New institutional setting, new organizational configurations: Redesigning the Danish emergency care system via a contingency approach

As a result of major administrative reform in 2007, the Danish emergency care system is undergoing the largest reorganization in decades (MHP, 2008; Vrangbaek, 2013). The number of acute hospitals has been reduced from more than 40 to 21 and new emergency departments (EDs) have been established (MHP, 2008; Wen et al., 2013, Mattsson, Mattsson & J\uf8rsboe, 2014). The EDs are the cornerstones of the Danish National Health System (NHS), as up to 70% of all acute care patients are evaluated there; they can be treated and discharged, or admitted for further care (MHP, 2008; Wen et al., 2013). The EDs therefore play a crucial role in determining the design of the overall healthcare, being a critical pathway for acute care and addressing hospital crowding. The Danish emergency care system represents an organizational field (DiMaggio & Powell, 1983) in which highly specialized healthcare actors, such as primary care physicians (PCPs), systems of out-of-hours care clinics, ambulance systems, and hospitals, have to coordinate their actions with the ultimate objective of providing a timely and appropriate response toward the collective. On the other hand, following the general reform of 2007, the National Board of Health in Denmark (NBHD) has recommended the delivery of emergency care through fewer, larger, and more centralized EDs. This was done to concentrate specialties and provide a higher level of care with greater efficiency in a system in which the patients\u2019 overall impression of hospitalization has traditionally been positive (MHP, 2008). Moreover, the overall reform generated (external) financial crunches for healthcare providers that predictably turned into internal pressures related to efficiency (e.g., Louis et al., 1999; Lega & DePietro, 2005; Reay & Hinings, 2005, 2009). The search for efficiency through the maximization of economies of scale, by concentrating specialized knowledge and equipment, is generating some symbiotic organizational effects. These can be studied at different levels of analysis (Hackman, 2003): a) at the macro level, through a general rationalization of public expense, in two ways: a.1) regions are in charge of the planning and delivery of healthcare, and new regional mechanisms for governance and funding, resulting in the diffusion of new performance appraisal approaches; a.2) positive operational spillovers are exploited amongst agents through coordination mechanisms based on healthcare networks, with several interdependent providers covering the various phases of emergency care; b) at the meso level, via the definition of structures, roles, and procedures of emergency care. In essence, each hospital designs its own ED, with different levels of managerial autonomy, human resource specialization, technological endowment, and design of internal processes. In short, the Danish emergency care system is trying to change toward a more cost-effective but also a more patient-oriented configuration; c) at the micro level, via the design of appropriate incentives for professionals. In Fearlie and Shortell\u2019s (2001) terms, \u201cA multilevel approach to change and the associated core properties can provide a framework for assessing progress on these and related issues over the next several years\u201d (p. 307). This paper presents the preliminary results of a larger research project called DESIGN-EM, aimed at designing effective and efficient EDs. In a dynamic environment, in which each of the 21 Danish hospitals is still configuring its own ED, this research project aims to determine if differences in organization designs affect efficiency, effectiveness, the quality of patient care, and resource utilization. It reports on the part of the project attempting to investigate the meso level of analysis (hospitals/EDs), and focuses on the research gap related to the adoption of the multi-contingency approach (Burton & Obel, 1988, 2004) in the design of emergency care, with a specific focus on the EDs (Table 1). Thus, this research addresses the following research question: How can hospitals design their EDs to adapt to institutional, technological, and clinical dynamics

Prenatal antidepressant exposure and child behavioural outcomes at 7 years of age: a study within the Danish National Birth Cohort

Objective: To investigate the impact of prenatal antidepressant exposure on behavioural problems in children at 7 years of age. Design: Nationwide population-based study. Setting: Danish National Birth Cohort. Population: A cohort of 49 178 pregnant women recruited between 1996 and 2002. Methods: Data obtained from computer-assisted telephone interviews twice during pregnancy were used to identify children born to: (i) depressed women who took antidepressants during pregnancy (n = 210); (ii) depressed women who did not take any antidepressants during pregnancy (n = 231); and (iii) healthy women who were not depressed (n = 48 737). Childhood behavioural problems at 7 years of age were examined using the validated Danish parent-report version of the Strengths and Difficulties Questionnaire (SDQ). Main outcome measures: SDQ scores. Results: No associations were observed between prenatal antidepressant exposure and abnormal SDQ scores for overall problem behaviour (adjusted relative risk, aRR 1.00; 95% confidence interval, 95% CI 0.49–2.05), hyperactivity/inattention (aRR 0.99; 95% CI 0.56–1.75), or peer problems (aRR 1.04; 95% CI 0.57–1.91). Although prenatal antidepressant exposure appeared to be associated with abnormal SDQ scores on the subscales of emotional symptoms (aRR 1.68; 95% CI 1.18–2.38) and conduct problems (aRR 1.58; 95% CI 1.03–2.42), these associations were significantly attenuated following adjustment for antenatal mood status (aRR 1.20; 95% CI 0.85–1.70 and aRR 1.19; 95% CI 0.77 1.83, respectively). Untreated prenatal depression was associated with an increased risk of all behavioural outcomes evaluated, compared with unexposed children, with significant attenuation following adjustment for antenatal mood status. Conclusions: The results of this study suggest that independent of maternal illness, prenatal antidepressant exposure is not associated with an increased risk of behavioural problems in children at 7 years of age.LE Grzeskowiak, JL Morrison, TB Henrikse, BH Bech, C Obel, J Olsen, LH Pederse

The association between preschool behavioural problems and internalizing difficulties at age 10-12 years

The aim was to study the association between preschool behavioural problems and emotional symptoms in 10- to 12-year-old children. The study was based on the Aarhus Birth cohort, Denmark, and included 1,336 children. Based on the parent-administered preschool behaviour questionnaire (PBQ), we identified three not mutually exclusive preschool behavioural categories: anxious–fearful (n = 146), hyperactive–distractible (n = 98), and hostile–aggressive (n = 170). Children without any known symptoms were considered well adjusted (n = 1,000). Borderline emotional (n = 105) and emotional difficulties (n = 136) were measured at age 10–12 years with the parent-administered strength and difficulties questionnaire (SDQ). Multinomial logistic regression analyses were used to adjust for potential confounding factors. We found that anxious–fearful behaviour and hostile–aggressive preschool behaviour were associated with twice the risk of school-age emotional difficulties. Comorbidity or confounding failed to explain these results. Hyperactive–distractible preschool behaviour was not associated with school-age emotional difficulties. Preschool anxious–fearful behaviour was associated with school-age emotional difficulties, suggesting internalizing symptom stability in some children from early childhood. Preschool hostile–aggressive behaviour was also associated with school-age emotional difficulties, which suggests transformation of one behavioural dimension into another through childhood, and the need to focus on both early internalizing difficulties and hostile–aggressive behaviour as risk factors for later internalizing difficulties

Brain glycogen—new perspectives on its metabolic function and regulation at the subcellular level

Glycogen is a complex glucose polymer found in a variety of tissues, including brain, where it is localized primarily in astrocytes. The small quantity found in brain compared to e.g., liver has led to the understanding that brain glycogen is merely used during hypoglycemia or ischemia. In this review evidence is brought forward highlighting what has been an emerging understanding in brain energy metabolism: that glycogen is more than just a convenient way to store energy for use in emergencies—it is a highly dynamic molecule with versatile implications in brain function, i.e., synaptic activity and memory formation. In line with the great spatiotemporal complexity of the brain and thereof derived focus on the basis for ensuring the availability of the right amount of energy at the right time and place, we here encourage a closer look into the molecular and subcellular mechanisms underlying glycogen metabolism. Based on (1) the compartmentation of the interconnected second messenger pathways controlling glycogen metabolism (calcium and cAMP), (2) alterations in the subcellular location of glycogen-associated enzymes and proteins induced by the metabolic status and (3) a sequential component in the intermolecular mechanisms of glycogen metabolism, we suggest that glycogen metabolism in astrocytes is compartmentalized at the subcellular level. As a consequence, the meaning and importance of conventional terms used to describe glycogen metabolism (e.g., turnover) is challenged. Overall, this review represents an overview of contemporary knowledge about brain glycogen and its metabolism and function. However, it also has a sharp focus on what we do not know, which is perhaps even more important for the future quest of uncovering the roles of glycogen in brain physiology and pathology

Incidence, risk factors and mortality of tuberculosis in Danish HIV patients 1995-2007

<p>Abstract</p> <p>Background</p> <p>Human Immunodeficiency Virus (HIV) infection predisposes to tuberculosis (TB). We described incidence, risk factors and prognosis of TB in HIV-1 infected patients during pre (1995-1996), early (1997-1999), and late Highly Active Antiretroviral Therapy (HAART) (2000-2007) periods.</p> <p>Methods</p> <p>We included patients from a population-based, multicenter, nationwide cohort. We calculated incidence rates (IRs) and mortality rates (MRs). Cox's regression analysis was used to estimate risk factors for TB infection with HAART initiation included as time updated variable. Kaplan-Meier was used to estimate mortality after TB.</p> <p>Results</p> <p>Among 2,668 patients identified, 120 patients developed TB during the follow-up period. The overall IR was 8.2 cases of TB/1,000 person-years of follow-up (PYR). IRs decreased during the pre-, early and late-HAART periods (37.1/1000 PYR, 12.9/1000 PYR and 6.5/1000 PYR respectively). African and Asian origin, low CD4 cell count and heterosexual and injection drug user route of HIV transmission were risk factors for TB and start of HAART reduced the risk substantially. The overall MR in TB patients was 34.4 deaths per 1,000 PYR (95% Confidence Interval: 22.0-54.0) and was highest in the first two years after the diagnosis of TB.</p> <p>Conclusions</p> <p>Incidence of TB still associated with conventional risk factors as country of birth, low CD4 count and route of HIV infection while HAART reduces the risk substantially. The mortality in this patient population is high in the first two years after TB diagnosis.</p

Novel model of neuronal bioenergetics: postsynaptic utilization of glucose but not lactate correlates positively with Ca2+ signalling in cultured mouse glutamatergic neurons

We have previously investigated the relative roles of extracellular glucose and lactate as fuels for glutamatergic neurons during synaptic activity. The conclusion from these studies was that cultured glutamatergic neurons utilize glucose rather than lactate during NMDA (N-methyl-d-aspartate)-induced synaptic activity and that lactate alone is not able to support neurotransmitter glutamate homoeostasis. Subsequently, a model was proposed to explain these results at the cellular level. In brief, the intermittent rises in intracellular Ca2+ during activation cause influx of Ca2+ into the mitochondrial matrix thus activating the tricarboxylic acid cycle dehydrogenases. This will lead to a lower activity of the MASH (malate–aspartate shuttle), which in turn will result in anaerobic glycolysis and lactate production rather than lactate utilization. In the present work, we have investigated the effect of an ionomycin-induced increase in intracellular Ca2+ (i.e. independent of synaptic activity) on neuronal energy metabolism employing 13C-labelled glucose and lactate and subsequent mass spectrometric analysis of labelling in glutamate, alanine and lactate. The results demonstrate that glucose utilization is positively correlated with intracellular Ca2+ whereas lactate utilization is not. This result lends further support for a significant role of glucose in neuronal bioenergetics and that Ca2+ signalling may control the switch between glucose and lactate utilization during synaptic activity. Based on the results, we propose a compartmentalized CiMASH (Ca2+-induced limitation of the MASH) model that includes intracellular compartmentation of glucose and lactate metabolism. We define pre- and post-synaptic compartments metabolizing glucose and glucose plus lactate respectively in which the latter displays a positive correlation between oxidative metabolism of glucose and Ca2+ signalling

CD4 cell count and the risk of AIDS or death in HIV-Infected adults on combination antiretroviral therapy with a suppressed viral load: a longitudinal cohort study from COHERE.

BACKGROUND: Most adults infected with HIV achieve viral suppression within a year of starting combination antiretroviral therapy (cART). It is important to understand the risk of AIDS events or death for patients with a suppressed viral load. METHODS AND FINDINGS: Using data from the Collaboration of Observational HIV Epidemiological Research Europe (2010 merger), we assessed the risk of a new AIDS-defining event or death in successfully treated patients. We accumulated episodes of viral suppression for each patient while on cART, each episode beginning with the second of two consecutive plasma viral load measurements 500 copies/µl, the first of two consecutive measurements between 50-500 copies/µl, cART interruption or administrative censoring. We used stratified multivariate Cox models to estimate the association between time updated CD4 cell count and a new AIDS event or death or death alone. 75,336 patients contributed 104,265 suppression episodes and were suppressed while on cART for a median 2.7 years. The mortality rate was 4.8 per 1,000 years of viral suppression. A higher CD4 cell count was always associated with a reduced risk of a new AIDS event or death; with a hazard ratio per 100 cells/µl (95% CI) of: 0.35 (0.30-0.40) for counts <200 cells/µl, 0.81 (0.71-0.92) for counts 200 to <350 cells/µl, 0.74 (0.66-0.83) for counts 350 to <500 cells/µl, and 0.96 (0.92-0.99) for counts ≥500 cells/µl. A higher CD4 cell count became even more beneficial over time for patients with CD4 cell counts <200 cells/µl. CONCLUSIONS: Despite the low mortality rate, the risk of a new AIDS event or death follows a CD4 cell count gradient in patients with viral suppression. A higher CD4 cell count was associated with the greatest benefit for patients with a CD4 cell count <200 cells/µl but still some slight benefit for those with a CD4 cell count ≥500 cells/µl