Update in acute lung injury and critical care 2010.
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ABSTRACT:
SUBMITTER: Vadasz I
PROVIDER: S-EPMC3114050 | biostudies-literature | 2011 May
REPOSITORIES: biostudies-literature
Publications
Update in acute lung injury and critical care 2010.
Vadász István I Sznajder Jacob I JI
American journal of respiratory and critical care medicine 20110501 9
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Project description:Perioperative acute lung injury (ALI) is a syndrome characterised by hypoxia and chest radiograph changes. It is a serious post-operative complication, associated with considerable mortality and morbidity. In addition to mechanical ventilation, remote organ insult could also trigger systemic responses which induce ALI. Currently, there are limited treatment options available beyond conservative respiratory support. However, increasing understanding of the pathophysiology of ALI and the biochemical pathways involved will aid the development of novel treatments and help to improve patient outcome as well as to reduce cost to the health service. In this review we will discuss the epidemiology of peri-operative ALI; the cellular and molecular mechanisms involved on the pathological process; the clinical considerations in preventing and managing perioperative ALI and the potential future treatment options.
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Project description:RationaleDespite advances in clinical management, there are currently no reliable diagnostic and therapeutic targets for acute respiratory distress syndrome (ARDS). The inflammasome/caspase-1 pathway regulates the maturation and secretion of proinflammatory cytokines (e.g., IL-18). IL-18 is associated with injury in animal models of systemic inflammation.ObjectivesWe sought to determine the contribution of the inflammasome pathway in experimental acute lung injury and human ARDS.MethodsWe performed comprehensive gene expression profiling on peripheral blood from patients with critical illness. Gene expression changes were assessed using real-time polymerase chain reaction, and IL-18 levels were measured in the plasma of the critically ill patients. Wild-type mice or mice genetically deficient in IL-18 or caspase-1 were mechanically ventilated using moderate tidal volume (12 ml/kg). Lung injury parameters were assessed in lung tissue, serum, and bronchoalveolar lavage fluid.Measurements and main resultsIn mice, mechanical ventilation enhanced IL-18 levels in the lung, serum, and bronchoalveolar lavage fluid. IL-18-neutralizing antibody treatment, or genetic deletion of IL-18 or caspase-1, reduced lung injury in response to mechanical ventilation. In human patients with ARDS, inflammasome-related mRNA transcripts (CASP1, IL1B, and IL18) were increased in peripheral blood. In samples from four clinical centers, IL-18 was elevated in the plasma of patients with ARDS (sepsis or trauma-induced ARDS) and served as a novel biomarker of intensive care unit morbidity and mortality.ConclusionsThe inflammasome pathway and its downstream cytokines play critical roles in ARDS development.
| S-EPMC3373064 | biostudies-literature
Project description:Purpose of reviewThis article outlines updates in point of care ultrasonography.Recent findingsImproving diagnostic accuracy and image quality is continuing to evolve in Point-of-care ultrasonography (POCUS). This include incorporating Artificial Intelligence (AI) and use of other modalities such as Doppler in lung ultrasonography. Transesophageal echocardiography is an emerging option when imaging is difficult to obtain via transthoracic echocardiography. POCUS is becoming instrumental when used during cardiac arrest. Ultrasound (VExUS) Grading System is a promising measurement to assess a patient's volume status. Given the multiple advantages of POCUS usage, competency in POCUS became a requirement of Critical Care fellowship training. POCUS is an important diagnostic modality and guide to medical management. New technological advances such as AI, can serve as a guide to enhance image quality and help accurately obtain quantitative assessments. POCUS has a major role during cardiac arrest and advanced cardiac life support. The clinical utility of POCUS was further substantiated during the COVID-19 pandemic. The Accreditation Council for Graduate Medical Education (ACGME) requires critical care programs to include competency in POCUS as part of their training.
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Project description:Pseudomonas aeruginosa is one of the most common nosocomial infections worldwide, and it frequently causes ventilator-associated acute pneumonia in immunocompromised patients. Abundant neutrophil extracellular traps (NETs) contribute to acute lung injury, thereby aggravating ventilator-induced lung damage. While pattern recognition receptors (PRRs) TLR4 and TLR5 are required for host defense against P. aeruginosa invasion, the PRR responsible for P. aeruginosa-induced NET formation, proinflammatory cytokine release, and acute lung injury remains unclear. We found that myeloid C-type lectin domain family 5 member A (CLEC5A) interacts with LPS of P. aeruginosa and is responsible for P. aeruginosa-induced NET formation and lung inflammation. P. aeruginosa activates CLEC5A to induce caspase-1-dependent NET formation, but it neither causes gasdermin D (GSDMD) cleavage nor contributes to P. aeruginosa-induced neutrophil death. Blockade of CLEC5A attenuates P. aeruginosa-induced NETosis and lung injury, and simultaneous administration of anti-CLEC5A mAb with ciprofloxacin increases survival rate and decreases collagen deposition in the lungs of mice challenged with a lethal dose of P. aeruginosa. Thus, CLEC5A is a promising therapeutic target to reduce ventilator-associated lung injury and fibrosis in P. aeruginosa-induced pneumonia.
| S-EPMC9676025 | biostudies-literature
Project description:Acute kidney injury (AKI) is associated with increased risk of morbidity and mortality in critically ill children and adults. Neonates remain an understudied group, although previous evidence suggests that this association holds true for them as well.Attention to the issue of neonatal AKI is increasing. New studies in very low-birthweight infants, infants with congenital heart disease who undergo cardiopulmonary bypass, those who receive extracorporeal membrane oxygenation and infants with perinatal depression continue to demonstrate that AKI is common in neonates and associated with increased risk of morbidity and mortality. Additional advances in the field of neonatal AKI include adaptation of modern, categorical AKI definitions, as well as further evaluation of novel urinary biomarkers (e.g., neutrophil gelatinase-associated lipocalin) in this patient group.AKI is an independent risk factor for poor outcomes in critically ill neonates. Our ability to improve outcomes for these patients depends on heightened awareness of this issue both at the bedside as well as in research, commitment to using standardized AKI definitions in order to pool and compare data more effectively and improvement in our diagnostic methods with better AKI biomarkers so that we can identify AKI and intervene much earlier in the disease course.
| S-EPMC5545784 | biostudies-other
Project description:In the intratracheal bleomycin (ITB) model of acute lung injury (ALI), macrophages are recruited to the lung and participate in the inflammation and resolution that follows injury. Macrophage origin is influential in determining activation; however, the specific phenotype of recruited and resident macrophages is not known. Inducible nitric oxide synthase (iNOS) has been implicated in the pathogenesis of ALI; however, the effects of its inhibition are mixed. Here we examined how macrophage origin determines the phenotypic response to ALI. Further, we hypothesize cell specific iNOS is key to determining activation and recruitment. Using a chimeric mouse approach, we have identified recruited and resident macrophage populations. We also used the chimeric mouse approach to create either pulmonary or bone marrow NOS2-/- mice and systemically inhibited iNOS via 1400 W. We evaluated macrophage populations at the peak of inflammation (8 days) and the beginning of resolution (15 days) following ITB. These studies demonstrate tissue resident macrophages adopt a M2 phenotype specifically, but monocyte originated macrophages activate along a spectrum. Additionally, we demonstrated that monocyte originating macrophage derived iNOS is responsible for recruitment to the lung during the inflammatory phase. Further, we show that macrophage activation is dependent upon cellular origin. Finally, these studies suggest pulmonary derived iNOS is detrimental to the lung following ITB. In conclusion, macrophage origin is a key determinant in response to ALI and iNOS is central to recruitment and activation.
| S-EPMC8822172 | biostudies-literature
Project description:This review summarizes new insights in the pathophysiologic implications of inflammation and microvascular alterations in organ dysfunction, as well as genetic factor contribution, from clinical and experimental studies that were published in 2010 in Critical Care in the fields of multiple organ dysfunction and sepsis. New diagnostic and prognostic markers of organ dysfunction are presented. Evaluations of novel therapeutic strategies, including implementation of international guidelines, modulation of inflammation and coagulation, and prevention of ventilator-induced lung injury and acute kidney injury, are reported. The results of these experimental studies and clinical trials are discussed in the context of the current relevant scientific and clinical background.
| S-EPMC3388699 | biostudies-literature
Project description:BackgroundTreatment of acute respiratory distress syndrome (ARDS) in children is largely based on extrapolated knowledge obtained from adults and which varies between different hospitals. This study explores ventilation treatment strategies for children with ARDS in the Nordic countries, and compares these with international practice.MethodsIn October 2012, a questionnaire covering ventilation treatment strategies for children aged 1 month to 6 years of age with ARDS was sent to 21 large Nordic intensive care units that treat children with ARDS. Pre-terms and children with congenital conditions were excluded.ResultsEighteen of the 21 (86%) targeted intensive care units responded to the questionnaire. Fifty per cent of these facilities were paediatric intensive care units. Written guidelines existed in 44% of the units. Fifty per cent of the units frequently used cuffed endotracheal tubes. Ventilation was achieved by pressure control for 89% vs. volume control for 11% of units. Bronchodilators were used by all units, whereas steroids usage was 83% and surfactant 39%. Inhaled nitric oxide and high frequency oscillation were available in 94% of the units. Neurally adjusted ventilator assist was used by 44% of the units. Extracorporeal membrane oxygenation could be started in 44% of the units.ConclusionVentilation treatment strategies for paediatric ARDS in the Nordic countries are relatively uniform and largely in accordance with international practice. The use of steroids and surfactant is more frequent than shown in other studies.
| S-EPMC6681019 | biostudies-literature