The Mixed Management of Patients' Medical Records: Responsibility Sharing Between the Patient and the Physician

Through this article, we propose a mixed management of patients' medical records, so as to share responsibilities between the patient and the Medical Practitioner by making Patients responsible for the validation of their administrative information, and MPs responsible for the validation of their Patients' medical information. Our proposal can be considered a solution to the main problem faced by patients, health practitioners and the authorities, namely the gathering and updating of administrative and medical data belonging to the patient in order to accurately reconstitute a patient's medical history. This method is based on two processes. The aim of the first process is to provide a patient's administrative data, in order to know where and when the patient received care (name of the health structure or health practitioner, type of care: out patient or inpatient). The aim of the second process is to provide a patient's medical information and to validate it under the accountability of the Medical Practitioner with the help of the patient if needed. During these two processes, the patient's privacy will be ensured through cryptographic hash functions like the Secure Hash Algorithm, which allows pseudonymisation of a patient's identity. The proposed Medical Record Search Engines will be able to retrieve and to provide upon a request formulated by the Medical ractitioner all the available information concerning a patient who has received care in different health structures without divulging the patient's identity. Our method can lead to improved efficiency of personal medical record management under the mixed responsibilities of the patient and the MP.

Bypass gastrique: prise en charge des complications et désagrements alimentaires [Gastric bypass: management of complications and food tolerance]

La chirurgie bariatrique est le seul traitement qui permette une perte pondérale significative sur le long terme mais le succès d'une telle intervention repose avant tout dans une sélection et une préparation attentive du patient. Une bonne connaissance des implications de l'opération permet de favoriser un changement de comportement alimentaire et par là aussi de diminuer les complications et les désagréments alimentaires. L'éducation du patient n'a de sens que si elle s'inscrit dans une prise en charge pluridisciplinaire, comprenant également un suivi diététique, planifié sur le long terme. La mastication, la vitesse d'ingestion des aliments, le fait de renoncer aux boissons gazeuses et de devoir boire régulièrement entre les repas, sont les éléments les plus difficiles à mettre en place pour le patient. Bariatric surgery is the only treatment inducing effective weight loss on the long term. The success of such an intervention is possible by carefully selecting and educating the candidates. Good understanding of the bariatric surgery implications allows the patients to modify their eating habits and thus decrease complications and food intolerance. Therefore patient education requires a multidisciplinary approach which implies the follow-up of a dietician on the long term. Mastication, speed of food ingestion, avoidance of carbonated beverages as well as the obligation to drink at frequent and regular intervals are the most difficult aspects to be taught to the patients

The region makes the difference: disparities in management of acute myocardial infaction within Switzerland

Purpose: To assess geographical differences within Switzerland regarding management and revascularization procedures for acute myocardial infarction (AMI). Methods: Swiss hospital discharge database for period 2007-2008. The main inclusion criterion was AMI as a primary discharge diagnosis. AMI revascularization procedures were identified and seven Swiss regions (Leman, Mittelland, Northwest, Zurich, Central, Eastern and Ticino) were analyzed. Results: Data from 25,674 AMI discharges were analyzed. Almost half (53.6%) of them were managed in a single hospital, the values ranging from 63.1% (Leman) to 31.4% (Ticino) see table. Relative to the total number of discharges, the highest Intensive Care Unit admission rate was in Leman (69.7%), the lowest (16.4%) in Ticino (Swiss average: 35.8%). Intracoronary revascularization rates were highest in Leman (51.6%) and lowest (30.8%) in Central Switzerland (Swiss average: 41.4%). Bare (non-drug-eluting) stents use was highest in Leman (33.1%) and lowest (7.0%) in Ticino (Swiss average: 15.8%), while drug eluting stent use was highest (32.8%) in Ticino and lowest (13.9%) in Central Switzerland (Swiss average: 24.0%). Coronary artery bypass graft rates were highest (4.6%) in Ticino and lowest (0.4%) in Eastern Switzerland (Swiss average: 2.6%). Mechanical circulatory assistance rates were highest (4.1%) in Zurich and lowest (0.4%) in Ticino (Swiss average: 1.7%). The differences in revascularization procedures remained after adjusting for age, single or multiple hospital management and gender. Conclusion: In Switzerland, significant geographical differences in management and revascularization procedures for AMI were found.

Risk factor profile and management of cerebrovascular patients in the REACH Registry.

BACKGROUND: Cerebrovascular disease (CVD) is a global public health problem. CVD patients are at high risk of recurrent stroke and other atherothrombotic events. Prevalence of risk factors, comorbidities, utilization of secondary prevention therapies and adherence to guidelines all influence the recurrent event rate. We assessed these factors in 18,992 CVD patients within a worldwide registry of stable outpatients. METHODS: The Reduction of Atherothrombosis for Continued Health Registry recruited >68,000 outpatients (44 countries). The subjects were mainly recruited by general practitioners (44%) and internists (29%) if they had symptomatic CVD, coronary artery disease, peripheral arterial disease (PAD) and/or >or=3 atherothrombotic risk factors. RESULTS: The 18,992 CVD patients suffered a stroke (53.7%), transient ischemic attack (TIA) (27.7%) or both (18.5%); 40% had symptomatic atherothrombotic disease in >or=1 additional vascular beds: 36% coronary artery disease; 10% PAD and 6% both. The prevalence of risk factors at baseline was higher in the TIA subgroup than in the stroke group: treated hypertension (83.5/82.0%; p = 0.02), body mass index >or=30 (26.7/20.8%; p < 0.0001), hypercholesterolemia (65.1/52.1%; p < 0.0001), atrial fibrillation (14.7/11.9%; p < 0.0001) and carotid artery disease (42.3/29.7%; p < 0.0001). CVD patients received antiplatelet agents (81.7%), oral anticoagulants (17.3%), lipid-lowering agents (61.2%) and antihypertensives (87.9%), but guideline treatment targets were frequently not achieved (54.5% had elevated blood pressure at baseline, while 4.5% had untreated diabetes). CONCLUSIONS: A high percentage of CVD patients have additional atherothrombotic disease manifestations. The risk profile puts CVD patients, especially the TIA subgroup, at high risk for future atherothrombotic events. Undertreatment is common worldwide and adherence to guidelines needs to be enforced.

Standards of care and novel approaches in the management of glioblastoma multiforme.

Glioblastoma multiforme (GBM) is the most common malignant primary brain tumor in adults. Standard therapeutic approaches provide modest improvement in the progression-free and overall survival, necessitating the investigation of novel therapies. We review the standard treatment options for GBM and evaluate the results obtained in clinical trials for promising novel approaches, including the inhibition of angiogenesis, targeted approaches against molecular pathways, immunotherapies, and local treatment with low voltage electric fields.

Determinants of the development of post-traumatic stress disorder, in the general population.

PURPOSE: To assess (1) the lifetime prevalence of exposure both to trauma and post-traumatic stress disorder (PTSD); (2) the risk of PTSD by type of trauma; and (3) the determinants of the development of PTSD in the community. METHODS: The Diagnostic Interview for Genetic Studies was administered to a random sample of an urban area (N = 3,691). RESULTS: (1) The lifetime prevalence estimates of exposure to trauma and PTSD were 21.0 and 5.0%; respectively, with a twice as high prevalence of PTSD in women compared to men despite a similar likelihood of exposure in the two sexes; (2) Sexual abuse was the trauma involving the highest risk of PTSD; (3) The risk of PTSD was most strongly associated with sexual abuse followed by preexisting bipolar disorder, alcohol dependence, antisocial personality, childhood separation anxiety disorder, being victim of crime, witnessing violence, Neuroticism and Problem-focused coping strategies. After adjustment for these characteristics, female sex was no longer found to be significantly associated with the risk of PTSD. CONCLUSIONS: The risk for the development of PTSD after exposure to traumatic events is associated with several factors including the type of exposure, preexisting psychopathology, personality features and coping strategies which independently contribute to the vulnerability to PTSD.

Treatment Options in the Management of Status Epilepticus

Status epilepticus treatment involves the use of several pharmacologic compounds, which are conceptually divided into three successive and additional lines of action. Because of their rapid onset of action, benzodiazepines represent the first approach; these are followed by classic antiepileptic drugs that are administered intravenously. In refractory episodes, pharmacologic coma induction with an appropriate anesthetic is advocated. Apart from first-line compounds, the level of evidence for medications used in status epilepticus is extremely limited. It is important to specifically address etiology in order to maximize the impact of the antiepileptic therapy. Fine-tuning of the treatment strategy, mainly regarding the choice of whether to induce coma, should be approached by balancing the benefits of rapid control of the status epilepticus with the risks of adverse effects. Although each status epilepticus episode should be treated as rapidly as possible, it appears advisable to reserve coma induction for those forms, such as generalized convulsive status, that have been shown to present a consistent risk of neurologic sequelae.

Prognostic factors and role of adjuvant therapies in the management of parasagittal meningiomas

L'objectif du présent travail de thèse est d'analyser rétrospectivement la série de méningiomes parasagittaux traités au CHUV, soit par traitements simples ou combinés (chirurgie et / ou radiochirurgie et radiothérapie fractionnée), afin de déterminer les facteurs qui influencent leur pronostic. Méthode: Entre Janvier 1999 et mai 2007, 37 méningiomes parasagittaux ont été traités dans notre centre. Nous avons analysé de manière rétrospective les différents paramètres du traitement de ces méningiomes ainsi que leur emplacement le long du sinus sagittal supérieur, leur volume, leur grade histologique et le degré de résection ainsi que le sexe et l'âge du patient afin de comprendre les facteurs qui influencent leur histoire naturelle. Résultats: Le suivi médian était de 6,7 ans (2,4 -12 ans). Les grades histologiques et le degré de résection tumorale (Simpson) étaient répartis uniformément le long du sinus sagittal supérieur. Le taux actuariel de contrôle global des tumeurs était de 65,9%. L'analyse de régression montre que le grade tumoral et le degré de résection sont deux facteurs extrêmement importants pour déterminer le contrôle tumoral (p <0,002 et ρ <0,008). La localisation le long du sinus sagittal supérieur a montré une baisse du taux de contrôle dans le tiers postérieur (p <0,002). Le sexe, l'âge et le volume de la tumeur n'étaient quand à eux pas des facteurs significatifs. Par ailleurs, et de façon inattendue, dans notre série, la proportion du traitement adjuvant a été beaucoup plus élevée que dans les séries décrites jusqu'à maintenant (39% vs 7%) mais avec un taux de contrôle similaire et diminution de la morbidité et la mortalité. Conclusions: Dans notre série, le grade histologique et le degré de résection tumorale (Simpson) sont des facteurs indépendants de récidive et de contrôle tumoral. Fait intéressant, l'emplacement dans le tiers postérieur du sinus sagittal supérieur semble être un autre facteur indépendant de récidive. Afin d'éviter les morbidités importantes liées à la chirurgie nous préconisons une utilisation précoce de traitements adjuvants pour les tumeurs grade histologique élevé et pour les tumeurs situées dans la partie postérieure du sinus sagittal supérieur

European expert opinion on the management of invasive candidiasis in adults.

This report discusses the present status of antifungal therapy and treatment options for candidaemia, considered by experts in the field in Europe. A conference of 26 experts from 13 European countries was held to discuss strategies for the treatment and prevention of invasive candidiasis, with the aim of providing a review on optimal management strategies. Published and unpublished comparative trials on antifungal therapy were analysed and discussed. Commonly asked questions about the management of candidaemia were selected, and possible responses to these questions were discussed. Panellists were then asked to respond to each question by using a touchpad answering system. After the initial conference, the viewpoint document has been reviewed and edited to include new insights and developments since the initial meeting. For many situations, consensus on treatment could not be reached, and the responses indicate that treatment is likely to be modified on a patient-to-patient basis, depending on factors such as degree of illness, prior exposure to azole antifungals, and the presence of potentially antifungal drug-resistant Candida species.

Mutations in tubulin genes are frequent causes of various foetal malformations of cortical development including microlissencephaly.

Complex cortical malformations associated with mutations in tubulin genes are commonly referred to as "Tubulinopathies". To further characterize the mutation frequency and phenotypes associated with tubulin mutations, we studied a cohort of 60 foetal cases. Twenty-six tubulin mutations were identified, of which TUBA1A mutations were the most prevalent (19 cases), followed by TUBB2B (6 cases) and TUBB3 (one case). Three subtypes clearly emerged. The most frequent (n = 13) was microlissencephaly with corpus callosum agenesis, severely hypoplastic brainstem and cerebellum. The cortical plate was either absent (6/13), with a 2-3 layered pattern (5/13) or less frequently thickened (2/13), often associated with neuroglial overmigration (4/13). All cases had voluminous germinal zones and ganglionic eminences. The second subtype was lissencephaly (n = 7), either classical (4/7) or associated with cerebellar hypoplasia (3/7) with corpus callosum agenesis (6/7). All foetuses with lissencephaly and cerebellar hypoplasia carried distinct TUBA1A mutations, while those with classical lissencephaly harbored recurrent mutations in TUBA1A (3 cases) or TUBB2B (1 case). The third group was polymicrogyria-like cortical dysplasia (n = 6), consisting of asymmetric multifocal or generalized polymicrogyria with inconstant corpus callosum agenesis (4/6) and hypoplastic brainstem and cerebellum (3/6). Polymicrogyria was either unlayered or 4-layered with neuronal heterotopias (5/6) and occasional focal neuroglial overmigration (2/6). Three had TUBA1A mutations and 3 TUBB2B mutations. Foetal TUBA1A tubulinopathies most often consist in microlissencephaly or classical lissencephaly with corpus callosum agenesis, but polymicrogyria may also occur. Conversely, TUBB2B mutations are responsible for either polymicrogyria (4/6) or microlissencephaly (2/6).

How to interprete subclinical thyroid dysfunction in the prevention and management of heart failure events? Individual participant data analysis from six prospective cohorts

Background: Guidelines of the Diagnosis and Management of Heart Failure (HF) recommend investigating exacerbating conditions, such as thyroid dysfunction, but without specifying impact of different TSH levels. Limited prospective data exist regarding the association between subclinical thyroid dysfunction and HF events. Methods: We performed a pooled analysis of individual participant data using all available prospective cohorts with thyroid function tests and subsequent follow-up of HF events. Individual data on 25,390 participants with 216,247 person-years of follow-up were supplied from 6 prospective cohorts in the United States and Europe. Euthyroidism was defined as TSH 0.45-4.49 mIU/L, subclinical hypothyroidism as TSH 4.5-19.9 mIU/L and subclinical hyperthyroidism as TSH <0.45 mIU/L, both with normal free thyroxine levels. HF events were defined as acute HF events, hospitalization or death related to HF events. Results: Among 25,390 participants, 2068 had subclinical hypothyroidism (8.1%) and 648 subclinical hyperthyroidism (2.6%). In age- and gender-adjusted analyses, risks of HF events were increased with both higher and lower TSH levels (P for quadratic pattern<0.01): hazard ratio (HR) was 1.01 (95% confidence interval [CI] 0.81-1.26) for TSH 4.5-6.9 mIU/L, 1.65 (CI 0.84-3.23) for TSH 7.0-9.9 mIU/L, 1.86 (CI 1.27-2.72) for TSH 10.0-19.9 mIUL/L (P for trend <0.01), and was 1.31 (CI 0.88-1.95) for TSH 0.10-0.44 mIU/L and 1.94 (CI 1.01-3.72) for TSH <0.10 mIU/L (P for trend=0.047). Risks remained similar after adjustment for cardiovascular risk factors. Conclusion: Risks of HF events were increased with both higher and lower TSH levels, particularly for TSH ≥10 mIU/L and for TSH <0.10 mIU/L. Our findings might help to interpret TSH levels in the prevention and investigation of HF.

Regulation of dendritic development by neurotrophic factors

AbstractEstablishment of a functional nervous system occurs through an orchestrated multistep process during embryogenesis. As dendrites are the primary sites of synaptic connections, development of dendritic arborization is essential for the formation of functional neural circuits. Maturation of dendritic arbor occurs through dynamic processes that are regulated by intrinsic genetic factors and external signals, such as environmental stimuli, neuronal activity and growth factors. Among the latter, the neurotrophic factor BDNF is a key regulator of dendritic growth. However, the mechanisms by which BDNF controls dendritic development remain elusive.In this study, we first showed that activation of the MAPK signaling pathway and phosphorylation of the transcription factor CREB are required to mediate the effects of BDNF on dendritic development of cortical neurons. However, phosphorylation of CREB alone is not sufficient to induce dendritic growth in response to BDNF. Thus, by using a mutant form of CREB unable to bind its coactivator CRTC1, we demonstrated that BDNF-induced dendritic elaboration requires the functional interaction between CREB and CRTC1. Consistent with these observations, inhibition of CRTC1 expression by shRNA-mediated knockdown was found to suppress the effects of BDNF on dendritic length and branching of cortical neurons.The nuclear translocation of CRTC1, a step necessary for the interaction between CREB and CRTC1, was shown to result from the activation of NMD A receptors by glutamate, leading to the dephosphorylation of CRTC1 by the protein phosphatase calcineurin. In line with these findings, prevention of CRTC1 nuclear translocation in the absence of glutamate, or by inhibiting NMDA receptors or calcineurin suppressed the promotion of dendritic growth by BDNF.Increasing evidence supports a role for the growth factor HGF in the regulation of dendritic morphology during brain development. Despite these observations, little is known about the cellular mechanisms underlying the effects of HGF on dendritic elaboration of cortical neurons. The second part of this study was aimed at elucidating the cellular processes that mediate the effects of HGF on dendritic differentiation. We found that HGF increases cortical dendritic growth through mechanisms that involve MAPK-dependent phosphorylation of CREB, and interaction of CREB with its coactivator CRTC1. These data indicate that the mechanisms underlying the promotion of dendritic growth by HGF are similar to those that mediate the effects of BDNF, suggesting that the role of CREB and CRTC1 in the regulation of dendritic development may not be limited to HGF and BDNF, but may extend to other neurotrophic factors that control dendritic differentiation.Together, these results identify a previously unrecognized mechanism by which CREB and its coactivator CRTC1 mediate the effects of BDNF and HGF on dendritic growth of cortical neurons. Moreover, these data highlight the important role of the cooperation between BDNF/HGF and glutamate that converges on CREB to stimulate the expression of genes that contribute to the development of dendritic arborization.RésuméL'établissement d'un système nerveux fonctionnel s'accomplit grâce à des mécanismes précis, orchestrés en plusieurs étapes au cours de l'embryogenèse. Les dendrites étant les principaux sites de connexions synaptiques, le développement de l'arborisation dendritique est essentiel à la formation de circuits neuronaux fonctionnels. La maturation de l'arbre dendritique s'effectue grâce à des processus dynamiques qui sont régulés par des facteurs génétiques intrinsèques ainsi que par des facteurs externes tels que les stimuli environnementaux, l'activité neuronale ou les facteurs de croissance. Parmi ces derniers, le facteur neurotrophique BDNF est - connu pour être un régulateur clé de la croissance dendritique. Cependant, les mécanismes par lesquels BDNF contrôle le développement dendritique demeurent mal connus.Au cours de cette étude, nous avons montré dans un premier temps que l'activation de la voie de signalisation de la MAPK et la phosphorylation du facteur de transcription CREB sont nécessaires aux effets du BDNF sur le développement dendritique des neurones corticaux. Toutefois, la phosphorylation de CREB en tant que telle n'est pas sûffisante pour permettre la pousse des dendrites en réponse au BDNF. Ainsi, en utilisant une forme mutée de CREB incapable de se lier à son coactivateur CRTC1, nous avons démontré que l'élaboration des dendrites induite par le BDNF nécessite également une interaction fonctionnelle entre CREB et CRTC1. Ces résultats ont été confirmés par d'autres expériences qui ont montré que l'inhibition de l'expression de CRTC1 par l'intermédiaire de shRNA supprime les effets du BDNF sur la longueur et le branchement dendritique des neurones corticaux.Les résultats obtenus au cours de ce travail montrent également que la translocation nucléaire de CRTC1, qui est une étape nécessaire à l'interaction entre CREB et CRTC1, résulte de l'activation des récepteurs NMDA par le glutamate, entraînant la déphosphorylation de CRTC1 par la protéine phosphatase calcineurine. De plus, le blocage de la translocation nucléaire de CRTC1 en absence de glutamate, ou suite à l'inhibition des récepteurs NMDA ou de la calcineurine, supprime complètement la pousse des dendrites induite par le BDNF.De nombreuses d'évidences indiquent que le facteur de croissance HGF joue également un rôle important dans la régulation de la morphologie dendritique au cours du développement cérébral. Malgré ces observations, peu d'éléments sont connus quant aux mécanismes cellulaires qui sous-tendent les effets du HGF sur la croissance dendritique des neurones corticaux. Le but de la seconde partie de cette étude a eu pour but d'élucider les processus cellulaires responsables des effets du HGF sur la différenciation dendritique des neurones corticaux. Au cours de ces expériences, nous avons pu mettre en évidence que le HGF induit la pousse dendritique par des mécanismes qui impliquent la phosphorylation de CREB par la MAPK, et l'interaction de CREB avec son coactivateur CRTC1. Ces données indiquent que les mécanismes impliqués dans la stimulation de la croissance dendritique par le HGF sont similaires à ceux régulant les effets du BDNF, ce qui suggère que le rôle de CREB et de CRTC1 dans la régulation du développement dendritique n'est vraisemblablement pas limité aux effets du HGF ou du BDNF, mais pourrait s'étendre à d'autres facteurs neurotrophiques qui contrôlent la différenciation dendritique.En conclusion, ces résultats ont permis l'identification d'un nouveau mécanisme par lequel CREB et son coactivateur CRTC1 transmettent les effets du BDNF et du HGF sur la croissance dendritique de neurones corticaux. Ces observations mettent également en évidence le rôle important joué par la coopération entre BDNF/HGF et le glutamate, dans l'activation de CREB ainsi que dans l'expression de gènes qui participent au développement de l'arborisation dendritique des neurones corticaux.

Management of faecal incontinence and constipation in adults with central neurological diseases.

BACKGROUND: People with neurological disease have a much higher risk of both faecal incontinence and constipation than the general population. There is often a fine line between the two conditions, with any management intended to ameliorate one risking precipitating the other. Bowel problems are observed to be the cause of much anxiety and may reduce quality of life in these people. Current bowel management is largely empirical with a limited research base. OBJECTIVES: To determine the effects of management strategies for faecal incontinence and constipation in people with neurological diseases affecting the central nervous system. SEARCH STRATEGY: We searched the Cochrane Incontinence Group Specialised Trials Register (searched 26 January 2005), the Cochrane Central Register of Controlled Trials (Issue 2, 2005), MEDLINE (January 1966 to May 2005), EMBASE (January 1998 to May 2005) and all reference lists of relevant articles. SELECTION CRITERIA: All randomised or quasi-randomised trials evaluating any types of conservative or surgical measure for the management of faecal incontinence and constipation in people with neurological diseases were selected. Specific therapies for the treatment of neurological diseases that indirectly affect bowel dysfunction were also considered. DATA COLLECTION AND ANALYSIS: Two reviewers assessed the methodological quality of eligible trials and two reviewers independently extracted data from included trials using a range of pre-specified outcome measures. MAIN RESULTS: Ten trials were identified by the search strategy, most were small and of poor quality. Oral medications for constipation were the subject of four trials. Cisapride does not seem to have clinically useful effects in people with spinal cord injuries (three trials). Psyllium was associated with increased stool frequency in people with Parkinson's disease but did not alter colonic transit time (one trial). Prucalopride, an enterokinetic did not demonstrate obvious benefits in this patient group (one study). Some rectal preparations to initiate defaecation produced faster results than others (one trial). Different time schedules for administration of rectal medication may produce different bowel responses (one trial). Mechanical evacuation may be more effective than oral or rectal medication (one trial). There appears to be a benefit to patients in one-off educational interventions from nurses. The clinical significance of any of these results is difficult to interpret. AUTHORS' CONCLUSIONS: There is still remarkably little research on this common and, to patients, very significant condition. It is not possible to draw any recommendation for bowel care in people with neurological diseases from the trials included in this review. Bowel management for these people must remain empirical until well-designed controlled trials with adequate numbers and clinically relevant outcome measures become available.