Active clinical trials for "Lung Injury"

Peri-operative fluid therapy is a controversial area with few randomized trials to guide practice. Fluid management has a significant influence on outcome following surgery. Yet practically, fluid prescription practice during this period is sub-optimal, resulting in avoidable iatrogenic complications. Several studies have assessed the effect of a 'liberal' vs. a 'restrictive' perioperative fluid regimen on post-operative outcome. However, most of these studies have focused primarily on intra-operative fluid management, whereas postoperative strategies have been less well defined, even though the immediate postoperative period is of critical importance to the patient's recovery. Moreover, whereas intra-operative fluid administration is monitored by the anesthesiologist, postoperatively it is less supervised and may result in excess or lack of intravenous (IV) fluids. Therefore, fluid management audit at the post-anesthesia care unit (PACU) is of paramount importance for patient healthcare. The objective of this study is to follow and report the current practice of fluid administration in the PACU of Tel Aviv Sourasky Medical Center, for an extended period of time as a first step towards establishing evidence-based guidelines for postoperative fluid management.

The acute respiratory distress syndrome (ARDS) remains a common and morbid complication of critical illness. Sepsis contribute to a lot of ARDS cases, but mechanisms by which non-pulmonary insults such as extrapulmonary sepsis propagate lung injury remain unclear. Most eukaryotic cells release small anuclear membrane-bound vesicles into the extracellular environment in either physiological or pathophysiological conditions, often called extracellular vesicles (EVs) .Through their cargo containing bioactive molecules such as proteins, mRNAs, and microRNAs and their interaction with target cells, EVs are recognized as important mediators of cellular communication. Mitochondrial contents are clearly present in EVs, and mitochondrial cargo within EVs have been shown to stimulate the production of proinflammatory cytokines, further enhancing LPS-induced inflammation. Among the mitochondrial contents, mtDNA was present at higher levels in EVs.Therefore, we hypothesis, EVs containing mtDNA play an important role in the occurrence and development of ARDS caused by extrapulmonary sepsis.

Efficacy of Lung ultrasound in monitoring fluid resuscitation in chest trauma patients with lung contusions

To carry out a prospective cohort study of healthy volunteers, assessing differences between baseline pulmonary inflammation, response to LPS inhalation and endothelial function, as measured by flow mediated dilation between, electronic cigarette uses, cigarette smokers and non smokers.

There is limited data on the respiratory system mechanics and ideal mode of ventilation for patients on veno-arterial extra-corporeal membrane oxygenation (VA ECMO) post cardiac arrest. In this observational study, the investigators will review and/or obtain laboratory, hemodynamic, respiratory system mechanical, and clinical data from patients on VA ECMO. The specific aims of this study are as follows: Aim 1: To characterize the lung ventilation strategy employed in patients on VA ECMO and its success. Aim 2: To characterize respiratory system mechanics while on ECMO using esophageal manometry and Electrical Impedance Tomography (EIT). Aim 3: To characterize right heart function and pulmonary vascular hemodynamics on the employed ventilation strategy. The overarching hypothesis is that fine-tuned individualized ventilation might be superior to an algorithm that does not account for cardiac and pulmonary functions. Therefore, the aims of this study are to identify areas in which the ventilation strategy may theoretically be suboptimal, which will guide future interventional studies investigating alternatives methods of ventilation which may reduce time on the ventilator after cardiac arrest, time in the intensive care unit, and need for veno-venous ECMO.

Acute lung injury is a highly prevalent disease in children, posing a serious threat to their health and causing economic burden on society and families. It has received high attention. Blocking the cascade immune inflammatory response that occurs in the respiratory tract and finding key targets for the prevention and treatment of acute lung injury has become an important challenge faced by the medical community. The pathogenesis of acute lung injury is complex, involving the combined action of multiple cells and cytokines in the immune system. Therefore, it is necessary to further study the function of immune cells and specific immune pathogenesis, providing new ideas and theoretical basis for clinical treatment of acute lung injury. The omics technology includes Genomics, Transcriptome, proteomics, metabolomics, etc. Through qualitative and quantitative analysis of changes in low molecular weight molecules or metabolites of biological samples, it provides a new way to find biomarkers and pathogenesis. We plan to study the peripheral blood of children with acute lung injury and healthy children, and use network analysis to screen for differential genes and related enrichment pathways in acute lung injury. We aim to explore the correlation between immune regulation and inflammatory repair in children with acute lung injury, and analyze the regulatory mechanisms between immune cells related to it. Provide assistance for clinical diagnosis and treatment.

Understanding the role VEGF plays in ARDS consequently provides an ideal opportunity to discover new therapies for ARDS.

The optimal amount caloric intake were still controversy in critically ill patients in literature. There were no significant outcome difference with different caloric intake in acute lung injury patients. In order to identify the optimal amount caloric intake in acute lung injury patients, we conduct a prospectively observational study to see whether the caloric differences influence hospital mortality.

Sepsis is the most frequent risk factor for ALI/ARDS. Meanwhile, Pulmonary is the most vulnerable organ to fail in response to sepsis, vascular endothelial dysfunction is a central event in the pathophysiology of sepsis. An improved understanding of endothelial response and associated biomarkers may lead to strategies to more accurately predict outcome and develop novel endothelium-directed therapies in sepsis. The human and mouse R-spondins encode a family of proteins that includes four paralogs (R-spo1-4). R-spondins are secreted proteins found primarily in the extracellular region and are known to promote β-catenin signaling. Among them, the embryonic lethal vascular remodeling phenotype of R-spondin3 (Rspo3) mutant mice suggests a role of EC derived Rspo3 in angiogenesis. Rspo3 protects tissues against mesenteric I/R by tightening endothelial cell junction and improving vascular intergrity. However, the role of Rspo3 in sepsis-induced pulmonary endothelial dysfunction remains unclear. Thus, it is worthwhile to explore the relationship between Rspo3 and sepsis-induced lung injury, which will be helpful for prevention and treatment of sepsis-induced lung injury and endothelial dysfunction.

The goal of this project is to find a marker expression that the investigators can use to trace symptom progression and develop a more efficient therapy to enhance ARDS patient survival rate and better post-ICU life quality.