Owning the cost of emergency medicine: beyond 2%.

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.

Developing Emergency Medicine Leaders: The AACEM/SAEM Chair Development Program at 5 Years.

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.

Too Big Too Fast? Potential Implications of the Rapid Increase in Emergency Medicine Residency Positions.

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.

Caught in a Double Bind: A Woman's Job Search Experience by Katelyn Moretti.

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.

Complex systems thinking in emergency medicine: A novel paradigm for a rapidly changing and interconnected health care landscape.

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.

Academic radiology and the emergency department: does it need changing?

RATIONAL AND OBJECTIVES: The increasing importance of imaging for both diagnosis and management in patient care has resulted in a demand for radiology services 7 days a week, 24 hours a day, especially in the emergency department (ED). We hypothesized the resident preliminary reports were better than generalist radiology interpretations, although inferior to subspecialty interpretations. MATERIALS AND METHODS: Total radiology volume through our Level I pediatric and adult academic trauma ED was obtained from the radiology information system. We conducted a literature search for error and discordant rates between radiologists of varying experience. For a 2-week prospective period, all preliminary reports generated by the residents and final interpretations were collected. Significant changes in the report were tabulated. RESULTS: The ED requested 72,886 imaging studies in 2004 (16% of the total radiology department volume). In a 2-week period, 12 of 1929 (0.6%) preliminary reports by residents were discordant to the final subspecialty dictation. In the 15 peer-reviewed publications documenting error rates in radiology, the error rate between American Board of Radiology (ABR)-certified radiologists is greater than that between residents and subspecialists in the literature and in our study. However, the perceived error rate by clinicians outside radiology is significantly higher. CONCLUSION: Sixteen percent of the volume of imaging studies comes through the ED. The residents handle off-hours cases with a radiology-detected error rate below the error rate between ABR-certified radiologists. To decrease the perceived clinician-identified error rate, we need to change how academic radiology handles ED cases.

Performance of the Hack's Impairment Index Score: A Novel Tool to Assess Impairment from Alcohol in Emergency Department Patients.

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.

Effects of ethanol on limited resuscitation in a model of traumatic brain injury and hemorrhagic shock.

OBJECT: Limited resuscitation following uncontrolled hemorrhagic shock (HS) has been associated with improved outcomes in various animal models, although it has not been previously studied in the setting of traumatic brain injury (TBI) and ethanol intoxication. The aim of the present study was to determine the effects of ethanol intoxication in a model of experimental TBI and HS treated with limited resuscitation. METHODS: After induction of anesthesia and the placement of instruments, swine were subjected to a fluid-percussion injury of 3 atm. Simultaneously, hemorrhage was induced from an arterial catheter via a computerized roller pump to a mean arterial blood pressure (MABP) of 50 mm Hg, at which time uncontrolled hemorrhage was induced by the creation of an aortic tear. When the MABP decreased to 30 mm Hg, limited resuscitation to a MABP of 60 mm Hg was begun. After 60 minutes, animals were aggressively resuscitated to baseline MABP levels. Two groups of animals were studied: those receiving tap water by gastrostomy tube and those receiving ethanol (4 g/kg) by gastrostomy tube. Animals were monitored for 180 minutes after TBI. Hemorrhage volumes were significantly greater in ethanol-infused animals (mean +/- standard deviation, 41 +/- 34 mm Hg) compared with tap water-infused animals (17 +/- 18 mm Hg; p = 0.048). Resuscitation requirements were significantly higher and metabolic parameters significantly worse in the ethanol group. Survival time was also significantly decreased in the animals infused with ethanol (81 +/- 60 minutes) compared with those infused with tap water (130 +/- 51 minutes; p = 0.035). CONCLUSIONS: Ethanol intoxication led to increased hemorrhage volume and worsened hemodynamic and metabolic profiles in this model of limited resuscitation after TBI and HS. Ethanol-exposed animals had increased resuscitation requirements and decreased survival times.

A New Panel of Blood Biomarkers for the Diagnosis of Mild Traumatic Brain Injury/Concussion in Adults.

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.

Guidelines for the management of severe head injury: are emergency physicians following them?

UNLABELLED: The Brain Trauma Foundation published "Guidelines for the Management of Severe Head Injury" in 1995. These evidence-based clinical guidelines (CGs) recommended against prophylactic hyperventilation and glucocorticoid use and advocated for aggressive blood pressure (BP) resuscitation, and the careful use of mannitol. OBJECTIVE: To survey Michigan emergency physicians (MEPs) to test their adherence to these guidelines. METHODS: An anonymous mail survey was sent to all 566 MEPs who are members of the American College of Emergency Physicians. Three clinical scenarios involving severe head injury were presented, all with Glasgow Coma Scale (GCS) scores of 8 or less. The physicians were asked to choose from 15 diagnostic and treatment options, which included: intubation and hyperventilation, BP resuscitation, intravenous (IV) mannitol administration, and IV glucocorticoid administration. RESULTS: Three hundred nineteen (56%) surveys were returned. Forty-six percent [95% confidence interval (95% CI) = 40% to 51%] of the MEPs elected to use prophylactic hyperventilation; very few administered IV glucocorticoids. Seventy-eight percent (95% CI = 75% to 81%) corrected hypotension with systolic BP < 90 mm Hg; 83% (95% CI = 80% to 86%) also administered mannitol appropriately. CONCLUSIONS: A majority of MEPs are managing severe head injury patients in accordance with the "Guidelines for the Management of Severe Head Injury," with the exception of avoiding prophylactic hyperventilation. More education and/or exposure to the evidence regarding prophylactic hyperventilation of severely head injured patients may improve adherence to the guidelines.

Posttraumatic invasion of monocytes across the blood-cerebrospinal fluid barrier.

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.

The Biology of Emergency Medicine: what have 30 years meant for Rosen's original concepts?

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.

Multiple sites of vasopressin synthesis in the injured brain.

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.

Blood-brain barrier pathophysiology in traumatic brain injury.

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.

Emerging concepts in the pathophysiology of traumatic brain injury.

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.

Vasopressin amplifies the production of proinflammatory mediators in traumatic brain injury.

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.