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BACKGROUND Ineffective communication procedures create openings for errors when health care professionals fail to transfer complete, consistent information. Deficient or absent clinical handovers, or failures to transfer information, responsibility, and accountability, can have severe consequences for hospitalized patients. Clinical handovers are practiced every day, in many ways, in all institutional health care settings. OBJECTIVE This study aimed to design an evidence-based, nursing handover standard for inpatients for use at shift changes or internal transfers between hospital wards. METHODS We carried out a modified, multiround, web-based, Delphi data collection survey of an anonymized panel sample of 264 nurse experts working at a multisite public hospital in Switzerland. Each survey round was built on responses from the previous one. The surveys ended with a focus group discussion consisting of a randomly selected panel of participants to explain why items for the evidence-based clinical nursing handover standard were selected or not selected. Items had to achieve a consensus of ≥70% for selection and inclusion. RESULTS The study presents the items selected by consensus for an evidence-based nursing handover standard for inpatients for use at shift changes or internal transfers. It also presents the reasons why survey items were or were not included. CONCLUSIONS This modified Delphi survey method enabled us to develop a consensus- and evidence-based nursing handover standard now being trialed at shift changes and the internal transfers of inpatients at our multisite public hospital in Switzerland.

BACKGROUND Poor communication processes create opportunities for errors when caregivers fail to transfer complete and consistent information. Inadequate or nonexistent clinical handovers or failures to transfer information, responsibility, and accountability can have dire consequences for hospitalized patients. Clinical handover is practiced every day, in a multitude of ways, in all health care settings. OBJECTIVE The goal of this study is to build a consensus, evidence-based nursing handover standard for inpatients during shift changes or internal transfers between hospital wards. The study will be based on papers published by Slade et al. METHODS This protocol describes a modified Delphi data-collection survey involving a targeted panel sample of 300 nurse experts. A multi-round survey will select an anonymous panel from a multi-site public hospital in Switzerland. Each survey stage will be described and will build on the previous one. The study will end with a focus group discussion involving a randomly selected panel to explain why items for the evidence-based clinical nursing handover standard were accepted or not accepted. An item must achieve a consensus of ≥70% for inclusion. RESULTS The present study’s expected outcome is a consensus-built, evidence-based nursing handover standard for inpatients during shift changes or internal transfers between the wards of a multi-site public hospital in Switzerland. CONCLUSIONS This survey will enable us to develop an evidence-based nursing handover standard for use during shift changes and internal inpatient transfers in a multi-site public hospital in Switzerland. INTERNATIONAL REGISTERED REPORT DERR1-10.2196/15910

Background Ineffective communication procedures create openings for errors when health care professionals fail to transfer complete, consistent information. Deficient or absent clinical handovers, or failures to transfer information, responsibility, and accountability, can have severe consequences for hospitalized patients. Clinical handovers are practiced every day, in many ways, in all institutional health care settings. Objective This study aimed to design an evidence-based, nursing handover standard for inpatients for use at shift changes or internal transfers between hospital wards. Methods We carried out a modified, multiround, web-based, Delphi data collection survey of an anonymized panel sample of 264 nurse experts working at a multisite public hospital in Switzerland. Each survey round was built on responses from the previous one. The surveys ended with a focus group discussion consisting of a randomly selected panel of participants to explain why items for the evidence-based clinical nursing handover standard were selected or not selected. Items had to achieve a consensus of ≥70% for selection and inclusion. Results The study presents the items selected by consensus for an evidence-based nursing handover standard for inpatients for use at shift changes or internal transfers. It also presents the reasons why survey items were or were not included. Conclusions This modified Delphi survey method enabled us to develop a consensus- and evidence-based nursing handover standard now being trialed at shift changes and the internal transfers of inpatients at our multisite public hospital in Switzerland.

Background Poor communication processes create opportunities for errors when caregivers fail to transfer complete and consistent information. Inadequate or nonexistent clinical handovers or failures to transfer information, responsibility, and accountability can have dire consequences for hospitalized patients. Clinical handover is practiced every day, in a multitude of ways, in all health care settings. Objective The goal of this study is to build a consensus, evidence-based nursing handover standard for inpatients during shift changes or internal transfers between hospital wards. The study will be based on papers published by Slade et al. Methods This protocol describes a modified Delphi data-collection survey involving a targeted panel sample of 300 nurse experts. A multi-round survey will select an anonymous panel from a multi-site public hospital in Switzerland. Each survey stage will be described and will build on the previous one. The study will end with a focus group discussion involving a randomly selected panel to explain why items for the evidence-based clinical nursing handover standard were accepted or not accepted. An item must achieve a consensus of ≥70% for inclusion. Results The present study’s expected outcome is a consensus-built, evidence-based nursing handover standard for inpatients during shift changes or internal transfers between the wards of a multi-site public hospital in Switzerland. Conclusions This survey will enable us to develop an evidence-based nursing handover standard for use during shift changes and internal inpatient transfers in a multi-site public hospital in Switzerland. International Registered Report Identifier (IRRID) DERR1-10.2196/15910

According to the Swiss hypothermia clinical staging, patients with stage III are unconscious with preserved vital signs, with core temperature usually between 24° and 28°C. With stage IV, vital signs are absent with core temperature24°C.To describe a patient presenting with HT stage III with vital signs but a core temperature of24°C, and to search for similar patients in the medical literature.MEDLINE was used to search for cases of deep accidental hypothermia (24°C) and preserved vital signs.We found 22 cases in addition to our case (n=23). Median age was 44 years (IQR 36; range 4-83) and median core temperature 22°C (IQR 1.7; 17-23.8). Vital signs were often minimal. Seven patients developed ventricular fibrillation (VF). Twenty patients survived with excellent neurological outcome.Vital signs can be present in hypothermic patients with core temperature24°C. In deeply hypothermic patients, a careful check and prolonged check of vital functions should be made, as vital signs may be minimal. The clinical Swiss staging remains valuable in the prehospital evaluation of hypothermic patients; its correlation with core temperature should be better defined.

Background. Continuous renal replacement therapy (CRRT) has been increasingly used in critically ill patients with acute kidney injury (AKI). One of the major properties that likely influence the catheter lifespan includes its surface specificity. We hypothesized that the improvement of blood-surface interaction by a reactive polymer film coating might reduce thrombogenic events in the vascular access device and subsequently lead to prolonged catheter survival in this clinical setting. Methods. We compared, in a randomized study, the clinical application of two temporary catheters (TCs): one surface-modified double-lumen catheter (smDLC) and one standard sDLC with identical geometry and flow design. Efficacy end points were defined as the ability to complete at least 72 h CRRT without interruption due to TC dysfunction and ability to achieve blood flow rates of ≥ 150 mL/min. Safety end points were defined as the occurrence of catheter-related (CR) bacteraemia or other CR complications. Results. We evaluated 236 critically ill patients (264 TCs) with AKI on CRRT (continuous venovenous haemodiafiltration) with age (mean ± SD) of 56.9 ± 17.9 years. The clinical investigation revealed that the number of hours before TC removal according to clinical requirements was significantly higher with smDLC as compared with sDLC (131 ± 38 vs 113 ± 21 h; P = 0.004). Temporary catheter dysfunction occurred in 5% for smDLC and 14% for sDLC; P = 0.001. Thrombosis of smDLC and sDLC was observed in 2.3 episodes per 1000 TC-days [95% confidence interval (CI), 1.9-2.5] and 4.2 episodes per 1000 TC-days (95% CI, 4.0-4.4), respectively; P = 0.021. The blood flow rate was 221 ± 29 mL/min vs 187 ± 36 mL/min for smDLC and sDLC, respectively; P = 0.012. Compared with the overall mean of TC dysfunction or thrombosis, the relative risk of premature removal (

With the current limited availability of organs for transplantation, it is important to consider marginal donor candidates, including survivors of potentially curable malignancies such as lymphoma. The absence of refractory/recurrent residual disease at the time of brain death can be difficult to establish. Therefore, it is critical to have objective data to decide whether to proceed or not with organ procurement and transplantation. We report a unique situation in which (18)F-fluorodeoxyglucose positron emission tomography (PET) was used to rule out Hodgkin's lymphoma recurrence in a 33-year-old, heart-beating, brain-dead, potential donor with a past history of Hodgkin's disease and a persistent mediastinal mass. PET showed no significant uptake in the mass, allowing organ donation and transplantation to occur. We present a new means of evaluating potential brain-dead donors with a past history of some lymphoma, whereby PET may help transplant physicians by optimizing donation safety while rationalizing the inclusion of marginal donors.

Invasive studies suggest that healthy children living at high altitude display pulmonary hypertension, but the data to support this assumption are sparse. Nitric oxide (NO) synthesized by the respiratory epithelium regulates pulmonary artery pressure, and its synthesis was reported to be increased in Aymara high-altitude dwellers. We hypothesized that pulmonary artery pressure will be lower in Aymara children than in children of European ancestry at high altitude, and that this will be related to increased respiratory NO. We therefore compared pulmonary artery pressure and exhaled NO (a marker of respiratory epithelial NO synthesis) between large groups of healthy children of Aymara (n = 200; mean +/- SD age, 9.5 +/- 3.6 years) and European ancestry (n = 77) living at high altitude (3,600 to 4,000 m). We also studied a group of European children (n = 29) living at low altitude. The systolic right ventricular to right atrial pressure gradient in the Aymara children was normal, even though significantly higher than the gradient measured in European children at low altitude (22.5 +/- 6.1 mm Hg vs 17.7 +/- 3.1 mm Hg, p < 0.001). In children of European ancestry studied at high altitude, the pressure gradient was 33% higher than in the Aymara children (30.0 +/- 5.3 mm Hg vs 22.5 +/- 6.1 mm Hg, p < 0.0001). In contrast to what was expected, exhaled NO tended to be lower in Aymara children than in European children living at the same altitude (12.4 +/- 8.8 parts per billion [ppb] vs 16.1 +/- 11.1 ppb, p = 0.06) and was not related to pulmonary artery pressure in either group. Aymara children are protected from hypoxic pulmonary hypertension at high altitude. This protection does not appear to be related to increased respiratory NO synthesis.

Nous rapportons le cas d’un patient connu pour une maladie de McArdle et une d’Alzheimer, qui nous a ete adresse pour un etat confusionnel aigu. Cliniquement et biologiquement le patient presentait une insuffisance renale aigue. Nous decrivons ci-dessous les demarches diagnostiques et evoquons son etiologie, puis nous discutons des glycogenoses musculaires, en particulier la physiopathologie, l’approche diagnostique et les traitements possibles.

We thank Lazdam et al and Yuan et al for their interesting comments on our study.1 Lazdam et al point out that in our study, birth weight in offspring of mothers with preeclampsia was significantly lower than in controls, and suggest that the vascular impairment in offspring was caused by a combination of the independent effects of preeclampsia and intrauterine growth restriction rather than by preeclampsia per se. To test this hypothesis, we performed a subgroup analysis of 15 offspring of mothers with preeclampsia and 15 controls matched for birth weight (3080±291 versus 3077±398 g; P =0.98). We found that the difference in flow-mediated dilation between birth-weight-matched offspring of preeclampsia and controls (6.4%±1.3% versus 8.9%±1.2%; P

Background— Adverse events in utero may predispose to cardiovascular disease in adulthood. The underlying mechanisms are unknown. During preeclampsia, vasculotoxic factors are released into the maternal circulation by the diseased placenta. We speculated that these factors pass the placental barrier and leave a defect in the circulation of the offspring that predisposes to a pathological response later in life. The hypoxia associated with high-altitude exposure is expected to facilitate the detection of this problem. Methods and Results— We assessed pulmonary artery pressure (by Doppler echocardiography) and flow-mediated dilation of the brachial artery in 48 offspring of women with preeclampsia and 90 offspring of women with normal pregnancies born and permanently living at the same high-altitude location (3600 m). Pulmonary artery pressure was roughly 30% higher (mean±SD, 32.1±5.6 versus 25.3±4.7 mm Hg; P P r =−0.61, P Conclusions— Preeclampsia leaves a persistent defect in the systemic and the pulmonary circulation of the offspring. This defect predisposes to exaggerated hypoxic pulmonary hypertension already during childhood and may contribute to premature cardiovascular disease in the systemic circulation later in life.

In the context of cerebral diseases the two main mechanisms responsible for non iatrogenic causes of hyponatremia are cerebral salt wasting syndrome (CSW) and inappropriate secretion of antidiuretic hormone (SIADH). Distinction between these two syndromes is difficult and is based on the assessment of the patient's volume status. In case of CSW, the volume status is low and the treatment is fluid and sodium replacement. In case of SIADH the volume status is normal or slightly expanded and the treatment is fluid restriction. To avoid centropontine myelinolysis, the speed of correction should not exceed 8 to 10 mmol/L over a 24-hour period. This article will describe practical tools to differentiate CSW from SIADH and therapeutic strategies useful in daily clinical practice.

BACKGROUND: nitric oxide (NO) plays an important role in the regulation of cardiovascular and glucose homeostasis. Mice lacking the gene encoding the neuronal isoform of nitric oxide synthase (nNOS) are insulin-resistant, but the underlying mechanism is unknown. nNOS is expressed in skeletal muscle tissue where it may regulate glucose uptake. Alternatively, nNOS driven NO synthesis may facilitate skeletal muscle perfusion and substrate delivery. Finally, nNOS dependent NO in the central nervous system may facilitate glucose disposal by decreasing sympathetic nerve activity. METHODS: in nNOS null and control mice, we studied whole body glucose uptake and skeletal muscle blood flow during hyperinsulinaemic clamp studies in vivo and glucose uptake in skeletal muscle preparations in vitro. We also examined the effects of alpha-adrenergic blockade (phentolamine) on glucose uptake during the clamp studies. RESULTS: as expected, the glucose infusion rate during clamping was roughly 15 percent lower in nNOS null than in control mice (89 (17) vs 101 (12) [-22 to -2]). Insulin stimulation of muscle blood flow in vivo, and intrinsic muscle glucose uptake in vitro, were comparable in the two groups. Phentolamine, which had no effect in the wild-type mice, normalised the insulin sensitivity in the mice lacking the nNOS gene. CONCLUSIONS: insulin resistance in nNOS null mice was not related to defective insulin stimulation of skeletal muscle perfusion and substrate delivery or insulin signaling in the skeletal muscle cell, but to a sympathetic alpha-adrenergic mechanism.

Studies of high-altitude populations, and in particular of maladapted subgroups, may provide important insight into underlying mechanisms involved in the pathogenesis of hypoxemia-related disease states in general. Over the past decade, studies involving short-term hypoxic exposure have greatly advanced our knowledge regarding underlying mechanisms and predisposing events of hypoxic pulmonary hypertension. Studies in high altitude pulmonary edema (HAPE)-prone subjects, a condition characterized by exaggerated hypoxic pulmonary hypertension, have provided evidence for the central role of pulmonary vascular endothelial and respiratory epithelial nitric oxide (NO) for pulmonary artery pressure homeostasis. More recently, it has been shown that pathological events during the perinatal period (possibly by impairing pulmonary NO synthesis), predispose to exaggerated hypoxic pulmonary hypertension later in life. In an attempt to translate some of this new knowledge to the understanding of underlying mechanisms and predisposing events of chronic hypoxic pulmonary hypertension, we have recently initiated a series of studies among high-risk subpopulations (experiments of nature) of high-altitude dwellers. These studies have allowed to identify novel risk factors and underlying mechanisms that may predispose to sustained hypoxic pulmonary hypertension. The aim of this article is to briefly review this new data, and demonstrate that insufficient NO synthesis/bioavailability, possibly related in part to augmented oxidative stress, may represent an important underlying mechanism predisposing to pulmonary hypertension in high-altitude dwellers.

Studies of high-altitude populations, and in particular of maladapted subgroups, may provide important insight into underlying mechanisms involved in the pathogenesis of hypoxemia-related disease states in general. Over the past decade, studies involving short-term hypoxic exposure have greatly advanced our knowledge regarding underlying mechanisms and predisposing events of hypoxic pulmonary hypertension. Studies in high altitude pulmonary edema (HAPE)-prone subjects, a condition characterized by exaggerated hypoxic pulmonary hypertension, have provided evidence for the central role of pulmonary vascular endothelial and respiratory epithelial nitric oxide (NO) for pulmonary artery pressure homeostasis. More recently, it has been shown that pathological events during the perinatal period (possibly by impairing pulmonary NO synthesis), predispose to exaggerated hypoxic pulmonary hypertension later in life. In an attempt to translate some of this new knowledge to the understanding of underlying mechanisms and predisposing events of chronic hypoxic pulmonary hypertension, we have recently initiated a series of studies among high-risk subpopulations (experiments of nature) of high-altitude dwellers. These studies have allowed to identify novel risk factors and underlying mechanisms that may predispose to sustained hypoxic pulmonary hypertension. The aim of this article is to briefly review this new data, and demonstrate that insufficient NO synthesis/bioavailability, possibly related in part to augmented oxidative stress, may represent an important underlying mechanism predisposing to pulmonary hypertension in high-altitude dwellers.

Obesity and insulin resistance are reaching epidemic proportions worldwide. Over the past decade, nitric oxide (NO) has emerged as a key player in the regulation of the metabolic and cardiovascular homeostasis. Here we will review recent data obtained in mice with disruption of the genes encoding for each of the three nitric oxide synthase isoforms. These data demonstrate that both defective and augmented NO synthesis have detrimental effects on the regulation of the metabolic and cardiovascular system. These observations provide the rationale for the use of NO-donors and/or inhibitors of NO overproduction in the treatment of insulin resistance.

Pulmonary embolism (PE) is a frequent pathology, the mortality of which remains elevated despite the efficacy of anticoagulation. This is mainly due to diagnostic difficulty, resulting from the low sensibility and specificity of clinical signs and routine exams in PE. The best diagnostic approach relies on decision making algorithms based on the determination of a clinical probability, which in turn dictates the choice of specialized exams (C-scan/scintigraphy, venous duplex, angiography and D-dimers). Risk stratification, which is based on the presence of hemodynamic alterations (right ventricular dysfunction, shock) is essential to guide therapy. In case of shock (massive embolism), treatment relies on systemic thrombolysis. In the presence of right ventricular dysfunction without shock (sub-massive embolism), the advantage of thrombolysis over anticoagulation alone has not been clearly demonstrated. In all other cases, as long as no contraindication exists, therapeutic anticoagulation with heparin must be initiated as soon as PE is suspected, since the mortality of this condition is highest in the two first hours following presentation.

BACKGROUND: Pulmonary edema results from a persistent imbalance between forces that drive water into the air space and the physiologic mechanisms that remove it. Among the latter, the absorption of liquid driven by active alveolar transepithelial sodium transport has an important role; a defect of this mechanism may predispose patients to pulmonary edema. Beta-adrenergic agonists up-regulate the clearance of alveolar fluid and attenuate pulmonary edema in animal models. METHODS: In a double-blind, randomized, placebo-controlled study, we assessed the effects of prophylactic inhalation of the beta-adrenergic agonist salmeterol on the incidence of pulmonary edema during exposure to high altitudes (4559 m, reached in less than 22 hours) in 37 subjects who were susceptible to high-altitude pulmonary edema. We also measured the nasal transepithelial potential difference, a marker of the transepithelial sodium and water transport in the distal airways, in 33 mountaineers who were prone to high-altitude pulmonary edema and 33 mountaineers who were resistant to this condition. RESULTS: Prophylactic inhalation of salmeterol decreased the incidence of high-altitude pulmonary edema in susceptible subjects by more than 50 percent, from 74 percent with placebo to 33 percent (P=0.02). The nasal potential-difference value under low-altitude conditions was more than 30 percent lower in the subjects who were susceptible to high-altitude pulmonary edema than in those who were not susceptible (P