The Emergency Medicine Physician Workforce: Projections for 2030.

STUDY OBJECTIVE: The goals of this study were to determine the current and projected supply in 2030 of contributors to emergency care, including emergency residency-trained and board-certified physicians, other physicians, nurse practitioners, and physician assistants. In addition, this study was designed to determine the current and projected demand for residency-trained, board-certified emergency physicians. METHODS: To forecast future workforce supply and demand, sources of existing data were used, assumptions based on past and potential future trends were determined, and a sensitivity analysis was conducted to determine how the final forecast would be subject to variance in the baseline inputs and assumptions. Methods included: (1) estimates of the baseline workforce supply of physicians, nurse practitioners, and physician assistants; (2) estimates of future changes in the raw numbers of persons entering and leaving that workforce; (3) estimates of the productivity of the workforce; and (4) estimates of the demand for emergency care services. The methodology assumes supply equals demand in the base year and estimates the change between the base year and 2030; it then compares supply and demand in 2030 under different scenarios. RESULTS: The task force consensus was that the most likely future scenario is described by: 2% annual graduate medical education growth, 3% annual emergency physician attrition, 20% encounters seen by a nurse practitioner or physician assistant, and 11% increase in emergency department visits relative to 2018. This scenario would result in a surplus of 7,845 emergency physicians in 2030. CONCLUSION: The specialty of emergency medicine is facing the likely oversupply of emergency physicians in 2030. The factors leading to this include the increasing supply of and changing demand for emergency physicians. An organized, collective approach to a balanced workforce by the specialty of emergency medicine is imperative.

Inhibition of N-type calcium channels in cardiac sympathetic neurons attenuates ventricular arrhythmogenesis in heart failure.

AIMS: Cardiac sympathetic overactivation is an important trigger of ventricular arrhythmias in patients with chronic heart failure (CHF). Our previous study demonstrated that N-type calcium (Cav2.2) currents in cardiac sympathetic post-ganglionic (CSP) neurons were increased in CHF. This study investigated the contribution of Cav2.2 channels in cardiac sympathetic overactivation and ventricular arrhythmogenesis in CHF. METHODS AND RESULTS: Rat CHF was induced by surgical ligation of the left coronary artery. Lentiviral Cav2.2-α shRNA or scrambled shRNA was transfected in vivo into stellate ganglia (SG) in CHF rats. Final experiments were performed at 14 weeks after coronary artery ligation. Real-time polymerase chain reaction and western blot data showed that in vivo transfection of Cav2.2-α shRNA reduced the expression of Cav2.2-α mRNA and protein in the SG in CHF rats. Cav2.2-α shRNA also reduced Cav2.2 currents and cell excitability of CSP neurons and attenuated cardiac sympathetic nerve activities (CSNA) in CHF rats. The power spectral analysis of heart rate variability (HRV) further revealed that transfection of Cav2.2-α shRNA in the SG normalized CHF-caused cardiac sympathetic overactivation in conscious rats. Twenty-four-hour continuous telemetry electrocardiogram recording revealed that this Cav2.2-α shRNA not only decreased incidence and duration of ventricular tachycardia/ventricular fibrillation but also improved CHF-induced heterogeneity of ventricular electrical activity in conscious CHF rats. Cav2.2-α shRNA also decreased susceptibility to ventricular arrhythmias in anaesthetized CHF rats. However, Cav2.2-α shRNA failed to improve CHF-induced cardiac contractile dysfunction. Scrambled shRNA did not affect Cav2.2 currents and cell excitability of CSP neurons, CSNA, HRV, and ventricular arrhythmogenesis in CHF rats. CONCLUSIONS: Overactivation of Cav2.2 channels in CSP neurons contributes to cardiac sympathetic hyperactivation and ventricular arrhythmogenesis in CHF. This suggests that discovering purely selective and potent small-molecule Cav2.2 channel blockers could be a potential therapeutic strategy to decrease fatal ventricular arrhythmias in CHF.

Dexamethasone Improves Wound Healing by Decreased Inflammation and Increased Vasculogenesis in Mouse Skin Frostbite Model.

INTRODUCTION: Frostbite is thought to result from initial vasoconstriction, ischemia, intracellular ice crystal formation, and inflammation caused by reperfusion injury. Corticosteroids have demonstrated beneficial anti-inflammatory effects in the treatment of other ischemia/reperfusion clinical conditions. The objective of this study was to determine the effect of dexamethasone (dex) on wound healing, inflammatory response, and vasculogenesis in a mouse skin frostbite model. METHODS: Treatment and control groups of C57/BL6 mice were subjected to frostbite using a previously described model. Treatment with intraperitoneal dex (1 mg·kg-1·d-1) began on the day of frostbite induction and lasted for 7 d. Over 4 wk, we compared wound diameter; morphology by visual inspection, hematoxylin-eosin staining, and Masson's trichrome staining; density of inflammatory cytokines IL-1ß and TNFα using Western blot analysis; and formation of microvasculature using immunofluorescence staining. Data were analyzed using 1-way or 1-way repeated-measures analysis of variance. RESULTS: After frostbite injury, morphological images demonstrated epidermal necrosis and loss in the frostbitten skin as well as infiltration of inflammation-related leukocytes. Increased production of inflammatory cytokines and disappearance of the microvasculature also occurred in the frostbitten skin. In comparison to the control group, treatment with dex promoted wound healing as demonstrated by decreased wound diameter; decreased levels of inflammatory cytokines, and accelerated formation of mature microvasculature. CONCLUSIONS: In this animal model, dex improved wound healing in frostbitten skin and demonstrated both anti-inflammatory effects and stimulation of vasculogenesis. This study suggests that the use of potent anti-inflammatory agents may be an effective strategy for mitigating frostbite injury.

American Board of Emergency Medicine Report on Residency and Fellowship Training Information (2018-2019).

The American Board of Emergency Medicine (ABEM) gathers extensive background information on emergency medicine-sponsored residency and fellowship programs, residents and fellows training in those programs, and all fellows for whom ABEM issues subspecialty certifications. We present the 2019 annual report on the status of US emergency medicine training programs.

Dexamethasone Protects Against Tourniquet-Induced Acute Ischemia-Reperfusion Injury in Mouse Hindlimb.

Extremity injuries with hemorrhage have been a significant cause of death in civilian medicine and on the battlefield. The use of a tourniquet as an intervention is necessary for treatment to an injured limb; however, the tourniquet and subsequent release results in serious acute ischemia-reperfusion (IR) injury in the skeletal muscle and neuromuscular junction (NMJ). Much evidence demonstrates that inflammation is an important factor to cause acute IR injury. To find effective therapeutic interventions for tourniquet-induced acute IR injuries, our current study investigated effect of dexamethasone, an anti-inflammatory drug, on tourniquet-induced acute IR injury in mouse hindlimb. In C57/BL6 mice, a tourniquet was placed on unilateral hindlimb (left hindlimb) at the hip joint for 3 h, and then released for 24 h to induce IR. Three hours of tourniquet and 24 h of release (24-h IR) caused gastrocnemius muscle injuries including rupture of the muscle sarcolemma and necrosis (42.8 ± 2.3% for infarct size of the gastrocnemius muscle). In the NMJ, motor nerve terminals disappeared, and endplate potentials were undetectable in 24-h IR mice. There was no gastrocnemius muscle contraction in 24-h IR mice. Western blot data showed that inflammatory cytokines (TNFα and IL-1ß) were increased in the gastrocnemius muscle after 24-h IR. Treatment with dexamethasone at the beginning of reperfusion (1 mg/kg, i.p.) significantly inhibited expression of TNFα and IL-1ß, reduced rupture of the muscle sarcolemma and infarct size (24.8 ± 2.0%), and improved direct muscle stimulation-induced gastrocnemius muscle contraction in 24-h IR mice. However, this anti-inflammatory drug did not improve NMJ morphology and function, and sciatic nerve-stimulated skeletal muscle contraction in 24-h IR mice. The data suggest that one-time treatment with dexamethasone at the beginning of reperfusion only reduced structural and functional impairments of the skeletal muscle but not the NMJ through inhibiting inflammatory cytokines.

American Board of Emergency Medicine Report on Residency and Fellowship Training Information (2017-2018).

The American Board of Emergency Medicine (ABEM) gathers extensive background information on emergency medicine-sponsored residency and fellowship programs, as well as the residents and fellows training in those programs. We present the 2018 annual report on the status of US emergency medicine training programs.

Obesity Does Not Increase Operative Time in Otologic Surgery: An Analysis of 5125 Cases.

OBJECTIVES: A large shoulder can impact otologic surgical access. The physical obstruction of a large shoulder may force the surgeon to adjust his or her posture or hand position. We sought to assess the effect of body mass index (BMI) on operative time in tympanoplasties and tympanomastoidectomies. STUDY DESIGN: Cross-sectional analysis. SETTING: National surgical quality improvement program dataset (NSQIP) 2011 to 2014. PATIENTS: Current procedural terminology (CPT) codes were used to identify patients undergoing tympanoplasties and tympanomastoidectomies. INTERVENTIONS: Otologic surgery as indicated by CPT code. MAIN OUTCOME MEASURES: Targeted variables included height, weight, and operative time. BMI was stratified to assess a range of body compositions (<25, 25-30, >30-35, >35-40, >40). Categorical variables were compared using χ tests and continuous variables were compared using Kruskal-Wallis tests. Correlation between operative time and BMI was assessed using Spearman's rho. A generalized linear model was used to analyze the variables affecting operative time. Surgical complications were assessed in binary logistic regression using the enter method. Two-tailed significance was set at α = 0.05. RESULTS: Two surgical groups were identified: tympanoplasty (n = 3,508) and tympanomastoidectomy (n = 1,617). There was not a significant difference in mean operative time across the BMI subgroups for either surgical group (p = 0.617, 0.859, respectively). Multivariate analyses showed no significant difference in operative times based on BMI classification. CONCLUSIONS: The body habitus of obese patients may force the otologic surgeon to adapt, but obese patients do not have a statistically significant longer mean operative time for tympanoplasties and tympanomastoidectomies than patients with a lower BMI.

Reduced N-Type Ca2+ Channels in Atrioventricular Ganglion Neurons Are Involved in Ventricular Arrhythmogenesis.

BACKGROUND: Attenuated cardiac vagal activity is associated with ventricular arrhythmogenesis and related mortality in patients with chronic heart failure. Our recent study has shown that expression of N-type Ca2+ channel α-subunits (Cav2.2-α) and N-type Ca2+ currents are reduced in intracardiac ganglion neurons from rats with chronic heart failure. Rat intracardiac ganglia are divided into the atrioventricular ganglion (AVG) and sinoatrial ganglion. Ventricular myocardium receives projection of neuronal terminals only from the AVG. In this study we tested whether a decrease in N-type Ca2+ channels in AVG neurons contributes to ventricular arrhythmogenesis. METHODS AND RESULTS: Lentiviral Cav2.2-α shRNA (2 µL, 2×107 pfu/mL) or scrambled shRNA was in vivo transfected into rat AVG neurons. Nontransfected sham rats served as controls. Using real-time single-cell polymerase chain reaction and reverse-phase protein array, we found that in vivo transfection of Cav2.2-α shRNA decreased expression of Cav2.2-α mRNA and protein in rat AVG neurons. Whole-cell patch-clamp data showed that Cav2.2-α shRNA reduced N-type Ca2+ currents and cell excitability in AVG neurons. The data from telemetry electrocardiographic recording demonstrated that 83% (5 out of 6) of conscious rats with Cav2.2-α shRNA transfection had premature ventricular contractions (P<0.05 versus 0% of nontransfected sham rats or scrambled shRNA-transfected rats). Additionally, an index of susceptibility to ventricular arrhythmias, inducibility of ventricular arrhythmias evoked by programmed electrical stimulation, was higher in rats with Cav2.2-α shRNA transfection compared with nontransfected sham rats and scrambled shRNA-transfected rats. CONCLUSIONS: A decrease in N-type Ca2+ channels in AVG neurons attenuates vagal control of ventricular myocardium, thereby initiating ventricular arrhythmias.

Therapeutic Mastoidectomy Does Not Increase Postoperative Complications in the Management of the Chronic Ear.

OBJECTIVE: Tympanoplasty with or without concurrent therapeutic mastoidectomy is a controversial topic in the management of chronic ear disease. We sought to describe whether there is a significant difference in postoperative complications. STUDY DESIGN: Retrospective cohort study. SETTING: American College of Surgeons National Surgical Quality Improvement Program public files. PATIENTS: Current procedural terminology codes were used to identify patients with chronic ear disease undergoing tympanoplasty ± concurrent mastoidectomy in the 2011 to 14 American College of Surgeons National Surgical Quality Improvement Program files. INTERVENTION: Therapeutic. MAIN OUTCOME MEASURES: Variables were compared with χ, Fischer's exact, and Mann-Whitney U tests, as appropriate to analyze postoperative complications between tympanoplasty with or without concurrent mastoidectomy. To account for confounding factors, presence of a complication was analyzed in binary logistic regression. Analysis considered sex, hypertension, obesity, advanced age, diabetes, smoking status, American Society of Anesthesiologists Physical status, procedure. RESULTS: There were 4,087 patients identified meeting criteria (tympanoplasty = 2,798, tympanomastoidectomy = 1,289). There was no statistical difference in postoperative complications (tympanoplasty n = 49 [1. 8%], tympanomastoidectomy n = 33 [2. 6%]; p = 0. 087) or return to the operating room (tympanoplasty = 4 [0. 1%], tympanomastoidectomy = 6 [0. 5%]; p = 0. 082). Binary logistic regression demonstrated smoking as a predictor of a postoperative complication (OR: 1. 758, 95% CI: 1. 084-2. 851; p = 0. 022), while concurrent mastoidectomy did not significantly increase the risk of complication (OR: 1. 440, 95% CI: 0. 915-2. 268; p = 0. 115). There was a significant difference in mean operative time between tympanoplasty and tympanomastoidectomy: 85.7 versus 154.23 min, p < 0. 001. CONCLUSION: In the management of chronic ear disease, tympanoplasty with concurrent mastoidectomy increases time under anesthesia, but it is not associated with any increased postoperative complications compared with tympanoplasty alone.

Impact of Resident Participation on Operative Time and Outcomes in Otologic Surgery.

Objectives To describe the impact of resident involvement in tympanoplasty on operative time and surgical complication rates. Study Design Case series with chart review. Setting Tertiary medical center. Subjects and Methods Current Procedural Terminology codes were used to identify patients in the 2011-2014 public use files of the American College of Surgeons National Surgical Quality Improvement Program who underwent a tympanoplasty or tympanomastoidectomy. Cases were included if the database indicated whether the operating room was staffed with an attending alone or an attending with residents. Categorical and continuous variables were compared with chi-square, Fisher's exact, and Mann-Whitney U tests. Generalized linear models with a log-link and gamma distribution were used to examine the factors affecting operative time. Results Overall, 1045 cases met our study criteria (tympanoplasty, n = 797; tympanomastoidectomy, n = 248). Resident involvement increased mean operative time for tympanoplasties by 46% (107 vs 73 minutes, P < .001) and tympanomastoidectomies by 49% (175 vs 117 minutes, P < .001). While controlling for confounding factors, the variable with the largest impact on operative time was resident involvement. There were no significant differences observed in the rate of surgical complications between attending-alone and attending-resident cases. Conclusion Resident involvement in tympanoplasty and tympanomastoidectomy did not affect the surgical complication rate. Resident involvement increased operative time for tympanoplasties and tympanomastoidectomies; however, the specific reasons for the increase are not explained by the available data.

Straight Line Scoring by Clinical Competency Committees Using Emergency Medicine Milestones.

BACKGROUND: In 2013, milestone ratings became a reporting requirement for emergency medicine (EM) residency programs. Programs rate each resident in the fall and spring on 23 milestone subcompetencies. OBJECTIVE: This study examined the incidence of straight line scoring (SLS) for EM Milestone ratings, defined as a resident being assessed the same score across the milestone subcompetencies. METHODS: This descriptive analysis measured the frequencies of SLS for all Accreditation Council for Graduate Medical Education (ACGME)-accredited EM programs during the 2015-2016 academic year. Outcomes were the frequency of SLS in the fall and spring milestone assessments, changes in the number of SLS reports, and reporting trends. Chi-square analysis compared nominal variables. RESULTS: There were 6257 residents in the fall and 6588 in the spring. Milestone scores were reported for 6173 EM residents in the fall (99% of 6257) and spring (94% of 6588). In the fall, 93% (5753 residents) did not receive SLS ratings and 420 (7%) did, with no significant difference compared with the spring (5776 [94%] versus 397 [6%]). Subgroup analysis showed higher SLS results for residents' first ratings (183 of 2136 versus 237 of 4220, P < .0001) and for their final ratings (200 of 2019 versus 197 of 4354, P < .0001). Twenty percent of programs submitted 10% or more SLS ratings, and a small percentage submitted more than 50% of ratings as SLS. CONCLUSIONS: Most programs did not submit SLS ratings. Because of the statistical improbability of SLS, any SLS ratings reduce the validity assertions of the milestone assessments.

Correlation of Ventricular Arrhythmogenesis with Neuronal Remodeling of Cardiac Postganglionic Parasympathetic Neurons in the Late Stage of Heart Failure after Myocardial Infarction.

Introduction: Ventricular arrhythmia is a major cause of sudden cardiac death in patients with chronic heart failure (CHF). Our recent study demonstrates that N-type Ca2+ currents in intracardiac ganglionic neurons are reduced in the late stage of CHF rats. Rat intracardiac ganglia are divided into the atrioventricular ganglion (AVG) and sinoatrial ganglion. Only AVG nerve terminals innervate the ventricular myocardium. In this study, we tested the correlation of electrical remodeling in AVG neurons with ventricular arrhythmogenesis in CHF rats. Methods and Results: CHF was induced in male Sprague-Dawley rats by surgical ligation of the left coronary artery. The data from 24-h continuous radiotelemetry ECG recording in conscious rats showed that ventricular tachycardia/fibrillation (VT/VF) occurred in 3 and 14-week CHF rats but not 8-week CHF rats. Additionally, as an index for vagal control of ventricular function, changes of left ventricular systolic pressure (LVSP) and the maximum rate of left ventricular pressure rise (LV dP/dtmax) in response to vagal efferent nerve stimulation were blunted in 14-week CHF rats but not 3 or 8-week CHF rats. Results from whole-cell patch clamp recording demonstrated that N-type Ca2+ currents in AVG neurons began to decrease in 8-week CHF rats, and that there was also a significant decrease in 14-week CHF rats. Correlation analysis revealed that N-type Ca2+ currents in AVG neurons negatively correlated with the cumulative duration of VT/VF in 14-week CHF rats, whereas there was no correlation between N-type Ca2+ currents in AVG neurons and the cumulative duration of VT/VF in 3-week CHF. Conclusion: Malignant ventricular arrhythmias mainly occur in the early and late stages of CHF. Electrical remodeling of AVG neurons highly correlates with the occurrence of ventricular arrhythmias in the late stage of CHF.

American Board of Emergency Medicine Report on Residency and Fellowship Training Information (2016-2017).

The American Board of Emergency Medicine (ABEM) gathers extensive background information on emergency medicine residency programs and the residents training in those programs. We present the 2017 annual report on the status of US emergency medicine training programs.

Morphological Regeneration and Functional Recovery of Neuromuscular Junctions after Tourniquet-Induced Injuries in Mouse Hindlimb.

Tourniquet application and its subsequent release cause serious injuries to the skeletal muscle, nerve, and neuromuscular junction (NMJ) due to mechanical compression and ischemia-reperfusion (IR). Monitoring structural and functional repair of the NMJ, nerve, and skeletal muscle after tourniquet-induced injuries is beneficial in exploring potential cellular and molecular mechanisms responsible for tourniquet-induced injuries, and for establishing effective therapeutic interventions. Here, we observed long-term morphological and functional changes of the NMJ in a murine model of tourniquet-induced hindlimb injuries. Unilateral hindlimbs of C57/BL6 mice were subjected to 3 h of tourniquet by placing an orthodontic rubber band, followed by varied periods of tourniquet release (1 day, 3 days, 1 week, 2 weeks, 4 weeks, and 6 weeks). NMJ morphology in the gastrocnemius muscle was imaged, and the endplate potential (EPP) was recorded to evaluate NMJ function. In NMJs, nicotinic acetylcholine receptor (nAChR) clusters normally displayed an intact, pretzel-like shape, and all nAChR clusters were innervated (100%) by motor nerve terminals. During 3 h of tourniquet application and varied periods of tourniquet release, NMJs in the gastrocnemius muscle were characterized by morphological and functional changes. At 1 day and 3 days of tourniquet release, nAChR clusters retained normal, pretzel-like shapes, whereas motor nerve terminals were completely destroyed and no EPPs recorded. From 1 to 6 weeks of tourniquet release, motor nerve terminals gradually regenerated, even reaching that seen in sham mice, whereas nAChR clusters were gradually fragmented with prolongation of tourniquet release. Additionally, the amplitude of EPPs gradually increased with prolongation of tourniquet release. However, even at 6 weeks after tourniquet release, the amplitude of EPPs did not restore to the level seen in sham mice (13.9 ± 1.1 mV, p < 0.05 vs. sham mice, 29.8 ± 1.0 mV). The data suggest that tourniquet application and subsequent release impair the structure and function of NMJs. Morphological change in motor nerve terminals is faster than in nAChR clusters in NMJs. Slow restoration of fragmented nAChR clusters possibly dampens neuromuscular transmission during the long phase following tourniquet release.

American Board of Emergency Medicine Report on Residency Training Information (2015-2016).

The American Board of Emergency Medicine (ABEM) gathers extensive background information on emergency medicine residency programs and the residents training in those programs. We present the 2016 annual report on the status of US emergency medicine training programs.

Altered ENaC is Associated With Aortic Baroreceptor Dysfunction in Chronic Heart Failure.

BACKGROUND: Abnormal baroreceptor function contributes to attenuated arterial baroreflex sensitivity in chronic heart failure (CHF). As a mechanosensor in mammalian nonepithelium, the epithelial sodium channel (ENaC) is an amiloride-sensitive and voltage-independent ion channel. The ENaC is thought to be a component of baroreceptor mechanosensitive ion channels in aortic baroreceptor cell bodies and nerve terminals. In this study, therefore, we measured the expression and activation of the ENaC in nodose neuronal cell bodies and aortic baroreceptor nerve terminals in sham and CHF rats. METHODS AND RESULTS: CHF was induced by surgical ligation of left coronary artery. The development of CHF was confirmed by hemodynamic and morphological characteristics. The aortic baroreceptor sensitivity was blunted in anesthetized CHF rats, compared with that in sham rats. The data from immunostaining and western blot analysis showed that the protein of ß- and γ-ENaC subunits was expressed in nodose neuronal cell bodies and aortic baroreceptor nerve terminals, whereas the protein of α-ENaC subunit was undetectable. CHF reduced protein expression of ß- and γ-ENaC subunits in nodose neuronal cell bodies and aortic baroreceptor nerve terminals. Additionally, the data recorded by the whole cell patch-clamp technique demonstrated that ENaC currents in aortic baroreceptor neurons were lower in CHF rats than that in sham rats. CONCLUSION: These results suggest that reduced protein expression of the ENaC decreases the ENaC activation, which could be involved in attenuation of the aortic baroreceptor sensitivity in the CHF state. Baroreceptors should be a potential therapeutic target for reducing mortality in CHF.

Angiotensin II-superoxide-NFκB signaling and aortic baroreceptor dysfunction in chronic heart failure.

Chronic heart failure (CHF) affects approximately 5.7 million people in the United States. Increasing evidence from both clinical and experimental studies indicates that the sensitivity of arterial baroreflex is blunted in the CHF state, which is a predictive risk factor for sudden cardiac death. Normally, the arterial baroreflex regulates blood pressure and heart rate through sensing mechanical alteration of arterial vascular walls by baroreceptor terminals in the aortic arch and carotid sinus. There are aortic baroreceptor neurons in the nodose ganglion (NG), which serve as the main afferent component of the arterial baroreflex. Functional changes of baroreceptor neurons are involved in the arterial baroreflex dysfunction in CHF. In the CHF state, circulating angiotensin II (Ang II) and local Ang II concentration in the NG are elevated, and AT1R mRNA and protein are overexpressed in the NG. Additionally, Ang II-superoxide-NFκB signaling pathway regulates the neuronal excitability of aortic baroreceptors through influencing the expression and activation of Nav channels in aortic baroreceptors, and subsequently causes the impairment of the arterial baroreflex in CHF. These new findings provide a basis for potential pharmacological interventions for the improvement of the arterial baroreflex sensitivity in the CHF state. This review summarizes the mechanisms responsible for the arterial baroreflex dysfunction in CHF.

Emergency Department Processes for the Evaluation and Management of Persons Under Investigation for Ebola Virus Disease.

INTRODUCTION: Due to the recent Ebola virus outbreak in West Africa, patients with epidemiologic risk for Ebola virus disease and symptoms consistent with Ebola virus disease are presenting to emergency departments (EDs) and clinics in the United States. These individuals, identified as a person under investigation for Ebola virus disease, are initially screened using a molecular assay for Ebola virus. If this initial test is negative and the person under investigation has been symptomatic for < 3 days, a repeat test is required after 3 days of symptoms to verify the negative result. In the time interval before the second test result is available, manifestations of the underlying disease process for the person under investigation, whether due to Ebola virus disease or some other etiology, may require further investigation to direct appropriate therapy. MATERIALS AND METHODS: ED administrators, physicians, and nurses proposed processes to provide care that is consistent with other ED patients. Biocontainment unit administrators, industrial hygienists, laboratory directors, physicians, and other medical personnel examined the ED processes and offered biocontainment unit personal protective equipment and process strategies designed to ensure safety for providers and patients. CONCLUSION: ED processes for the safe and timely evaluation and management of the person under investigation for Ebola virus disease are presented with the ultimate goals of protecting providers and ensuring a consistent level of care while confirmatory testing is pending.

American Board of Emergency Medicine report on residency training information (2014-2015).

The American Board of Emergency Medicine (ABEM) gathers extensive background information on emergency medicine residency programs and the residents in those programs. We present the 2015 annual report on the status of US emergency medicine training programs.