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Objectives We characterize physician workflow in two distinctive emergency departments (ED). Physician practices mediated by electronic health records (EHR) are explored within the context of organizational complexity for the delivery of care. Methods Two urban clinical sites, including an academic teaching ED, were selected. Fourteen physicians were recruited. Overall, 62 hours of direct clinical observations were conducted characterizing clinical activities (EHR use, team communication, and patient care). Data were analyzed using qualitative open-coding techniques and descriptive statistics. Timeline belts were used to represent temporal events. Results At site 1, physicians, engaged in more team communication, followed by direct patient care. Although physicians spent 61% of their clinical time at workstations, only 25% was spent on the EHR, primarily for clinical documentation and review. Site 2 physicians engaged primarily in direct patient care spending 52% of their time at a workstation, and 31% dedicated to EHRs, focused on chart review. At site 1, physicians showed nonlinear complex workflow patterns with a greater frequency of multitasking and interruptions, resulting in workflow fragmentation. In comparison, at site 2, a less complex environment with a unique patient assignment system, resulting in a more linear workflow pattern. Conclusion The nature of the clinical practice and EHR-mediated workflow reflects the ED work practices. Physicians in more complex organizations may be less efficient because of the fragmented workflow. However, these effects can be mitigated by effort distribution through team communication, which affords inherent safety checks.

Highlights • Intravenous iron supplementation provides symptomatic relief in patients with heart failure and concomitant iron deficiency. • The current definition of iron deficiency based on ferritin, Summary To date, 3 clinical trials have shown symptomatic benefit from the use of intravenous (IV) iron in patients with heart failure (HF) with low serum iron. This has led to recommendations in support of the use of IV iron in this population. However, the systemic and cellular mechanisms of iron homeostasis in cardiomyocyte health and disease are distinct, complex, and poorly understood. Iron metabolism in HF appears dysregulated, but it is still unclear whether the changes are maladaptive and pathologic or compensatory and protective for the cardiomyocytes. The serum markers of iron deficiency in HF do not accurately reflect cellular and mitochondrial iron levels, and the current definition based on the ferritin and transferrin saturation values is broad and inclusive of patients who do not need IV iron. This is particularly relevant in view of the potential risks that are associated with the use of IV iron. Reliable markers of cellular iron status may differentiate subgroups of HF patients who would benefit from cellular and mitochondrial iron chelation rather than IV iron.

Objective To quantify the impact of two approaches (directed and query-based) to health information exchange (HIE) on potentially avoidable use of health care services. Data sources/study setting Data on ambulatory care providers' adoption of HIE were merged with Medicare fee-for-service claims from 2008 to 2014. Providers were from 13 counties in New York served by the Rochester Regional Health Information Organization (RHIO). Study design Linear regression models with provider and year fixed effects were used to estimate changes in the probability of utilization outcomes for Medicare beneficiaries attributed to providers adopting directed and/or query-based HIE compared with beneficiaries attributed to providers who had not adopted HIE. Data collection Providers' HIE adoption status was determined through Rochester RHIO registration records. RHIO and claims data were linked via National Provider Identifiers. Principal findings Query-based HIE adoption was associated with a 0.2 percentage point reduction in the probability of an ambulatory care sensitive hospitalization and a 1.1 percentage point decrease in the likelihood of an unplanned readmission. Directed HIE adoption was not associated with any outcome. Conclusions The Centers for Medicare & Medicaid Services' (CMS) EHR certification criteria includes requirements for directed HIE, but not query-based HIE. Pending further research, certification criteria should place equal weight on facilitating query-based and directed exchange.

Iron plays an important role in mammalian physiological processes. It is a critical component for the function of many proteins, including enzymes that require heme and iron-sulfur clusters. However, excess iron is also detrimental because of its ability to catalyze the formation of reactive oxygen species. As a result, cellular and systemic iron levels are tightly regulated to prevent oxidative damage. Iron deficiency can lead to a number of pathological conditions, the most prominent being anemia. Iron deficiency should be corrected to improve adult patients' symptoms and to facilitate normal growth during fetal development and childhood. However, inappropriate use of intravenous iron in chronic conditions, such as cancer and heart failure, in the absence of clear iron deficiency can lead to unwanted side effects. Thus, this form of therapy should be reserved for certain patients who cannot tolerate oral iron and need rapid iron replenishment. Here, we will review cellular and systemic iron homeostasis and will discuss complications of iron deficiency.

Chronic loss of Augmenter of Liver Regeneration (ALR) results in mitochondrial myopathy with cataracts; however, the mechanism for this disorder remains unclear. Here, we demonstrate that loss of ALR, a principal component of the MIA40/ALR protein import pathway, results in impaired cytosolic Fe/S cluster biogenesis in mammalian cells. Mechanistically, MIA40/ALR facilitates the mitochondrial import of ATP-binding cassette (ABC)-B8, an inner mitochondrial membrane protein required for cytoplasmic Fe/S cluster maturation, through physical interaction with ABCB8. Downregulation of ALR impairs mitochondrial ABCB8 import, reduces cytoplasmic Fe/S cluster maturation, and increases cellular iron through the iron regulatory protein-iron response element system. Our finding thus provides a mechanistic link between MIA40/ALR import machinery and cytosolic Fe/S cluster maturation through the mitochondrial import of ABCB8, and offers a potential explanation for the pathology seen in patients with ALR mutations.

Chronic loss of Augmenter of Liver Regeneration (ALR) results in mitochondrial myopathy with cataracts, however, the mechanism for this disorder remains unclear. Here, we demonstrate that loss of ALR, a principal component of the MIA40/ALR protein import pathway, results in impaired cytosolic Fe/S cluster biogenesis in mammalian cells. Mechanistically, MIA40/ALR facilitates the mitochondrial import of ATP binding cassette (ABC)-B8, an inner mitochondrial membrane protein required for cytoplasmic Fe/S cluster maturation, through physical interaction with ABCB8. Downregulation of ALR impairs mitochondrial ABCB8 import, reduces cytoplasmic Fe/S cluster maturation, and increases cellular iron through the iron regulatory protein-iron response element system. Our finding provides a mechanistic link between MIA40/ALR import machinery and cytosolic Fe/S cluster maturation through the mitochondrial import of ABCB8, and offers a potential explanation for the pathology seen in patients with ALR mutations.

Introduction: A loss of function mutation in the mRNA binding protein ZFP36L2 has been associated with congenital heart diseases in humans, although the mechanism remains unclear. Objectives: We sought to elucidate the role of ZFP36L2 in the heart using mice with cardiac-specific ZFP36L2 deletion. Results: Cardiac-specific Zfp36l2 knockout (cs-L2KO) female mice exhibit a dramatic phenotype in which the majority of mice die after repeated pregnancies due to heart failure. We performed RNA-seq in H9c2 cells with ZFP36L2 KD, and found the expression of multiple mTOR pathway genes were altered, including marked repression of Redd1 and Sesn2 . Consistent with the RNA-seq data, the activity of mTORC1 was increased in cs-L2KO mouse hearts and in ZFP36L2 KD H9c2 cells. Loss of TSC2 mitigated mTORC1 hyperactivity in ZFP36L2 KD cells, indicating that ZFP36L2 regulates mTORC1 activity through the TSC2 complex. Overexpression of REDD1 rescued increased mTORC1 activity with ZFP36L2 KD, suggesting that ZFP36L2 regulates mTORC1, in-part through REDD1. Under total amino acid starvation, we observed higher p-S6K T389 levels in ZFP36L2 KD cells, and SESN2 overexpression mitigated p-S6K T389 , indicating loss of ZFP36L2 also regulates mTORC1 through amino acid sensing. p53 is a transcriptional activator of both REDD1 and SESN2, and we found that ZFP36L2 was required to maintain p53 levels by directly destabilizing MDM2 mRNA. Accordingly, administration of Nutlin3, an MDM2 inhibitor, reversed the reduction in p53, REDD1 and SESN2 protein levels, and prevented the increase in S6K phosphorylation in response to ZFP36L2 KD. Next, we treated pregnant mice with rapamycin, and cs-L2KO mice treated with rapamycin displayed significantly improved cardiac function after delivery. Finally, we analyzed human heart samples from patients with peri-partum cardiomyopathy and found ZFP36L2 protein to be significantly decreased and p-S6K T389 levels increased, compared to healthy controls. Conclusions: Our studies demonstrate that ZFP36L2 regulates mTORC1 activity through modifying p53 stability, and that the disruption of this pathway induces peri-partum cardiomyopathy. Inhibition of mTORC1 hyperactivity with rapamycin can be a potential therapy for this disease.

Introduction: A loss of function mutation in the mRNA binding protein ZFP36L2 has been associated with congenital heart diseases in humans, although the mechanism remains unclear. Objectives: We sought to elucidate the role of ZFP36L2 in the heart using mice with cardiac-specific ZFP36L2 deletion. Results: Cardiac-specific Zfp36l2 knockout (cs-L2KO) female mice exhibit a dramatic phenotype in which the majority of mice die after repeated pregnancies due to heart failure. We performed RNA-seq in H9c2 cells with ZFP36L2 KD, and found the expression of multiple mTOR pathway genes were altered, including marked repression of Redd1 and Sesn2 . Consistent with the RNA-seq data, the activity of mTORC1 was increased in cs-L2KO mouse hearts and in ZFP36L2 KD H9c2 cells. Loss of TSC2 mitigated mTORC1 hyperactivity in ZFP36L2 KD cells, indicating that ZFP36L2 regulates mTORC1 activity through the TSC2 complex. Overexpression of REDD1 rescued increased mTORC1 activity with ZFP36L2 KD, suggesting that ZFP36L2 regulates mTORC1, in-part through REDD1. Under total amino acid starvation, we observed higher p-S6K T389 levels in ZFP36L2 KD cells, and SESN2 overexpression mitigated p-S6K T389 , indicating loss of ZFP36L2 also regulates mTORC1 through amino acid sensing. p53 is a transcriptional activator of both REDD1 and SESN2, and we found that ZFP36L2 was required to maintain p53 levels by directly destabilizing MDM2 mRNA. Accordingly, administration of Nutlin3, an MDM2 inhibitor, reversed the reduction in p53, REDD1 and SESN2 protein levels, and prevented the increase in S6K phosphorylation in response to ZFP36L2 KD. Next, we treated pregnant mice with rapamycin, and cs-L2KO mice treated with rapamycin displayed significantly improved cardiac function after delivery. Finally, we analyzed human heart samples from patients with peri-partum cardiomyopathy and found ZFP36L2 protein to be significantly decreased and p-S6K T389 levels increased, compared to healthy controls. Conclusions: Our studies demonstrate that ZFP36L2 regulates mTORC1 activity through modifying p53 stability, and that the disruption of this pathway induces peri-partum cardiomyopathy. Inhibition of mTORC1 hyperactivity with rapamycin can be a potential therapy for this disease.

Objective With federal mandates and incentives since the turn of this decade, electronic health records (EHR) have been widely adopted and used for clinical care. Over the last several years, we have seen both positive and negative perspectives on its use. Using an analysis of log files of EHR use, we investigated the nature of EHR use and their effect on an emergency department's (ED) throughput and efficiency. Methods EHR logs of time spent by attending physicians on EHR-based activities over a 6-week period (n = 2,304 patients) were collected. For each patient encounter, physician activities in the EHR were categorized into four activities: documentation, review, orders, and navigation. Four ED-based performance metrics were also captured: door-to-provider time, door-to-doctor time, door-to-disposition time, and length of stay (LOS). Association between the four EHR-based activities and corresponding ED performance metrics were evaluated. Results We found positive correlations between physician review of patient charts, and door-to-disposition time (r = 0.43, p Conclusion The results highlight that longer time spent on reviewing information on the EHR is potentially associated with decreased ED throughput efficiency. Balancing these competing goals is often a challenge of physicians, and its implications for patient safety is discussed.

Excess cellular iron increases reactive oxygen species (ROS) production and causes cellular damage. Mitochondria are the major site of iron metabolism and ROS production; however, few studies have investigated the role of mitochondrial iron in the development of cardiac disorders, such as ischemic heart disease or cardiomyopathy (CM). We observe increased mitochondrial iron in mice after ischemia/reperfusion (I/R) and in human hearts with ischemic CM, and hypothesize that decreasing mitochondrial iron protects against I/R damage and the development of CM. Reducing mitochondrial iron genetically through cardiac‐specific overexpression of a mitochondrial iron export protein or pharmacologically using a mitochondria‐permeable iron chelator protects mice against I/R injury. Furthermore, decreasing mitochondrial iron protects the murine hearts in a model of spontaneous CM with mitochondrial iron accumulation. Reduced mitochondrial ROS that is independent of alterations in the electron transport chain's ROS producing capacity contributes to the protective effects. Overall, our findings suggest that mitochondrial iron contributes to cardiac ischemic damage, and may be a novel therapeutic target against ischemic heart disease.

SIRT2 is a cytoplasmic sirtuin that plays a role in various cellular processes, including tumorigenesis, metabolism, and inflammation. Since these processes require iron, we hypothesized that SIRT2 directly regulates cellular iron homeostasis. Here, we have demonstrated that SIRT2 depletion results in a decrease in cellular iron levels both in vitro and in vivo. Mechanistically, we determined that SIRT2 maintains cellular iron levels by binding to and deacetylating nuclear factor erythroid-derived 2-related factor 2 (NRF2) on lysines 506 and 508, leading to a reduction in total and nuclear NRF2 levels. The reduction in nuclear NRF2 leads to reduced ferroportin 1 (FPN1) expression, which in turn results in decreased cellular iron export. Finally, we observed that Sirt2 deletion reduced cell viability in response to iron deficiency. Moreover, livers from Sirt2-/- mice had decreased iron levels, while this effect was reversed in Sirt2-/- Nrf2-/- double-KO mice. Taken together, our results uncover a link between sirtuin proteins and direct control over cellular iron homeostasis via regulation of NRF2 deacetylation and stability.

The role of posttranscriptional metabolic gene regulatory programs in diabetes is not well understood. Here, we show that the RNA-binding protein tristetraprolin (TTP) is reduced in the livers of diabetic mice and humans and is transcriptionally induced in response to insulin treatment in murine livers in vitro and in vivo. Liver-specific Ttp-KO (lsTtp-KO) mice challenged with high-fat diet (HFD) have improved glucose tolerance and peripheral insulin sensitivity compared with littermate controls. Analysis of secreted hepatic factors demonstrated that fibroblast growth factor 21 (FGF21) is posttranscriptionally repressed by TTP. Consistent with increased FGF21, lsTtp-KO mice fed HFD have increased brown fat activation, peripheral tissue glucose uptake, and adiponectin production compared with littermate controls. Downregulation of hepatic Fgf21 via an adeno-associated virus-driven shRNA in mice fed HFD reverses the insulin-sensitizing effects of hepatic Ttp deletion. Thus, hepatic TTP posttranscriptionally regulates systemic insulin sensitivity in diabetes through liver-derived FGF21.

Cells respond to iron deficiency by activating iron-regulatory proteins to increase cellular iron uptake and availability. However, it is not clear how cells adapt to conditions when cellular iron uptake does not fully match iron demand. Here, we show that the mRNA-binding protein tristetraprolin (TTP) is induced by iron deficiency and degrades mRNAs of mitochondrial Fe/S-cluster-containing proteins, specifically Ndufs1 in complex I and Uqcrfs1 in complex III, to match the decrease in Fe/S-cluster availability. In the absence of TTP, Uqcrfs1 levels are not decreased in iron deficiency, resulting in nonfunctional complex III, electron leakage, and oxidative damage. Mice with deletion of Ttp display cardiac dysfunction with iron deficiency, demonstrating that TTP is necessary for maintaining cardiac function in the setting of low cellular iron. Altogether, our results describe a pathway that is activated in iron deficiency to regulate mitochondrial function to match the availability of Fe/S clusters.

Study objective Frequent emergency department (ED) users are of interest to policymakers and hospitals. The objective of this study is to examine the effect of health information exchange size on the identification of frequent ED users. Methods We retrospectively analyzed data from Healthix, a health information exchange in New York that previously included 10 hospitals and then grew to 31 hospitals. We divided patients into 3 cohorts: high-frequency ED users with 4 or more visits in any 30-day period, medium-frequency ED users with 4 or more visits in any year, and infrequent ED users with fewer than 4 visits in any year. For both the smaller (10-hospital) and larger (31-hospital) health information exchanges, we compared the identification rate of frequent ED users that was based on hospital-specific data with the corresponding rates that were based on health information exchange data. Results The smaller health information exchange (n=1,696,279 unique ED patients) identified 11.4% more high-frequency users (33,467 versus 30,057) and 9.5% more medium-frequency users (109,497 versus 100,014) than the hospital-specific data. The larger health information exchange (n=3,684,999) identified 19.6% more high-frequency patients (52,727 versus 44,079) and 18.2% more medium-frequency patients (222,574 versus 192,541) than the hospital-specific data. Expanding from the smaller health information exchange to the larger one, we found an absolute increase of 8.2% and 8.7% identified high- and medium-frequency users, respectively. Conclusion Increasing health information exchange size more accurately reflects how patients access EDs and ultimately improves not only the total number of identified frequent ED users but also their identification rate.

SummaryBackground: Hospital closures are becoming increasingly common in the United States. Patients who received care at the closing hospitals must travel to different, often farther hospitals for care, and nearby remaining hospitals may have difficulty coping with a sudden influx of patients.Objectives: Our objectives are to analyze the dispersion patterns of patients from a closing hospital and to correlate that with distance from the closing hospital for three specific visit types: emergency, inpatient, and ambulatory.Methods: In this study, we used data from a health information exchange to track patients from Saint Vincent’s Medical Center, a hospital in New York City that closed in 2010, to determine where they received emergency, inpatient, and ambulatory care following the closure.Results: We found that patients went to the next nearest hospital for their emergency and inpatient care, but ambulatory encounters did not correlate with distance.Discussion: It is likely that patients followed their ambulatory providers as they transitioned to another hospital system. Additional work should be done to determine predictors of impact on nearby hospitals when another hospital in the community closes in order to better prepare for patient dispersion.Citation: Garg N, Husk G, Nguyen T, Onyile A, Echezona S, Kuperman G, Shapiro JS. Hospital closure and insights into patient dispersion: the closure of Saint Vincent’s Catholic Medical Center in New York City. Appl Clin Inf 2015; 6: 185–199http://dx.doi.org/10.4338/ACI-2014-10-RA-0090

Iron chelation rather than supplementation would be beneficial to patients with heart diseases. More effort should be devoted to the development of iron chelators that could target mitochondrial iron. Iron is an essential trace mineral for normal mammalian physiology. It is incorporated into iron/sulfur (Fe/S) clusters that serve as important cofactors for many enzymes, including the mitochondrial respiratory chain, and it gives blood and muscle their signature red color through its presence in heme.1 Because of its involvement in many important cellular processes, dysregulation of iron often causes disease. There are 2 broad categories of diseases associated with iron dysregulation—iron overload and iron deficiency. Each category can be further subdivided based on whether the changes in iron occur at the cellular or at the systemic level. Iron is critical for developmental processes, and studies have linked severe systemic iron deficiency to impaired brain development in children.2 However, most of these studies were conducted in developing countries where iron deficiency tends to be more severe. In developed countries, the major disorder associated with iron deficiency is anemia. Although systemic iron deficiency and anemia may have been used interchangeably, these 2 terms refer to different conditions. Systemic iron deficiency refers to low amounts of iron in circulation because of limited iron absorption or excess iron loss. Anemia is defined as low hemoglobin content within red blood cells and can be caused by low systemic iron, mutations in hemoglobin genes, vitamin B12 deficiency, or underlying chronic diseases. Limited oxygen-carrying capacity secondary to anemia can cause fatigue; however, it generally does not cause mortality or major damage to vital organs. Except for high-output heart failure (HF) associated with severe anemia, iron deficiency and anemia are not associated with any other major cardiac disorders. Cellular iron deficiency is a rare phenomenon, and except …

Introduction: Type II diabetes mellitus (T2DM) is a growing health problem affecting over 29 million Americans and individuals with T2DM have increased mortality after myocardial infarction and stroke. Thus, it is imperative to find novel treatments for diabetes to offset the increased risk of cardiovascular disease (CVD) related mortality. Tristetraprolin (TTP) is an mRNA binding protein first identified as an insulin responsive gene. It binds to AU-rich elements (AREs) in the 3’ untranslated region (UTR) of certain transcripts and promotes their degradation. Reduced TTP expression has been observed in human patients with obesity and insulin resistance, and computational analysis suggests that TTP may bind to and degrade the mRNA of key enzymes involved in glucose oxidation. Thus, we hypothesized that downregulation of TTP would increase glucose oxidation and protect against T2DM. Results: We found hepatic expression of TTP to be decreased in diabetic mice. Using an in silico analysis to identify mRNAs that are targeted by TTP and play a role in glucose metabolism, we identified the pyruvate dehydrogenase-E2 subunit (PDH-E2) to contain several conserved TTP binding sites in its 3’ UTR. PDH-E2 expression was significantly increased (mRNA > 1.4-fold; protein > 2-fold) in hepatocytes isolated from liver-specific TTP knockout (KO) mice. Furthermore, measurement of PDH-E2 mRNA stability showed that PDH-E2 mRNA is significantly stabilized with TTP deletion, indicating that TTP regulates PDH-E2 mRNA. We then assessed whether the regulation of PDH-E2 by TTP alters glucose metabolism. Using Seahorse, we found a 1.7-fold increase in oxidative metabolism in TTP KO cells fed with glucose and pyruvate. This increase was reversed with siRNA mediated downregulation of PDH-E2. Systemically, liver-specific TTP KO mice fed a high-fat diet had significantly lower blood glucose levels after glucose tolerance tests and insulin tolerance tests. Conclusion: Our results suggest that a decrease in TTP protects against the development of T2DM by increasing PDH-E2 expression and subsequent glucose oxidation in the liver. Together, these data provide a novel, potential therapeutic target for T2DM, a significant modifiable risk factor contributing to CVD mortality.

Objectives: To describe (1) the predictability of frequent emergency department (ED) use (a marker of inadequate disease control and/or poor access to care), and (2) the demographics, comorbidities, and use of health services of frequent ED users, among people with epilepsy. Methods: We obtained demographics, comorbidities, and 2 years of encounter data for 8,041 people with epilepsy from a health information exchange in New York City. Using a retrospective cohort design, we explored bivariate relationships between baseline characteristics (year 1) and subsequent frequent ED use (year 2). We then built, evaluated, and compared predictive models to identify frequent ED users (≥4 visits year 2), using multiple techniques (logistic regression, lasso, elastic net, CART [classification and regression trees], Random Forests, AdaBoost, support vector machines). We selected a final model based on performance and simplicity. Results: People with epilepsy who, in year 1, were adults (rather than children or seniors), male, Manhattan residents, frequent users of health services, users of multiple health systems, or had medical, neurologic, or psychiatric comorbidities, were more likely to frequently use the ED in year 2. Predictive techniques identified frequent ED visitors with good positive predictive value (approximately 70%) but poor sensitivity (approximately 20%). A simple strategy, selecting individuals with 11+ ED visits in year 1, performed as well as more sophisticated models. Conclusions: People with epilepsy with 11+ ED visits in a year are at highest risk of continued frequent ED use and may benefit from targeted intervention to avoid preventable ED visits. Future work should focus on improving the sensitivity of predictions.

Emergency physicians often must make critical, time-sensitive decisions with a paucity of information with the realization that additional unavailable health information may exist. Health information exchange enables clinician access to patient health information from multiple sources across the spectrum of care. This can provide a more complete longitudinal record, which more accurately reflects the way most patients obtain care: across multiple providers and provider organizations. This information article explores various aspects of health information exchange that are relevant to emergency medicine and offers guidance to emergency physicians and to organized medicine for the use and promotion of this emerging technology. This article makes 5 primary emergency medicine–focused recommendations, as well as 7 additional secondary generalized recommendations, to health information exchanges, policymakers, and professional groups, which are crafted to facilitate health information exchange's purpose and demonstrate its value.

Background: The management of acute stroke is time-sensitive. Clinical decision making requires data not only from laboratory testing and neuroimaging, but also from a detailed history and neurologic examination. The neurologic examination provides baseline information and assists in differentiating acute stroke from its mimickers. There is a need for tools to facilitate the evaluation and decision making in the acute stroke patient to make the correct diagnosis and, when indicated, to properly administer intravenous thrombolytic therapy. Objectives: The goals of this project were to create a standardized, handheld software program to aid physicians in their evaluation of patients presenting to the emergency department (ED) with acute ischemic stroke, and to create an educational tool with which residents and other health care professionals can gain a level of proficiency in treating these patients. Results: A comprehensive handheld tool was created that incorporates a National Institutes of Health Stroke Scale (NIHSS) calculator, inclusion criteria, absolute contraindications, and relative warnings for thrombolytic use (i.e., recombinant tissue plasminogen activator), and a weight-based dosing calculator that flows in a logical and clinically relevant format. Additionally, the program includes reference materials and guidelines for clinical management to further assist the clinician. Conclusions: Applications of this program include reformatting for use as a data-gathering tool in future clinical studies investigating the treatment of stroke patients, increasing the use and documentation of the NIHSS within the ED in acute ischemic stroke patients, and improving protocol adherence for rt-PA use.

For more than 25 years, emergency medicine researchers have examined 72-hour return visits as a marker for high-risk patient visits and as a surrogate measure for quality of care. Individual emergency departments frequently use 72-hour returns as a screening tool to identify deficits in care, although comprehensive departmental reviews of this nature may consume considerable resources. We discuss the lack of published data supporting the use of 72-hour return frequency as an overall performance measure and examine why this is not a valid use, describe a conceptual framework for reviewing 72-hour return cases as a screening tool, and call for future studies to test various models for conducting such quality assurance reviews of patients who return to the emergency department within 72 hours.

Summary Objective Hospital crossover occurs when people seek care at multiple hospitals, creating information gaps for physicians at the time of care. Health information exchange (HIE) is technology that fills these gaps, by allowing otherwise unaffiliated physicians to share electronic medical information. However, the potential value of HIE is understudied, particularly for chronic neurologic conditions like epilepsy. We describe the prevalence and associated factors of hospital crossover among people with epilepsy, in order to understand the epidemiology of who may benefit from HIE. Methods We used a cross-sectional study design to examine the bivariate and multivariable association of demographics, comorbidity, and health service utilization variables with hospital crossover, among people with epilepsy. We identified 8,074 people with epilepsy from the International Classification of Diseases, Ninth Revision (ICD-9) codes, obtained from an HIE that linked seven hospitals in Manhattan, New York. We defined hospital crossover as care from more than one hospital in any setting (inpatient, outpatient, emergency, or radiology) over 2 years. Results Of 8,074 people with epilepsy, 1,770 (22%) engaged in hospital crossover over 2 years. Crossover was associated with younger age (children compared with adults, adjusted odds ratio [OR] 1.4, 95% confidence interval [CI] 1.2–1.7), living near the hospitals (Manhattan vs. other boroughs of New York City, adjusted OR 1.6, 95% CI 1.4–1.8), more visits in the emergency, radiology, inpatient, and outpatient settings (p

We hypothesized that using communitywide data from a health information exchange (HIE) could improve the ability to identify frequent emergency department (ED) users—those with four or more ED visits in thirty days—by allowing ED use to be measured across unaffiliated hospitals. When we analyzed HIE-wide data instead of site-specific data, we identified 20.3 percent more frequent ED users (5,756 versus 4,785) and 16.0 percent more visits by them to the ED (53,031 versus 45,771). Additionally, we found that 28.8 percent of frequent ED users visited multiple EDs during the twelve-month study period, versus 3.0 percent of all ED users. All three differences were significant ( p < 0.001 ). An improved ability to identify frequent ED users allows better targeting of case management and other services that can improve frequent ED users’ health and reduce their use of costly emergency medical services.

Background The trend towards hospitalist medicine can lead to disjointed patient care. Outpatient clinicians may be unaware of patients’ encounters with a disparate healthcare system. Electronic notifications to outpatient clinicians of patients’ emergency department (ED) visits and inpatient admissions and discharges using health information exchange can inform outpatient clinicians of patients’ hospital-based events.Objective Assess outpatient clinicians’ impressions of a new, secure messaging-based, patient event notification system.Methods Twenty outpatient clinicians receiving notifications of hospital-based events were recruited and 14 agreed to participate. Using a semi-structured interview, clinicians were asked about their use of notifications and the impact on their practices.Results Nine of 14 interviewed clinicians (64%) thought that without notifications, they would have heard about fewer than 10% of ED visits before the patient’s next visit. Nine clinicians (64%) thought that without notifications, they would have heard about fewer than 25% of inpatient admissions and discharges before the patient’s next visit. Six clinicians (43%) reported that they call the inpatient team more often because of notifications. Eight users (57%) thought that notifications improved patient safety by increasing their awareness of the patients’ clinical events and their medication changes. Key themes identified were the importance of workflow integration and a desire for more clinical information in notifications.Conclusions The notification system is perceived by clinicians to be of value. These findings should instigate further message-oriented use of health information exchange and point to refinements that can lead to even greater benefits.

The Health Information Technology for Economic and Clinical Health Act of 2009 and the Centers for Medicare & Medicaid Services "meaningful use" incentive programs, in tandem with the boundless additional requirements for detailed reporting of quality metrics, have galvanized hospital efforts to implement hospital-based electronic health records. As such, emergency department information systems (EDISs) are an important and unique component of most hospitals' electronic health records. System functionality varies greatly and affects physician decisionmaking, clinician workflow, communication, and, ultimately, the overall quality of care and patient safety. This article is a joint effort by members of the Quality Improvement and Patient Safety Section and the Informatics Section of the American College of Emergency Physicians. The aim of this effort is to examine the benefits and potential threats to quality and patient safety that could result from the choice of a particular EDIS, its implementation and optimization, and the hospital's or physician group's approach to continuous improvement of the EDIS. Specifically, we explored the following areas of potential EDIS safety concerns: communication failure, wrong order-wrong patient errors, poor data display, and alert fatigue. Case studies are presented that illustrate the potential harm that could befall patients from an inferior EDIS product or suboptimal execution of such a product in the clinical environment. The authors have developed 7 recommendations to improve patient safety with respect to the deployment of EDISs. These include ensuring that emergency providers actively participate in selection of the EDIS product, in the design of processes related to EDIS implementation and optimization, and in the monitoring of the system's ongoing success or failure. Our recommendations apply to emergency departments using any type of EDIS: custom-developed systems, best-of-breed vendor systems, or enterprise systems.

Summary Objectives: Emergency physicians are trained to make decisions quickly and with limited patient information. Health Information Exchange (HIE) has the potential to improve emergency care by bringing relevant patient data from non-affiliated organizations to the bedside. NYCLIX (New York CLinical Information eXchange) offers HIE functionality among multiple New York metropolitan area provider organizations and has pilot users in several member emergency departments (EDs). Methods: We conducted semi-structured interviews at three participating EDs with emergency physicians trained to use NYCLIX. Among “users” with > 1 login, responses to questions regarding typical usage scenarios, successful retrieval of data, and areas for improving the interface were recorded. Among “non-users” with ≤1 login, questions about NYCLIX accessibility and utility were asked. Both groups were asked to recall items from prior training regarding data sources and availability. Results: Eighteen NYCLIX pilot users, all board certified emergency physicians, were interviewed. Of the 14 physicians with more than one login, half estimated successful retrieval of HIE data affecting patient care. Four non-users (one login or less) cited forgotten login information as a major reason for non-use. Though both groups made errors, users were more likely to recall true NYCLIX member sites and data elements than non-users. Improvements suggested as likely to facilitate usage included a single automated login to both the ED information system (EDIS) and HIE, and automatic notification of HIE data availability in the EDIS All respondents reported satisfaction with their training. Conclusions: Integrating HIE into existing ED workflows remains a challenge, though a substantial fraction of users report changes in management based on HIE data. Though interviewees believed their training was adequate, significant errors in their understanding of available NYCLIX data elements and participating sites persist.

Aim: To determine the accuracy of troponin laboratory results versus International Classification of Diseases clinical modification codes (ICD-9-CM) in identifying acute coronary syndrome (ACS) rule-out (R/O) patients who present to emergency departments (EDs). Materials & methods: Retrospective data analysis and chart review (to establish gold standard) were conducted on ED patients. Data retrieved from a clinical data warehouse were reviewed to identify patients with two or more troponins within 24 h of ED registration and ICD-9-CM codes consistent with ACS R/O. Results: Of 329 charts reviewed, 17 were determined to be ACS R/O. A total of 31 out of 329 (9.42%, 95% CI: 6.26–12.58%) had two or more troponins with a sensitivity of 100% (95% CI: 77.08–100%) and specificity of 95.51% (95% CI: 92.42–97.43%). A total of 32 out of 329 patients (9.73%, 95% CI: 6.53–12.93%) had R/O ICD-9-CM codes with a sensitivity of 76.47% (95% CI: 49.76–83.00%) and specificity of 93.91% (95% CI: 90.50–96.19%). All 17 gold-standard ACS R/O patients were identified using troponins while ICD-9-CM identified 13 out of 17. Conclusion: Clinical data (two troponins) availability is timelier and compares well with billing data (ICD-9-CM codes) in ACS R/O patient identification. Clinical data use may be generalized to identify other disease specific cohorts for clinical research.

Health information exchange (HIE) initiatives are in various stages of development across the United States. They aim to bring previously unavailable clinical data from patients’ disparate health records, which may be spread over multiple provider and payer networks, to the point of care where clinicians and their patients need it most. The implications of these initiatives on public health are numerous. This article provides general evaluation methods for measuring the impact of HIE on public health in six use cases: (1) mandated reporting of laboratory diagnoses, (2) mandated reporting of physician-based diagnoses, (3) public health investigation, (4) disease-based non-reportable laboratory data, (5) antibiotic-resistant organism surveillance, and (6) population-level quality monitoring.

Background Health information exchange (HIE) is a potentially powerful technology that can improve the quality of care delivered in emergency departments, but little is known about emergency physicians’ current perceptions of HIE. Objectives This study sought to assess emergency physicians’ perceived needs and knowledge of HIE. Methods A questionnaire was developed based on heuristics from the literature and implemented in a Web-based tool. The survey was sent as a hyperlink via e-mail to 371 attending emergency physicians at 12 hospitals in New York City. Results The response rate was 58% (n = 216). Although 63% said more than one quarter of their patients would benefit from external health information, the barriers to obtain it without HIE are too high—85% said it was difficult or very difficult to obtain external data, taking an average of 66 minutes, 72% said that their attempts fail half of the time, and 56% currently attempt to obtain external data less than 10% of the time. When asked to create a rank-order list, electrocardiograms (ECGs) were ranked the highest, followed by discharge summaries. Respondents also chose images over written reports for ECGs and X-rays, but preferred written reports for advanced imaging and cardiac studies. Conclusion There is a strong perceived need for HIE, most respondents were not aware of HIE prior to this study, and there are certain types of data and presentations of data that are preferred by emergency physicians in the New York City region.

Fueled by a decade-long increase in emergency department (ED) visits with a concomitant decrease in hospital bed capacity and the number of hospital EDs, ED crowding has reached crisis proportions. Robust information systems and process redesign are two strategies to improve the safety and quality of emergency care. At the ED at the Mount Sinai Medical Center, an urban, tertiary care academic medical center in New York City, elements of departmental work flow were redesigned to streamline patient throughput before implementation of a fully integrated emergency department information system (EDIS) with patient tracking, computerized charting and order entry, and direct access to patient historical data from the hospital data repository. Pre- and postintervention data were analyzed to examine the impact on (ED) efficiency.The length of stay for all patients (arrival to time patient left ED) decreased by 1.94 hours, from 6.69 (n = 508) pre-intervention to 4.75 (n = 691) postintervention (p.001); doctor-to-disposition time (first doctor-patient contact to disposition decision) decreased by 1.90 hours, from 3.64 (n = 508) to 1.74 (n = 691; p.001); door-to-doctor time (triage to first doctor-patient contact) decreased by 0.54 hours, from 1.22 (n = 508) to 0.68 (n = 691; p.001). X-ray turnaround time (TAT) decreased by 0.18 hours from 0.92 (n = 60) to 0.74 (n = 108; p = .179); computerized tomography (CT) scan TAT decreased by 1.56 hours, from 3.89 (n = 40) to 2.33 (n = 29; p.001), lab TAT decreased by 0.59 hours, from 2.03 (n = 121) to 1.44 (n = 271; p = .006).Increasing the clinical information available at the bedside and improving departmental work flow through EDIS implementation and process redesign led to decreased patient throughput times and improved ED efficiency.