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Objective: Candidaemia is a life-threatening infectious disease, associated with septic shock, multiple organ failure, and a high mortality rate. In France, reported data on the incidence of ICU-acquired candidaemia and the causative Candida species are scarce. The objective of this study was to determine temporal trends in epidemiology and risk factors of intensive care unit-acquired candidaemia (ICU-Cand) and ICU mortality among a very large population of ICU patients., Method: Demographics, patient risk factors, invasive device exposure and nosocomial infection in ICU patient were collected from 2004 to 2013 in a national network of 213 ICUs: REA-RAISIN. Incidence and risk factors for candidaemia and ICU mortality were assessed., Results: Out of 246,459 ICU patients, 851 developed an ICU-cand, representing 0.3 per 1000 patients-days. The incidence rose sharply over time. Candida albicans was the main species. The overall and ICU mortality was 52.4% in ICU-cand patients. The main risk factors of ICU-cand were length of stay, severity of illness and antimicrobial therapy at ICU admission, immune status and use of invasive procedure. ICU-cand was an independent risk factor of mortality (OR: 1.53; 95%CI [1.40-1.70]); in a sub-group analysis, independent effects on mortality were observed with C. albicans (OR: 1.45 [1.23-1.71]), Candida tropicalis (OR: 2.11 [1.31-3.39]) and "other" Candida species (OR: 1.64 [1.09-2.45])., Conclusion: ICU candidaemia ranked sixth among bloodstream infections, and its average annual incidence was 0.3 per 1000 patients days. Despite of new therapy and international recommendation, the incidence rose sharply during the study period, and ICU mortality remained high., (Copyright © 2017 The British Infection Association. Published by Elsevier Ltd. All rights reserved.)

Objective: To evaluate whether different indicators using for guiding volume expansion are valuable tools to assess edematous lung injury in patients with septic shock., Design and Setting: Prospective observational clinical study in a university intensive care unit., Patients: Sixteen consecutive mechanically ventilated patients developing septic shock with evidence of pulmonary edema on chest radiograph and severe hypoxemia (PaO(2)/FIO(2) <250 mmHg)., Measurements and Results: A pulmonary artery catheter was used for the measurement of cardiac index (CI), central venous pressure (CVP), and pulmonary artery occlusion pressure (PAOP). A fiberoptic catheter was placed in the descending aorta. Measurements of extravascular lung water index (EVLWI), intrathoracic blood volume index (ITBVI), and total end-diastolic volume index (TEDVI) were obtained using the thermal dye dilution technique. Measurements were taken just after placement of catheters and 24 h later. Fluid balance was also estimated within the first 24 h. TEDVI and ITBVI were significantly correlated with EVLWI, but not CVP and PAOP. Analysis of 24-h changes showed that the changes in TEDVI and in ITBVI reflected the change in EVLWI, whereas PAOP, CVP, and fluid balance did not., Conclusions: Volume variables (TEDVI, ITBVI) are more useful indicators than pressure variables (CVP, PAOP) for assessment of EVLWI in septic patients with pulmonary edema.

Vascular endothelial growth factor (VEGF) is a potent endothelial cell growth and permeability factor highly expressed in rodent alveolar epithelium after injury and repair. To investigate VEGF synthesis in human lung epithelial cells, we examined VEGF expression by cultured cells under basal conditions and after cytokine treatment or oxidative stress. Basal VEGF expression was detected in transformed human epithelial cell lines (A549 and 1HAEo-) and in primary human bronchial epithelial cells with RT-PCR, Western blot, and immunocytochemistry. Among the cytokines tested, only transforming growth factor-beta1 increased the levels of excreted VEGF(165) as measured by ELISA. Under hypoxia (0% O(2) for 24 h), the VEGF(165) level increased fivefold, and this effect was O(2) concentration dependent. VEGF concentrations in the medium of all the cell types studied reached values similar to those found in bronchoalveolar lavage fluids from normal patients. Endothelial cells (human umbilical vein endothelial cells) exposed to conditioned medium from primary bronchial epithelial cell cultures showed an increased growth rate, which was inhibited in the presence of a specific neutralizing antibody to VEGF. These results suggest that lung epithelial cells participate in the endothelial repair and angiogenesis that follow lung injury through the synthesis of VEGF.

In mechanically ventilated patients with acute circulatory failure related to sepsis, we investigated whether the respiratory changes in arterial pressure could be related to the effects of volume expansion (VE) on cardiac index (CI). Forty patients instrumented with indwelling systemic and pulmonary artery catheters were studied before and after VE. Maximal and minimal values of pulse pressure (Pp(max) and Pp(min)) and systolic pressure (Ps(max) and Ps(min)) were determined over one respiratory cycle. The respiratory changes in pulse pressure (DeltaPp) were calculated as the difference between Pp(max) and Pp(min) divided by the mean of the two values and were expressed as a percentage. The respiratory changes in systolic pressure (DeltaPs) were calculated using a similar formula. The VE-induced increase in CI was >/= 15% in 16 patients (responders) and < 15% in 24 patients (nonresponders). Before VE, DeltaPp (24 +/- 9 versus 7 +/- 3%, p < 0.001) and DeltaPs (15 +/- 5 versus 6 +/- 3%, p < 0.001) were higher in responders than in nonresponders. Receiver operating characteristic (ROC) curves analysis showed that DeltaPp was a more accurate indicator of fluid responsiveness than DeltaPs. Before VE, a DeltaPp value of 13% allowed discrimination between responders and nonresponders with a sensitivity of 94% and a specificity of 96%. VE-induced changes in CI closely correlated with DeltaPp before volume expansion (r(2) = 0. 85, p < 0.001). VE decreased DeltaPp from 14 +/- 10 to 7 +/- 5% (p < 0.001) and VE-induced changes in DeltaPp correlated with VE-induced changes in CI (r(2) = 0.72, p < 0.001). It was concluded that in mechanically ventilated patients with acute circulatory failure related to sepsis, analysis of DeltaPp is a simple method for predicting and assessing the hemodynamic effects of VE, and that DeltaPp is a more reliable indicator of fluid responsiveness than DeltaPs.

Normobaric oxygen toxicity is well described in all animal species. However susceptibility to oxygen exposure is highly variable according to age, species and strains. Similarly in humans, prolonged high oxygen exposure is reported to induce cough, shortness of breath, decrease vital capacity and increase alveolo-capillary permeability. The toxic FIO2 threshold (length of exposure and level) is still debated. In patients with previous lung injury, this threshold is even more difficult to delineate as pathologic pulmonary lesions might result from hyperoxia or primary lung insult. Oxygen free-radicals play a key role in the pathophysiology of oxygen toxicity. Oxygen resistance or tolerance is obtained with intraperitoneal, intravenous and intratracheal endotoxin or cytokines administration. Previous exposure to high oxygen concentration is also reported to increase survival rate and decrease pulmonary lesions in animal models. Protection may rely on antioxidant enzymes synthesis, nitric oxide production, neutrophils recruitment and modulation of alveolar macrophages activity. In humans, oxygen tolerance might be suspected through several clinical studies reporting favorable outcome after long term-oxygen exposure. Better knowledge of the risks of prolonged high oxygen exposure is important to re-evaluate the goals of mechanical ventilation (FIO2, SaO2, PEEP) and/or to develop treatments to prevent oxygen toxicity (surfactant, antioxidant enzymes).

At the Symposium entitled "Health, Culture, and Quality of Life" held in Hanoi in 1993, the authors of this report met the physicians in charge of the Traditional Medicine Institute of Hanoi which works with the World Health Organization for traditional medicine. After an historical overview of the foundation of this center providing research, care, and training under the auspices of the Hanoi School of Medicine, Professor Hoang Bao Chau described a practice based on revision of ancestral traditions in accordance with scientific methods, the resulting synthesis being up-to-date yet in keeping with heritage. This novel and pragmatic approach, which takes into account the complexity of man, offers an opportunity to reflect on the current status of medical practices in the world and on their adaptation to each population at a time when the experience of the Other seems almost impossible to communicate.

The purely technologic realm of modern medicine is not, at first glance, compatible with the expectations of populations that still considered disease to have a magical dimension. The gap is obvious between physicians and patients coming from different cultures but it can also be detected even when the two parties are from the same background. This medico-cultural conflict is probably one of the main causes of resistance, reticence, omissions, and disappointments that have hindered efforts to better public health. Improvement of individual well-being and sanitary conditions depends not only on available facilities but also on the mentality of those that implement their use. Cultural context should be given serious consideration in strategic decision-making. More extensive use of quality-of-life surveys could be helpful in this regard.