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International audience; Air pollution is a public health issue and the toxicity of ambient particulate matter (PM) is well-recognized. Although it does not mostly contribute to the total mass of PM, increasing evidence indicates that the ultrafine fraction has generally a greater toxicity than the others do. A better knowledge of the underlying mechanisms involved in the pathological disorders related to nanoparticles (NPs) remains essential. Hence, the goal of this study was to determine better whether the exposure to a relatively low dose of well-characterized iron-rich NPs (Fe-NPs) might alter some critical toxicological endpoints in a relevant primary culture model of human bronchial epithelial cells (HBECs). We sought to use Fe-NPs representative of those frequently found in the industrial smokes of metallurgical industries. After having noticed the effective internalization of Fe-NPs, oxidative, inflammatory, DNA repair, and apoptotic endpoints were investigated within HBECs, mainly through transcriptional screening. Taken together, these results revealed that, despite it only produced relatively low levels of reactive oxygen species without any significant oxidative damage, low-dose Fe-NPs quickly significantly deregulated the transcription of some target genes closely involved in the proinflammatory response. Although this inflammatory process seemed to stay under control over time in case of this acute scenario of exposure, the future study of its evolution after a scenario of repeated exposure could be very interesting to evaluate the toxicity of Fe-NPs better. K E Y W O R D S gene expression profiling, human bronchial epithelial cells, inflammation, iron nanoparticles, oxidative stress, physicochemical characterization 1 | INTRODUCTION Air pollution still constitutes the major threat to human health, whereas the adverse impacts and the underlying mechanisms of air pollution-derived particulate matter (PM) are not clearly defined

In December 2019, in Wuhan, a new human infectious pathology was born, COVID-19, consisting above all in pneumoniae, induced by the coronavirus named SARS-CoV-2 because of the respiratory distress it caused (SARS for severe acute respiratory syndrome, and CoV for Coronavirus). A real health and planetary crisis has appeared, much more substantial than that linked to SARS-CoV-1 in 2002-2004 and to MERS-CoV (Middle East Respiratory Syndrome Coronavirus) in 2012. In addition to respiratory damage that can be dramatic, this pathology is complicated by the frequency of cardiovascular, renal and coagulation diseases. Health care systems have had to adapt urgently, in the absence of hindsight from the pathology, and without effective therapeutic weapons. Through this review of the literature, we detail our local practices for the overall management of patients hospitalized in Intensive care.En décembre 2019, à Wuhan, une nouvelle pathologie infectieuse humaine est née, le COVID-19, consistant avant tout en une pneumonie, induite par le coronavirus nommé SARS-CoV-2 en lien avec l’intensité de la détresse respiratoire qu’il entraîne (SARS pour syndrome respiratoire aigu sévère, et CoV pour coronavirus). Une véritable crise sanitaire et planétaire est apparue, bien plus conséquente que celle liée au SARS-CoV-1 en 2002-2004 et au MERS-CoV (Middle East Respiratory Syndrome Coronavirus) en 2012. Outre une atteinte respiratoire pouvant être dramatique, cette pathologie est complexifiée par la fréquence des atteintes cardiovasculaires, rénales et de la coagulation. Les systèmes de soins de santé ont dû s’adapter urgemment, en l’absence de recul face à la pathologie, et sans armes thérapeutiques efficaces. Au travers de cette revue de la littérature, nous détaillons nos pratiques locales pour la prise en charge globale des patients hospitalisés aux Soins intensifs.

Air pollution and particulate matter (PM) are classified as carcinogenic to humans. Pollutants evidence for public health concern include coarse (PM10) and fine (PM2.5) particles. However, ultrafine particles (PM0.1) are assumed to be more toxic than larger particles, but data are still needed to better understand their mechanism of action. In this context, the aim of our work was to investigate the in vitro and in vivo genotoxic potential of fine (PM2.5-018) and quasi ultra-fine (PM0.18) particles from an urban-industrial area (Dunkirk, France) by using comet, micronucleus and/or gene mutation assays. In vitro assessment was performed with 2 lung immortalized cell lines (BEAS-2B and NCI-H292) and primary normal human bronchial epithelial cells (NHBE) grown at the air-liquid interface or in submerged conditions (5 µg PM/cm2). For in vivo assessment, tests were performed after acute (24 h, 100 µg PM/animal), subacute (1 month, 10 µg PM/animal) and subchronic (3 months, 10 µg PM/animal) intranasal exposure of BALB/c mice. In vitro, our results show that PM2.5-018 and PM0.18 induced primary DNA damage but no chromosomal aberrations in immortalized cells. Negative results were noted in primary cells for both endpoints. In vivo assays revealed that PM2.5-018 and PM0.18 induced no significant increases in DNA primary damage, chromosomal aberrations or gene mutations, whatever the duration of exposure. This investigation provides initial answers regarding the in vitro and in vivo genotoxic mode of action of PM2.5-018 and PM0.18 at moderate doses and highlights the need to develop standardized specific methodologies for assessing the genotoxicity of PM. Moreover, other mechanisms possibly implicated in pulmonary carcinogenesis, e.g. epigenetics, should be investigated.

Nowadays ambient particulate matter (PM) levels still regularly exceed the guideline values established by World Health Organization in most urban areas. Numerous experimental studies have already demonstrated the airway toxicity of the fine fraction of PM (FP), mainly triggered by oxidative stress-induced airway inflammation. However, only few studies have actually paid close attention to the ultrafine fraction of PM (UFP), which is likely to be more easily internalized in cells and more biologically reactive. Mitochondria are major endogenous sources of reactive oxygen species (ROS) through oxidative metabolism, and coordinate many critical cellular signaling processes. Mitochondria have been often studied in the context of PM toxicity and generally associated with apoptosis activation. However, little is known about the underlying adaptation mechanisms that could occur following exposure at sub-apoptotic doses of ambient PM. Here, normal human bronchial epithelial BEAS-2B cells were acutely or repeatedly exposed to relatively low doses (5 µg.cm

Since its first description in 1967, a lot of progress has been made in understanding the pathophysiology, diagnosis and management of acute respiratory distress syndrome (ARDS). This nosological entity is based on the appearance of a diffuse alveolar damage associating pulmonary epithelial barrier disruption with an alveolar filling, both responsible of profound hypoxemia and important morbi-mortality. Nowadays, ARDS remains a frequent syndrome, associated with various etiologies. Diagnosis is based on the occurrence of acute hypoxic respiratory failure not explained by cardiac insufficiency or volume overload, within 7 days after a recognized risk factor, and in the presence of bilateral pulmonary opacities not fully explained by effusions, atelectasis or nodules on the chest radiography. Survivors present an increased risk of developing cognitive decline, depression, post-traumatic stress, and typical ICU related side-effects such as polyneuropathy and sarcopenia. In this context and not withstanding significant recent progress in the field of mechanical ventilation and extra-corporeal respiratory assistance, early diagnosis remains essential to identify patients with ARDS in order to offer them the most appropriate therapy.Depuis sa première description en 1967, des progrès majeurs ont été réalisés dans la compréhension de la physiopathologie, le diagnostic et la prise en charge du syndrome de détresse respiratoire aiguë (SDRA). Cette entité nosologique repose sur l’apparition d’un dommage alvéolaire diffus associant une rupture de la barrière épithéliale pulmonaire avec un comblement alvéolaire à l’origine d’une hypoxémie profonde. De nos jours, le SDRA reste un syndrome fréquent, grevé d’une mortalité élevée, et prenant source dans de multiples situations pathologiques. Le diagnostic du SDRA repose sur l’apparition d’une insuffisance respiratoire aiguë hypoxique non expliquée par une insuffisance cardiaque ou une surcharge volémique, dans un délai de 7 jours suivant l’apparition d’un facteur de risque reconnu, en présence d’opacités pulmonaires bilatérales non complètement expliquées par des épanchements, des atélectasies ou des nodules. Les survivants sont à haut risque de développer un déclin cognitif, une dépression, ou un stress post-traumatique en plus des effets secondaires classiques d’une longue hospitalisation en unité de soins intensifs que sont la polyneuropathie ou la sarcopénie. Dans ce contexte, et en dépit de progrès importants dans le domaine de la ventilation mécanique et de l’assistance respiratoire par circulation extra-corporelle, il reste primordial d’identifier précocement les patients souffrant de SDRA afin de leur proposer la thérapeutique la plus appropriée dès les premiers signes cliniques.

Air pollution and particulate matter (PM) are classified as carcinogenic to humans. Pollutants evidence for public health concern include coarse (PM

The knowledge of the underlying mechanisms by which particulate matter (PM) exerts its health effects is still incomplete since it may trigger various symptoms as some persons may be more susceptible than others. Detailed studies realized in more relevant in vitro models are highly needed. Healthy normal human bronchial epithelial (NHBE), asthma-diseased human bronchial epithelial (DHBE), and COPD-DHBE cells, differentiated at the air-liquid interface, were acutely or repeatedly exposed to fine (i.e., PM

The effects of iron nanoparticles on bryophytes (Physcomitrella patens) were studied following foliar exposure. We used iron nanoparticles (Fe–NP) representative of industrial emissions from the metallurgical industries. After a characterization of iron nanoparticles and the validation of nanoparticle internalization in cells, the effects (cytotoxicity, oxidative stress, lipid peroxidation of membrane) of iron nanoparticles were determined through the axenic culturing of Physcomitrella patens exposed at five different concentrations (5 ng, 50 ng, 500 ng, 5 µg and 50 µg per plant). Following exposure, the plant health, measured as ATP concentrations, was not impacted. Moreover, we studied oxidative stress in three ways: through the measure of reactive oxygen species (ROS) production, through malondialdehyde (MDA) production and also through glutathione regulation. At concentrations tested over a short period, the level of ROS, MDA and glutathione were not significantly disturbed.

International audience

The knowledge of the underlying mechanisms by which particulate matter (PM) exerts its health effects is still incomplete since it may trigger various symptoms as some persons may be more susceptible than others. Detailed studies realized in more relevant in vitro models are highly needed. Healthy normal human bronchial epithelial (NHBE), asthma-diseased human bronchial epithelial (DHBE), and COPD-DHBE cells, differentiated at the air-liquid interface, were acutely or repeatedly exposed to fine (i.e., PM2.5-0.18, also called FP) and quasi-ultrafine (i.e., PM0.18, also called UFP) particles. Immunofluorescence labelling of pan-cytokeratin, MUC5AC, and ZO-1 confirmed their specific cell-types. Baselines of the inflammatory mediators secreted by all the cells were quite similar. Slight changes of TNFα, IL-1β, IL-6, IL-8, GM-CSF, MCP-1, and/or TGFα, and of H3K9 histone acetylation supported a higher inflammatory response of asthma- and especially COPD-DHBE cells, after exposure to FP and especially UFP. At baseline, 35 differentially expressed genes (DEG) in asthma-DHBE, and 23 DEG in COPD-DHBE, compared to NHBE cells, were reported. They were involved in biological processes implicated in the development of asthma and COPD diseases, such as cellular process (e.g., PLA2G4C, NLRP1, S100A5, MUC1), biological regulation (e.g., CCNE1), developmental process (e.g., WNT10B), and cell component organization and synthesis (e.g., KRT34, COL6A1, COL6A2). In all the FP or UFP-exposed cell models, DEG were also functionally annotated to the chemical metabolic process (e.g., CYP1A1, CYP1B1, CYP1A2) and inflammatory response (e.g., EREG). Another DEG, FGF-1, was only down-regulated in asthma and specially COPD-DHBE cells repeatedly exposed. While RAB37 could help to counteract the down-regulation of FGF-1 in asthma-DHBE cells, the deregulation of FGR, WNT7B, VIPR1, and PPARGC1A could dramatically contribute to make it worse in COPD-DHBE cells. Taken together, these data contributed to support the highest effects of UFP versus FP and highest sensitivity of asthma- and notably COPD-DHBE versus NHBE cells.

Training in ultrasound techniques for intensive care medicine physicians should aim at achieving competencies in three main areas: (1) general critical care ultrasound (GCCUS), (2) "basic" critical care echocardiography (CCE), and (3) advanced CCE. A group of 29 experts representing the European Society of Intensive Care Medicine (ESICM) and 11 other critical care societies worldwide worked on a potential framework for organizing training adapted to each area of competence. This framework is mainly aimed at defining minimal requirements but is by no means rigid or restrictive: each training organization can be adapted according to resources available. There was 100% agreement among the participants that general critical care ultrasound and "basic" critical care echocardiography should be mandatory in the curriculum of intensive care unit (ICU) physicians. It is the role of each critical care society to support the implementation of training in GCCUS and basic CCE in its own country.

The present study reports a case of biopsy-proven pulmonary veno-occlusive disease as a cause of severe pulmonary hypertension in a patient suffering from a chronic myeloproliferative disorder. The pulmonary disease evolved favourably under treatment with defibrotide, a pro-fibrinolytic medication used in hepatic veno-occlusive disease.

Iron nanoparticles (nFe) prepared by vaporization and cryogenic condensation process (10–100 nm) has been exposed to Hank's balanced salt solution (HBSS) and the B-Ali cell growth fluids. These media can be used for cellular growth to study nFe penetration through cell membrane and its induced cytotoxicity. Surface chemistry of nFe exposed to such complex fluids has been characterized as the nanoparticles surface can be strongly changed by adsorption or corrosion processes before reaching intracellular medium. Particle size and surface chemistry have been characterized by scanning electron microscopy (SEM) and high-resolution X-ray photoelectron spectroscopy (HR-XPS). Exposition of nFe particles to growth and differentiation media leads to the formation of an oxy-hydroxide layer containing chlorinated species. We found that the passivated Fe2O3 layer of the bare nFe particles is rapidly transformed into a thicker oxy-hydroxide layer that has a greater ability to adsorb molecular ions or ionic biomolecules like proteins or DNA.

Iron nanoparticles were produced in a radiofrequency levitation furnace and their dimensions and purity determined by scanning electron microscopy and x-ray microanalysis. Confocal microscopy revealed that these particles penetrated the leaves of Aphanorrhegma when applied to the plants as mineral water suspensions. This, the first demonstration of nanoparticle uptake by a bryophyte, opens the way to nanotoxicological studies paralleling those in higher plants. The actual penetration mechanism in both groups remains unknown.

A 65-year-old man was scheduled for an on-pump coronary artery bypass graft procedure because of a three-vessels coronary artery disease. A right atrial mass appended to the interatrial septum was discovered during intraoperative transoesophageal echocardiography. Therefore, the right atrium was opened. Gross examination revealed a fatty lesion of the interatrial septum. A biopsy was performed before the atrium was closed. A histological diagnosis of lipomatous hypertrophy of the interatrial septum was made. Lipomatous hypertrophy of the interatrial septum is a mass of adipocytes infiltrating the interatrial septum. The aspect of "dumbbell" produced by the sparing of the Fossa Ovalis is typical. The lesion is benign and remains asymptomatic most of the time although it can be responsible for cardiac arrhythmias or circulatory obstruction. The typical echographic aspect should be known to avoid unnecessary surgical resection.

ExtraCorporeal Membrane Oxygenation (ECMO) is a cardiopulmonary assistance device able to support patients in cardiac arrest, refractory cardiogenic shock or refractory hypoxemia otherwise sentenced to death. Recent technical progresses, early indication decision, bedside multidisciplinary implant, specific complications screening and echocardiographic weaning testing are crucial points to allow success of this exceptional technique.

We report a case of pneumopericardium occuring after cardiac surgery. Pneumopericardium is a rare condition; trauma is the most frequent etiology. Nontraumatic causes include fistulae in relationship with the bronchial tree or oesophagus and intrapericardial gazeous production due to bacterial pericarditis. Pericardiocentesis is indicated in case of air tamponade and local infection.

We report the case of a 67-year-old patient who presented with a myelodysplastic syndrome and who developed a pulmonary mucormycosis with a rare extension to the dorsal spine. A decompressive laminectomy was attempted after failure of broad-spectrum antifungal treatment (Cancidas, V-Fend). The diagnosis was obtained after surgical biopsy. The scheduled lobectomy could not be performed because of altered clinical condition. The patient eventually died despite adapted antifungal treatment (Abelcet, Posaconazole). Pulmonary mucormycosis is a rare cause of mycotic infection that reaches most of the time immunocompromised patients. The pathogenic agent is part of zygomyces that have angio-invasive ability. Perineural propagation was recently described. Immunodepression, late diagnosis and lack of response to new generation antifungal drugs (V-Fend, Cancidas) are responsible for therapeutic failure in this disease. This case emphasizes the risk inherent to empirical antifungal treatment and the need of early biopsy in cases that do not respond to treatment.

Over the last ten years, much progress has been achieved in intensive care medicine. Large randomized studies, most often their multicentric, were performed and their results were translated into rules to be followed for the most appropriate treatment of life-threatening organ failures. The place of non-invasive ventilation in the management of hypercapnic or hypoxic respiratory insufficiencies was thus defined, and the methods for less traumatic mechanical ventilation were specified. The techniques of renal replacement therapy were compared and the optimal doses of dialysis or hemofiltration were established. The metabolic support of the patients was also altered following landmark studies, such as the management of blood glucose, which deeply influenced the approach to critically ill patients.

We report the case of a 31-year-old woman who died in a context of haemophagocytic syndrome with multiple opportunist infections:viral, mycobacterial and fungal. To our knowledge, this is the tenth case of invasive aspergillosis manifested by an aspergillus pericarditis with cardiac tamponade. Search for HIV infection, neoplasia, haematological malignancies was negative. In addition, the patient carried on a nonviral, non-ethylic cirrhosis, the etiology of which remained unknow. We will particularly develop the aspergillus pericarditis with cardiac tamponade and the haemophagocytic syndrome.

A case of dilated ischemic cardiomyopathy, with severely impaired left ventricular systolic function, treated by endoventriculoplasty and CABG, is reported. The authors discuss the modern concepts regarding the surgical treatment of large anterior asynergic scars following occlusion of the LAD. Since there are more similarities between akinesia and dyskinesia than previously thought, the endoventriculoplasty of DOR may constitute a new way to surgically remodel the left ventricle in dilated cardiomyopathies with large anterior akinesia. This surgery significantly improves the ventricular function and the overall patients' prognosis at short and mid term follow up.

With the emergence of rapid extubation protocols following cardiac surgery, providing adequate analgesia in the early postoperative period is important. This prospective randomised double-blind study investigated the benefits of pre-operative intrathecal administration of low dose morphine in patients undergoing coronary artery bypass graft surgery. Postoperative analgesia, pulmonary function, stress response and postoperative recovery profile were assessed. Thirty patients were allocated into two groups, receiving either 500 mug of morphine intrathecally prior to anaesthesia and intravenous patient-controlled analgesia with morphine postoperatively following tracheal extubation, or only postoperative intravenous patient-controlled analgesia. In the intrathecal group, the total consumption of intravenous morphine following surgery was significantly reduced by 40% and patients reported lower pain scores at rest, during the first 24 h following extubation. Peak expiratory flow rate was greater and postoperative catecholamine release was significantly lower. Patients in the control group had a higher incidence of reduced respiratory rate following extubation.

We report two cases of "fulminant" endocarditis due to Staphyloccoccus aureus. In both cases, the echocardiographic and bacteriologic diagnosis was esthablished in a clinical picture of severe sepsis and thrombocytopenia evolving after a fever of less than 3 days duration.

Portal venous gas is a rare radiological symptom related to several possible causes. Its severity is only correlated with the severity of the primary disease. We report the case of a portal pneumatose. The diagnosis was made by ultrasound and CT scan.

We discuss two cases of abdominal candidiasis in critically ill patients with multiple organ failure and sepsis. Microbiological and clinical courses remained unresponsive to apparently appropriate antifungal therapy with azole or polyene derivatives. Both microbiological and clinical outcomes dramatically improved after starting caspofungin therapy. Lack of cross-resistance, lack of toxicity and potent fungicidal activity make caspofungin a very attractive drug in life threatening abdominal candidiasis. The optimal treatment of life threatening candidiasis remains a controversial issue. Because of recent advances in the field, we propose a critical review of the problem of refractory candidiasis.

The diagnosis of tamponade is confirmed by Doppler echocardiography. Early examination by this means is capital which implies easy access to this facility whenever the clinician suspects this condition. The diagnostic value of classical clinical and Doppler echocardiographic signs requires a model of circumferential pericardial effusion exerting compressive effects in the context of spontaneous ventilation. The underlying pathologies, assisted, ventilation, localised pericardial effusions, are responsible for over- or under-diagnostic errors.

We report the case of a massive tension-pneumoperitoneum developing immediately after starting mechanical ventilation (barotrauma). Careful analysis of CT-data provided meaningful informations in assessing the non surgical pulmonary source of pneumo peritoneum.

We report a case of severe dyskinetic syndrome, consisting of intense myoclonia movements, associated with choreiform activity involving the face and upper extremities. The abnormal movements occurred in a patient with confusion and visual hallucinations. This syndrome had an abrupt onset in a patient recovering from coronary artery bypass surgery complicated by an early post-operative cardiac arrest and acute renal failure. Dyskinesia appeared several days after intravenous administration of ranitidine for stress ulcer prophylaxis. Several etiologies were raised in this case among which were post-anoxic myoclonia and metabolic encephalopathy. Cessation of histamine receptor blocker therapy for 48 hours was associated with return of normal cognitive function and disappearance of abnormal movements. This confirmed the iatrogenic nature of the syndrome related to administration of ranitidine.

Severity scoring systems are of great interest for the intensive care physicians. They provide major objective information regarding their patients and their medical practice. Scoring systems have been regularly improved over the two last decades. The different existing systems present advantages and disadvantages which influence their use in the intensive care. These scoring systems offer a wide range of analysis, however they are often underused. In this paper we suggest recommendations that could help to maximise the information provided by these systems.

A 75 year old woman was found to have a posterior cerebellar lesion which after surgical removal was shown to be a meningioma. Her postoperative course was complicated by a MRSA meningitis and on day 23 after resection, a polyuria up to 11.7 1/24 h became apparent. The diagnosis of cerebral wasting syndrome (CSWS) was made based on biological and clinical features such as an excessive natriuresis (143 mmol/l) resulting in hyponatremia (130 mmol/l) and an osmolarity higher in urine than in blood. A low central venous pressure and a low wedge pressure confirming a volumic depletion indicated the diagnosis of CSWS. This syndrome has marked similarities with the Inappropriate Secretion of Antidiuretic Hormone Syndrome (SIADH) in terms of biological finding with regards to clinical context and presentation. Without an adequate assessment, a patient with CSWS may be misdiagnosed as SIADH. However recognition is important, as water restriction which is part of SIADH treatment, is detrimental to patients with CSWS and can possibly be lethal.