkable essay. I hired her, and her husband. I was pleased to bring them both on board as promising new faculty members. This article is protected by copyright. All rights reserved.
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INTRODUCTION: The specialty of emergency medicine is experiencing the convergence of a number of transformational forces in the United States, including health care reform, technological advancements, and societal shifts. These bring both opportunity and uncertainty. 21ST CENTURY CHALLENGES: Persistent challenges such as the opioid epidemic, rising health care costs, misaligned incentives, patients with multiple chronic diseases, and emergency department crowding continue to plague the acute, unscheduled care system. REDUCTIONISM AND COMPLEX SYSTEMS THINKING: The traditional approach to health care practice and improvement-reductionism-is not adequate for the complexity of the twenty-first century. Reductionist thinking will likely continue to produce unintended consequences and suboptimal outcomes. Complex systems thinking provides a perspective and set of tools better suited for the challenges and opportunities facing public health in general, and emergency medicine more specifically. IMPLICATIONS FOR EMERGENCY MEDICINE: This article introduces complex systems thinking and argues for its application in the context of emergency medicine by drawing on the history of the circumstances surrounding the formation of the specialty and by providing examples of its application to several practice challenges.
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Medicina de Emergencia/organización & administración , Análisis de Sistemas , Innovación Organizacional , Incertidumbre , Estados UnidosRESUMEN
BACKGROUND: Over 35 million alcohol-impaired (AI) patients are cared for in emergency departments (EDs) annually. Emergency physicians are charged with ensuring AI patients' safety by identifying resolution of alcohol-induced impairment. The most common standard evaluation is an extemporized clinical examination, as ethanol levels are not reliable or predictive of clinical symptoms. There is no standard assessment of ED AI patients. OBJECTIVE: The objective was to evaluate a novel standardized ED assessment of alcohol impairment, Hack's Impairment Index (HII score), in a busy urban ED. METHODS: A retrospective chart review was performed for all AI patients seen in our busy urban ED over 24 months. Trained nurses evaluated AI patients with both "usual" and HII score every 2 hours. Patients were stratified by frequency of visits for AI during this time: high (≥ 6), medium (2-5), and low (1). Within each category, comparisons were made between HII scores, measured ethanol levels, and usual nursing assessment of AI. Changes in HII scores over time were also evaluated. RESULTS: A total of 8,074 visits from 3,219 unique patients were eligible for study, including 7,973 (98.7%) with ethanol levels, 5,061 (62.7%) with complete HII scores, and 3,646 (45.2%) with health care provider assessments. Correlations between HII scores and ethanol levels were poor (Pearson's R2 = 0.09, 0.09, and 0.17 for high-, medium-, and low-frequency strata). HII scores were excellent at discriminating nursing assessment of AI, while ethanol levels were less effective. Omitting extrema, HII scores fell consistently an average 0.062 points per hour, throughout patients' visits. CONCLUSIONS: The HII score applied a quantitative, objective assessment of alcohol impairment. HII scores were superior to ethanol levels as an objective clinical measure of impairment. The HII declines in a reasonably predictable manner over time, with serial evaluations corresponding well with health care provider evaluations.
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Intoxicación Alcohólica/diagnóstico , Servicio de Urgencia en Hospital , Adulto , Femenino , Humanos , Masculino , Persona de Mediana Edad , Evaluación en Enfermería/métodos , Valor Predictivo de las Pruebas , Estudios RetrospectivosRESUMEN
No routine tests currently exist to objectively diagnose mild traumatic brain injury (mTBI)/concussion. Previously reported biomarkers for mTBI represented proteins released from damaged neurons or glia. However, low levels of these proteins, and/or the complexity of assays used for their detection, limits implementation of these biomarkers in routine practice. Here, we sought to identify proteins whose synthesis is altered post-mTBI and whose blood levels could be measured using standard immunoassays. Adult patients sustaining a concussion within the past 24 h were enrolled. Controls were uninjured subjects and patients with orthopedic injury (OI). Four candidate biomarkers were identified: copeptin; galectin 3 (LGALS3); matrix metalloproteinase 9 (MMP9); and occludin (OCLN). A 3.4-fold decrease (p<0.0001) in plasma concentration of copeptin was found in mTBI patients within 8 h after accident, compared to uninjured controls. Plasma levels of LGALS3, MMP9, and OCLN increased 3.6- to 4.5-fold (p<0.0001) within the same time frame postinjury. Levels of at least two biomarkers were altered beyond their respective cut-off values in 90% of mTBI patients, whereas in none of uninjured controls were levels of two biomarkers simultaneously changed. A positive correlation (r=0.681; p<0.001) between plasma levels of LGALS3 and OCLN was also found in mTBI patients, whereas in OI patients or uninjured subjects, these variables did not correlate. This panel of biomarkers discerns, with high accuracy, patients with isolated concussion from uninjured individuals within the first 8 h after accident. These biomarkers can also aid in diagnosing concussion in the presence of OI.
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Biomarcadores/sangre , Conmoción Encefálica/sangre , Galectina 3/sangre , Glicopéptidos/sangre , Metaloproteinasa 9 de la Matriz/sangre , Ocludina/sangre , Adulto , Femenino , Humanos , Masculino , Persona de Mediana EdadRESUMEN
This article evaluates current evidence on the cost of emergency care. First, we reviewed data from national data sets and found that aggregate spending on emergency care is 5% to 6% of national health expenditures but could be as high as 10%. These figures are significantly higher than those previously published. Second, we reviewed the literature on economic models of the cost of emergency care and found that the results are inconclusive and incomplete. As an alternative, we discussed activity-based cost accounting and concluded that it is a promising research methodology for emergency medicine. We conclude by advocating for a strategy to demonstrate the value and strategic importance of emergency medicine rather than minimizing its role in national health care costs.
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Servicios Médicos de Urgencia/economía , Servicio de Urgencia en Hospital/economía , Costos de la Atención en Salud , Servicio de Urgencia en Hospital/estadística & datos numéricos , Encuestas de Atención de la Salud , Humanos , Escalas de Valor Relativo , Estados Unidos , United States Agency for Healthcare Research and QualityRESUMEN
The invasion of inflammatory cells occurring after ischemic or traumatic brain injury (TBI) has a detrimental effect on neuronal survival and functional recovery after injury. We have recently demonstrated that not only the blood-brain barrier, but also the blood-cerebrospinal fluid (CSF) barrier (BCSFB), has a role in posttraumatic recruitment of neutrophils. Here, we show that TBI results in a rapid increase in synthesis and release into the CSF of a major chemoattractant for monocytes, CCL2, by the choroid plexus epithelium, a site of the BCSFB. Using an in vitro model of the BCSFB, we also show that CCL2 is released across the apical and basolateral membranes of the choroidal epithelium, a pattern of chemokine secretion that promotes leukocyte migration across epithelial barriers. Immunohistochemical and electron microscopic analyses of choroidal tissue provide evidence for the movement of monocytes, sometimes in tandem with neutrophils, along the paracellular pathways between adjacent epithelial cells. These data further support the pathophysiological role of BCSFB in promoting the recruitment of inflammatory cells to the injured brain.
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Barrera Hematoencefálica/inmunología , Lesiones Encefálicas/inmunología , Líquido Cefalorraquídeo/inmunología , Plexo Coroideo/inmunología , Monocitos/citología , Animales , Membrana Basal/inmunología , Membrana Basal/ultraestructura , Barrera Hematoencefálica/ultraestructura , Western Blotting , Lesiones Encefálicas/sangre , Lesiones Encefálicas/líquido cefalorraquídeo , Células Cultivadas , Líquido Cefalorraquídeo/citología , Quimiocina CCL2/inmunología , Quimiocina CCL2/metabolismo , Quimiotaxis de Leucocito/inmunología , Plexo Coroideo/irrigación sanguínea , Plexo Coroideo/ultraestructura , Modelos Animales de Enfermedad , Ensayo de Inmunoadsorción Enzimática , Células Epiteliales/inmunología , Uniones Intercelulares/inmunología , Uniones Intercelulares/ultraestructura , Masculino , Microscopía Electrónica de Transmisión , Monocitos/inmunología , Monocitos/ultraestructura , Infiltración Neutrófila/inmunología , Ratas , Ratas Long-Evans , Reacción en Cadena en Tiempo Real de la Polimerasa , Reacción en Cadena de la Polimerasa de Transcriptasa InversaRESUMEN
In 1979 Peter Rosen, MD, a leading academic figure in the developing field of emergency medicine (EM), wrote an article, "The Biology of Emergency Medicine," in response to criticism from other specialties and medical leaders that there was no unique biology of EM that would qualify it as a legitimate medical specialty. This essay received much attention at the time and served as rallying cry for emergency physicians (EPs) who were trying to find their places in the house of medicine and especially in medical schools and academic teaching hospitals. Thirty years later, the opposition that prompted many of Rosen's strongly worded impressions and observations on the biology of EM, clinical emergency department (ED) practice, education, and research has largely faded. Many of Rosen's predictions on the eventual success of EM have come true. However, core issues that existed then continue to present challenges for academic EM and clinical emergency practice.
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Medicina de Emergencia/historia , Publicaciones Periódicas como Asunto/historia , Investigación Biomédica/historia , Medicina de Emergencia/educación , Historia del Siglo XX , Historia del Siglo XXI , Humanos , Medicina , Rol del Médico/historia , Estados UnidosRESUMEN
Previous studies have indicated that the primary targets for vasopressin actions on the injured brain are the cerebrovascular endothelium and astrocytes, and that vasopressin amplifies the posttraumatic production of proinflammatory mediators. Here, the controlled cortical impact model of traumatic brain injury in rats was used to identify the sources of vasopressin in the injured brain. Injury increased vasopressin synthesis in the hypothalamus and cerebral cortex adjacent to the posttraumatic lesion. In the cortex, vasopressin was predominantly produced by activated microglia/macrophages, and, to a lesser extent, by the cerebrovascular endothelium. These data further support the pathophysiological role of vasopressin in brain injury.
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Química Encefálica/fisiología , Lesiones Encefálicas/metabolismo , Vasopresinas/biosíntesis , Animales , Arginina Vasopresina/biosíntesis , Lesiones Encefálicas/patología , Corteza Cerebral/lesiones , Corteza Cerebral/metabolismo , Corteza Cerebral/patología , Endotelio Vascular/fisiología , Hipernatremia/metabolismo , Hipotálamo/lesiones , Hipotálamo/metabolismo , Hipotálamo/patología , Inmunohistoquímica , Macrófagos/fisiología , Masculino , Microglía/fisiología , Microscopía Confocal , ARN Mensajero/biosíntesis , ARN Mensajero/genética , Ratas , Ratas Long-Evans , Reacción en Cadena de la Polimerasa de Transcriptasa InversaRESUMEN
The blood-brain barrier (BBB) is formed by tightly connected cerebrovascular endothelial cells, but its normal function also depends on paracrine interactions between the brain endothelium and closely located glia. There is a growing consensus that brain injury, whether it is ischemic, hemorrhagic, or traumatic, leads to dysfunction of the BBB. Changes in BBB function observed after injury are thought to contribute to the loss of neural tissue and to affect the response to neuroprotective drugs. New discoveries suggest that considering the entire gliovascular unit, rather than the BBB alone, will expand our understanding of the cellular and molecular responses to traumatic brain injury (TBI). This review will address the BBB breakdown in TBI, the role of blood-borne factors in affecting the function of the gliovascular unit, changes in BBB permeability and post-traumatic edema formation, and the major pathophysiological factors associated with TBI that may contribute to post-traumatic dysfunction of the BBB. The key role of neuroinflammation and the possible effect of injury on transport mechanisms at the BBB will also be described. Finally, the potential role of the BBB as a target for therapeutic intervention through restoration of normal BBB function after injury and/or by harnessing the cerebrovascular endothelium to produce neurotrophic growth factors will be discussed.
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A complex set of molecular and functional reactions is set into motion by traumatic brain injury (TBI). New research that extends beyond pathological effects on neurons suggests a key role for the blood-brain barrier, neurovascular unit, arginine vasopressin, and neuroinflammation in the pathophysiology of TBI. The prevalence of molecular derangements in TBI holds promise for the identification and use of biomarkers to assess severity of injury, determine prognosis, and perhaps direct therapy. Hopefully, improved knowledge of these elements of pathophysiology will provide the mechanistic clues that lead to improved treatment of TBI.
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Arginina Vasopresina/metabolismo , Barrera Hematoencefálica/fisiopatología , Lesiones Encefálicas/fisiopatología , Encéfalo/fisiopatología , Estrés Oxidativo/inmunología , Biomarcadores , Encéfalo/inmunología , Encéfalo/metabolismo , Lesiones Encefálicas/inmunología , Lesiones Encefálicas/metabolismo , Lesiones Encefálicas/terapia , Humanos , Pronóstico , Índice de Severidad de la Enfermedad , Resultado del TratamientoRESUMEN
Arginine vasopressin (AVP) has previously been shown to promote disruption of the blood-brain barrier, exacerbate edema, and augment the loss of neural tissue in various forms and models of brain injury. However, the mechanisms underlying these AVP actions are not well understood. These mechanisms were studied in AVP-deficient Brattleboro rats (Avp(di/di)), and their parental Long-Evans strain, using a controlled cortical impact model of traumatic brain injury (TBI). The increased influx of inflammatory cells into the injured cortex in wild-type versus Avp(di/di) rats was associated with higher levels of cortical synthesis of the CXC and CC chemokines found in wild-type versus Avp(di/di) rats. These chemokines were predominantly produced by the cerebrovascular endothelium and astrocytes. In astrocyte and brain endothelial cell cultures, AVP acted synergistically with tumor necrosis factor-alpha (TNF-alpha) to increase the TNF-alpha-dependent production of CXC and CC chemokines. These AVP actions were mediated by c-Jun N-terminal kinase (JNK), as shown by Western blotting and pharmacological inhibition of JNK activity. The activity of JNK was increased in response to injury, and the differences in the magnitude of its post-traumatic activation between Avp(di/di) and wild-type rats were observed. These data demonstrate that AVP plays an important role in exacerbating the brain inflammatory response to injury.
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Lesiones Encefálicas/metabolismo , Mediadores de Inflamación/metabolismo , Vasopresinas/genética , Vasopresinas/fisiología , Animales , Western Blotting , Encéfalo/patología , Lesiones Encefálicas/patología , Células Cultivadas , Quimiocina CCL2/biosíntesis , Quimiocina CXCL1/metabolismo , Quimiocina CXCL2/metabolismo , Inmunohistoquímica , Inmunoprecipitación , Proteínas Quinasas JNK Activadas por Mitógenos/antagonistas & inhibidores , Proteínas Quinasas JNK Activadas por Mitógenos/metabolismo , Masculino , Ratas , Ratas Brattleboro , Ratas Long-Evans , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Factor de Necrosis Tumoral alfa/metabolismo , Vasopresinas/deficienciaRESUMEN
Traumatic brain injury (TBI) frequently results in neuroinflammation, which includes the invasion of neutrophils. After TBI, neutrophils infiltrate the choroid plexus (CP), a site of the blood-cerebrospinal fluid (CSF) barrier (BCSFB), and accumulate in the CSF space near the injury, from where these inflammatory cells may migrate to brain parenchyma. We have hypothesized that the CP functions as an entry point for neutrophils to invade the injured brain. Using the controlled cortical impact model of TBI in rats and an in vitro model of the BCSFB, we show that the CP produces CXC chemokines, such as cytokine-induced neutrophil chemoattractant (CINC)-1 or CXCL1, CINC-2alpha or CXCL3, and CINC-3 or CXCL2. These chemokines are secreted both apically and basolaterally from the choroidal epithelium, a prerequisite for neutrophil migration across epithelial barriers. Consistent with these findings, we also provide electron microscopic evidence that neutrophils infiltrate the choroidal stroma and subsequently reach the intercellular space between choroidal epithelial cells. This is the first detailed analysis of the BCSFB function related to neutrophil trafficking. Our observations support the role of this barrier in posttraumatic neutrophil invasion.
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Lesiones Encefálicas/inmunología , Plexo Coroideo , Neutrófilos/inmunología , Animales , Barrera Hematoencefálica/fisiología , Células Cultivadas , Corteza Cerebral/metabolismo , Quimiocina CXCL1/metabolismo , Quimiocinas CXC/genética , Quimiocinas CXC/inmunología , Plexo Coroideo/citología , Plexo Coroideo/metabolismo , Citocinas/genética , Citocinas/inmunología , Interleucina-1beta/genética , Interleucina-1beta/inmunología , Masculino , Neutrófilos/citología , Ratas , Ratas Long-Evans , Ratas Sprague-Dawley , Factor de Necrosis Tumoral alfa/genética , Factor de Necrosis Tumoral alfa/inmunologíaRESUMEN
OBJECTIVES: This study sought to account for trends in medical student specialty choice by examining the importance of lifestyle factors. Emergency medicine (EM) is among several medical specialties classified as having a "controllable lifestyle." The primary objective of this study was to determine if medical students choosing careers in EM have a different profile of influences, values, and expectations from students choosing other specialties or specialty groups. Of secondary interest was how much lifestyle influenced students choosing EM compared to students choosing controllable lifestyle (CL) specialties. METHODS: Using data from the 2005 and 2006 Association of American Medical Colleges (AAMC) graduation questionnaire (GQ) supplemental surveys, we grouped responses according to desired specialty choice: EM (n = 963), CL (n = 3,681), primary care (PC; n = 3,191), or surgical specialty (SS; n = 1,694). The survey requires students to rate the influence of nine specific factors in determining their specialty choice: lifestyle, competitiveness, high level of educational debt, mentors and role models, options for fellowship training, salary expectations, length of residency training, family expectations, and medical school career planning activities. Using one-way analysis of variance (ANOVA) and nonparametric statistics, we assessed responses among the four subgroups for differences in the importance attributed to these factors. RESULTS: A total of 13,440 students completed the two supplemental surveys of the GQ. Of these students, 9,529 identified a specialty choice that fell within one of the four comparison groups and were included in the analysis. Compared to other specialty groups, students choosing EM reported lifestyle and length of residency as strong influences, while attributing less influence to mentors and options for fellowship training. CONCLUSIONS: Students choosing a career in EM have distinctly different priorities and influences than students entering PC and SS. The profile of students who choose EM is very similar to those choosing traditional CL specialties. A more thorough understanding of the values and priorities that shape medical student career selection may allow educators to provide better career counseling.
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Selección de Profesión , Medicina de Emergencia , Medicina/estadística & datos numéricos , Especialización , Estudiantes de Medicina/psicología , Adulto , Análisis de Varianza , Movilidad Laboral , Estudios Transversales , Medicina de Emergencia/educación , Becas , Femenino , Humanos , Internet , Internado y Residencia , Estilo de Vida , Masculino , Mentores , Especialidades Quirúrgicas , Encuestas y Cuestionarios , Estados Unidos , Adulto JovenRESUMEN
Traumatic brain injury is a major source of death and disability worldwide. Significant success has been achieved in improving short-term outcomes in severe traumatic brain injury victims; however, there are still great limitations in our ability to return severe traumatic brain injury victims to high levels of functioning. Primary brain injury, due to initial injury forces, causes tissue distortion and destruction in the early postinjury period. Clinical outcomes depend in large part on mediating the bimolecular and cellular changes that occur after the initial injury. These secondary injuries from traumatic brain injury lead to alterations in cell function and propagation of injury through processes such as depolarization, excitotoxicity, disruption of calcium homeostasis, free-radical generation, blood-brain barrier disruption, ischemic injury, edema formation, and intracranial hypertension. The best hope for improving outcome in traumatic brain injury patients is a better understanding of these processes and the development of therapies that can limit secondary brain injury.