The Experts below are selected from a list of 810 Experts worldwide ranked by ideXlab platform

Arthur S. Slutsky - One of the best experts on this subject based on the ideXlab platform.

  • Lung–Kidney Cross-Talk in the Critically Ill Patient
    American journal of respiratory and critical care medicine, 2016
    Co-Authors: Faeq Husain-syed, Arthur S. Slutsky, Claudio Ronco
    Abstract:

    Discoveries have emerged highlighting the complex nature of the interorgan cross-talk between the kidney and the lung. Vascular rigidity, neurohormonal activation, tissue hypoxia, and abnormal immune cell signaling have been identified as common pathways leading to the development and progression of chronic kidney disease. However, our understanding of the causal relationships between lung injury and kidney injury is not precise. This review discusses a number of features and mechanisms of renal dysfunction in pulmonary disorders in relation to respiratory acidosis, impaired gas exchange, systemic congestion, respiratory support/replacement therapies, and other issues relevant to the clinical care of these patients. Biotrauma due to injurious ventilatory strategies can lead to the release of mediators into the lung, which may then translocate into the systemic circulation and cause end-organ dysfunction, including renal dysfunction. Right ventricular dysfunction and congestive states may contribute to alterations of renal perfusion and oxygenation, leading to diuretic resistance and recurrent hospitalization. In patients with concomitant respiratory failure, noninvasive ventilation represents a promising treatment option for the correction of impaired renal microcirculation and endothelial dysfunction. In patients requiring extracorporeal membrane oxygenation, short- and long-term monitoring of kidney function is warranted, as they are at highest risk of developing acute kidney injury and fluid overload.

  • Biotrauma and Ventilator-Induced Lung Injury: Clinical Implications
    Chest, 2016
    Co-Authors: Gerard F. Curley, John G. Laffey, Haibo Zhang, Arthur S. Slutsky
    Abstract:

    The pathophysiological mechanisms by which mechanical ventilation can contribute to lung injury, termed "ventilator-induced lung injury" (VILI), is increasingly well understood. "Biotrauma" describes the release of mediators by injurious ventilatory strategies, which can lead to lung and distal organ injury. Insights from preclinical models demonstrating that traditional high tidal volumes drove the inflammatory response helped lead to clinical trials demonstrating lower mortality in patients who underwent ventilation with a lower-tidal-volume strategy. Other approaches that minimize VILI, such as higher positive end-expiratory pressure, prone positioning, and neuromuscular blockade have each been demonstrated to decrease indices of activation of the inflammatory response. This review examines the evolution of our understanding of the mechanisms underlying VILI, particularly regarding Biotrauma. We will assess evidence that ventilatory and other "adjunctive" strategies that decrease Biotrauma offer great potential to minimize the adverse consequences of VILI and to improve the outcomes of patients with respiratory failure.

  • Ventilator-induced lung injury. Similarity and differences between children and adults.
    American journal of respiratory and critical care medicine, 2014
    Co-Authors: Martin C. J. Kneyber, Haibo Zhang, Arthur S. Slutsky
    Abstract:

    It is well established that mechanical ventilation can injure the lung, producing an entity known as ventilator-induced lung injury (VILI). There are various forms of VILI, including volutrauma (i.e., injury caused by overdistending the lung), atelectrauma (injury due to repeated opening/closing of lung units), and Biotrauma (release of mediators that can induce lung injury or aggravate pre-existing injury, potentially leading to multiple organ failure). Experimental data in the pediatric context are in accord with the importance of VILI, and appear to show age-related susceptibility to VILI, although a conclusive link between use of large Vts and mortality has not been demonstrated in this population. The relevance of VILI in the pediatric intensive care unit population is thus unclear. Given the physiological and biological differences in the respiratory systems of infants, children, and adults, it is difficult to directly extrapolate clinical practice from adults to children. This Critical Care Perspec...

  • Novel approaches to minimize ventilator-induced lung injury
    BMC medicine, 2013
    Co-Authors: Eddy Fan, Jesús Villar, Arthur S. Slutsky
    Abstract:

    Despite over 40 years of research, there is no specific lung-directed therapy for the acute respiratory distress syndrome (ARDS). Although much has evolved in our understanding of its pathogenesis and factors affecting patient outcome, supportive care with mechanical ventilation remains the cornerstone of treatment. Perhaps the most important advance in ARDS research has been the recognition that mechanical ventilation, although necessary to preserve life, can itself aggravate or cause lung damage through a variety of mechanisms collectively referred to as ventilator-induced lung injury (VILI). This improved understanding of ARDS and VILI has been important in designing lung-protective ventilatory strategies aimed at attenuating VILI and improving outcomes. Considerable effort has been made to enhance our mechanistic understanding of VILI and to develop new ventilatory strategies and therapeutic interventions to prevent and ameliorate VILI with the goal of improving outcomes in patients with ARDS. In this review, we will review the pathophysiology of VILI, discuss a number of novel physiological approaches for minimizing VILI, therapies to counteract Biotrauma, and highlight a number of experimental studies to support these concepts.

  • the contribution of biophysical lung injury to the development of Biotrauma
    Annual Review of Physiology, 2006
    Co-Authors: Claudia Dos C Santos, Arthur S. Slutsky
    Abstract:

    Patients with severe acute respiratory distress syndrome who die usually succumb to multiorgan failure as opposed to hypoxia. Despite appropriate resuscitation, some patients' symptoms persist on a downward spiral, apparently propagated by an uncontained systemic inflammatory response. This phenomenon is not well understood. However, a novel hypothesis to explain this observation proposes that it is related to the life-saving ventilatory support used to treat the respiratory failure. According to this hypothesis, mechanical ventilation per se, by altering both the magnitude and the pattern of lung stretch, can cause changes in gene expression and/or cellular metabolism that ultimately can lead to the development of an overwhelming inflammatory response-even in the absence of overt structural damage. This mechanism of injury has been termed Biotrauma. In this review we explore the Biotrauma hypothesis, the causal relationship between biophysical injury and organ failure, and its implications for the future therapy and management of critically ill patients.

Cobi Jacoba Johanna Heijnen - One of the best experts on this subject based on the ideXlab platform.

  • Ventilator-induced lung injury and multiple system organ failure: a critical review of facts and hypotheses
    Intensive Care Medicine, 2004
    Co-Authors: Frans B. Plötz, Arthur S. Slutsky, Adrianus J. Vught, Cobi Jacoba Johanna Heijnen
    Abstract:

    Objective To review how Biotrauma leads to the development of multiple system organ failure (MSOF). Design and setting Published articles on experimental and clinical studies and review articles in the English language were collected and analyzed. Results The concept that ventilation strategies using “large” tidal volumes and zero PEEP of injured lungs can enhance injury by the release of inflammatory mediators into the lungs and circulation, a mechanism that has been called Biotrauma, is supported by evidence from experimental models ranging from mechanically stressed cell systems, to isolated lungs, intact animals, and humans. Biotrauma may lead to MSOF via spillover of lung-borne inflammatory mediators into the systemic circulation. However, spillover of other agents such as bacteria and soluble proapoptotic factors may also contribute to the onset of MSOF. Other less well studied mechanisms such as peripheral immunosuppression and translocation of bacteria and/or products from the gut may play an important role. Finally, genetic variability is a crucial factor. Conclusions The development of MSOF is a multifactorial process. Our proposed mechanisms linking mechanical ventilation and MSOF suggest several novel therapeutic approaches. However, it will first be necessary to study the mechanisms described above to delineate more precisely the contribution of each proposed factor, their interrelationships, and their time course. We suggest that scientific advances in immunology may offer novel approaches for prevention of MSOF secondary to ventilator-induced lung injury.

  • ventilator induced lung injury and multiple system organ failure a critical review of facts and hypotheses
    Intensive Care Medicine, 2004
    Co-Authors: Frans B. Plötz, Arthur S. Slutsky, Adrianus J Van Vught, Cobi Jacoba Johanna Heijnen
    Abstract:

    Objective To review how Biotrauma leads to the development of multiple system organ failure (MSOF).

Frans B. Plötz - One of the best experts on this subject based on the ideXlab platform.

  • The Kidney During Mechanical Ventilation
    Critical Care Nephrology, 2019
    Co-Authors: Jan Willem Kuiper, A. B. Johan Groeneveld, Frans B. Plötz
    Abstract:

    Abstract Mechanical ventilation (MV) has been of great value in improving the survival of many patients suffering from respiratory failure. Although lifesaving in many patients, MV is associated with acute lung injury, termed ventilator-induced lung injury (VILI), and multiple organ failure including acute kidney injury (AKI). MV can triple the risk of in-hospital death in critically ill patients with AKI. MV exerts systemic hemodynamic effects through a complex interaction among intrathoracic pressure, intravascular volume, and cardiac performance. In addition, MV directly affects PaCO2 and PaO2 levels in patients. Mechanical stress caused by MV can affect cellular and molecular processes in the lung, a mechanism that has been called Biotrauma. The Biotrauma hypothesis consists of two pathways: first, mediators are released, and second, these mediators have biologic activity. Through effects on systemic hemodynamics MV can affect renal blood flow. Also effects on regulatory hormonal mechanisms may affect renal function, but more research is needed. Hypercapnia and severe hypoxemia resulting from or associated with MV have been found to correlate inversely with renal blood flow. Finally, an increasing number of mediators have been reported to increase in systemic circulation during MV and potentially may contribute to AKI. These mediators may exert their effect through several mechanisms: mediators can have effect on vasoactivity, inflammation, and apoptosis. In conclusion, MV is critical to survival in critically ill patients with effects on the kidney through several interacting mechanisms. This process is complicated further by the underlying disease.

  • Mechanical ventilation and acute renal failure
    Critical Care Medicine, 2005
    Co-Authors: Jan Willem Kuiper, A. B. Johan Groeneveld, Arthur S. Slutsky, Frans B. Plötz
    Abstract:

    Objective: To review the current literature on possible mechanisms by which mechanical ventilation may initiate or aggravate acute renal failure. Data Source: A Medline database and references from identified articles were used to perform a literature search relating to mechanical ventilation and acute renal failure. Data Synthesis: Acute renal failure may be initiated or aggravated by mechanical ventilation through three different mechanisms. First, strategies such as permissive hypercapnia or permissive hypoxemia may compromise renal blood flow. Second, through effects on cardiac output, mechanical ventilation affects systemic and renal hemodynamics. Third, mechanical ventilation may cause Biotrauma-a pulmonary inflammatory reaction that may generate systemic release of inflammatory mediators. The harmful effects of mechanical ventilation may become more significant when a comorbidity is present. In these situations, it is more difficult to maintain normal gas exchange, and moderate arterial hypoxemia and hypercapnia are often accepted. Renal blood flow is compromised due to a decreased cardiac output as a consequence of high intrathoracic pressures. Furthermore, the effects of Biotrauma are not limited to the lungs but may lead to a systemic inflammatory reaction. Conclusions: The development of acute renal failure during mechanical ventilation likely represents a multifactorial process that may become more important in the presence of comorbidities. Development of optimal interventional strategies requires an understanding of physiologic principles and greater insight into the precise molecular and cellular mechanisms that may also play a role.

  • Ventilator-induced lung injury and multiple system organ failure: a critical review of facts and hypotheses
    Intensive Care Medicine, 2004
    Co-Authors: Frans B. Plötz, Arthur S. Slutsky, Adrianus J. Vught, Cobi Jacoba Johanna Heijnen
    Abstract:

    Objective To review how Biotrauma leads to the development of multiple system organ failure (MSOF). Design and setting Published articles on experimental and clinical studies and review articles in the English language were collected and analyzed. Results The concept that ventilation strategies using “large” tidal volumes and zero PEEP of injured lungs can enhance injury by the release of inflammatory mediators into the lungs and circulation, a mechanism that has been called Biotrauma, is supported by evidence from experimental models ranging from mechanically stressed cell systems, to isolated lungs, intact animals, and humans. Biotrauma may lead to MSOF via spillover of lung-borne inflammatory mediators into the systemic circulation. However, spillover of other agents such as bacteria and soluble proapoptotic factors may also contribute to the onset of MSOF. Other less well studied mechanisms such as peripheral immunosuppression and translocation of bacteria and/or products from the gut may play an important role. Finally, genetic variability is a crucial factor. Conclusions The development of MSOF is a multifactorial process. Our proposed mechanisms linking mechanical ventilation and MSOF suggest several novel therapeutic approaches. However, it will first be necessary to study the mechanisms described above to delineate more precisely the contribution of each proposed factor, their interrelationships, and their time course. We suggest that scientific advances in immunology may offer novel approaches for prevention of MSOF secondary to ventilator-induced lung injury.

  • ventilator induced lung injury and multiple system organ failure a critical review of facts and hypotheses
    Intensive Care Medicine, 2004
    Co-Authors: Frans B. Plötz, Arthur S. Slutsky, Adrianus J Van Vught, Cobi Jacoba Johanna Heijnen
    Abstract:

    Objective To review how Biotrauma leads to the development of multiple system organ failure (MSOF).

Alain Combes - One of the best experts on this subject based on the ideXlab platform.

  • Ultra-Protective Ventilation Reduces Biotrauma in Patients on Venovenous Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome*
    Critical care medicine, 2019
    Co-Authors: Sacha Rozencwajg, Amélie Guihot, Guillaume Franchineau, Mickael Lescroat, Nicolas Bréchot, Guillaume Hékimian, Guillaume Lebreton, Brigitte Autran, Charles-edouard Luyt, Alain Combes
    Abstract:

    Introduction:Ventilator settings for patients with severe acute respiratory distress syndrome supported by venovenous extracorporeal membrane oxygenation are currently set arbitrarily. The impact on serum and pulmonary Biotrauma markers of the transition to ultra-protective ventilation settings foll

  • Ultra-Protective Ventilation Reduces Biotrauma in Patients on Venovenous Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome*
    Critical Care Medicine, 2019
    Co-Authors: Sacha Rozencwajg, Amélie Guihot, Guillaume Franchineau, Mickael Lescroat, Nicolas Bréchot, Guillaume Hékimian, Guillaume Lebreton, Brigitte Autran, Charles-edouard Luyt, Alain Combes
    Abstract:

    INTRODUCTION: Ventilator settings for patients with severe acute respiratory distress syndrome supported by venovenous extracorporeal membrane oxygenation are currently set arbitrarily. The impact on serum and pulmonary Biotrauma markers of the transition to ultra-protective ventilation settings following extracorporeal membrane oxygenation implantation, and different mechanical ventilation strategies while on extracorporeal membrane oxygenation were investigated. DESIGN: Randomized clinical trial. SETTINGS: Nine-month monocentric study. PATIENTS: Severe acute respiratory distress syndrome patients on venovenous extracorporeal membrane oxygenation. INTERVENTIONS: After starting extracorporeal membrane oxygenation, patients were switched to the bi-level positive airway pressure mode with 1 second of 24 cm H2O high pressure and 2 seconds of 12 cm H2O low pressure for 24 hours. A computer-generated allocation sequence randomized patients to receive each of the following three experimental steps: 1) high pressure 24 cm H2O and low pressure 20 cm H2O (very high positive end-expiratory pressure-very low driving pressure); 2) high pressure 24 cm H2O and low pressure 5 cm H2O (low positive end-expiratory pressure-high driving pressure); and 3) high pressure 17 cm H2O and low pressure 5 cm H2O (low positive end-expiratory pressure-low driving pressure). Plasma and bronchoalveolar lavage soluble receptor for advanced glycation end-products, plasma interleukin-6, and monocyte chemotactic protein-1 were sampled preextracorporeal membrane oxygenation and after 12 hours at each step. MEASUREMENTS AND MAIN RESULTS: Sixteen patients on ECMO after 7 days (1-11 d) of mechanical ventilation were included. "Ultra-protective" mechanical ventilation settings following ECMO initiation were associated with significantly lower plasma sRAGE, interleukin-6, and monocyte chemotactic protein-1 concentrations. Plasma sRAGE and cytokines were comparable within each on-ECMO experimental step, but the lowest bronchoalveolar lavage sRAGE levels were obtained at minimal driving pressure. CONCLUSIONS: ECMO allows ultra- protective ventilation, which combines significantly lower plateau pressure, tidalvolume, and driving pressure. This ventilation strategy significantly limited pulmonary Biotrauma, which couldtherefore decrease ventilator-induced lung injury. However, the optimal ultra-protective ventilation strategy once ECMO is initiated remains undetermined and warrants further investigations.

Andreas Güldner - One of the best experts on this subject based on the ideXlab platform.