The Experts below are selected from a list of 106959 Experts worldwide ranked by ideXlab platform
Michael A. Matthay - One of the best experts on this subject based on the ideXlab platform.
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Early acute Lung Injury: Criteria for identifying Lung Injury prior to the need for positive pressure ventilation
Critical Care Medicine, 2013Co-Authors: Joseph E. Levitt, Carolyn S. Calfee, Benjamin A. Goldstein, Rosemary Vojnik, Michael A. MatthayAbstract:Objective:Mortality associated with acute Lung Injury remains high. Early identification of acute Lung Injury prior to onset of respiratory failure may provide a therapeutic window to target in future clinical trials. The recently validated Lung Injury Prediction Score identifies patients at risk fo
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hyperoxic acute Lung Injury
Respiratory Care, 2013Co-Authors: Richard H Kallet, Michael A. MatthayAbstract:Prolonged breathing of very high FIO2 (FIO2 ≥ 0.9) uniformly causes severe hyperoxic acute Lung Injury (HALI) and, without a reduction of FIO2, is usually fatal. The severity of HALI is directly proportional to PO2 (particularly above 450 mm Hg, or an FIO2 of 0.6) and exposure duration. Hyperoxia produces extraordinary amounts of reactive O2 species that overwhelms natural anti-oxidant defenses and destroys cellular structures through several pathways. Genetic predisposition has been shown to play an important role in HALI among animals, and some genetics-based epidemiologic research suggests that this may be true for humans as well. Clinically, the risk of HALI likely occurs when FIO2 exceeds 0.7, and may become problematic when FIO2 exceeds 0.8 for an extended period of time. Both high-stretch mechanical ventilation and hyperoxia potentiate Lung Injury and may promote pulmonary infection. During the 1960s, confusion regarding the incidence and relevance of HALI largely reflected such issues as the primitive control of FIO2, the absence of PEEP, and the fact that at the time both ALI and ventilator-induced Lung Injury were unknown. The advent of PEEP and precise control over FIO2, as well as Lung-protective ventilation, and other adjunctive therapies for severe hypoxemia, has greatly reduced the risk of HALI for the vast majority of patients requiring mechanical ventilation in the 21st century. However, a subset of patients with very severe ARDS requiring hyperoxic therapy is at substantial risk for developing HALI, therefore justifying the use of such adjunctive therapies.
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Treatment of Acute Lung Injury
2012Co-Authors: Michael A. MatthayAbstract:This presentation at the 2007 Aspen Lung Injury and Repair Conference provided a brief historical perspective from the 1998 Aspen Conference on Acute Lung Injury, highlighting the discussion of clinical definitions. There was also a review of the National Heart, Lung, and Blood Institute ARDS Network clinical trials, with an emphasis on the success of the Lung-protective ventilation strategy in reducing mortality. In addition, there was a discussion of the recently completed fluid and catheter treatment trial, which demonstrated no benefit for pulmonary arterial catheterization over central venous catheterization for monitoring patients with acute Lung Injury (ALI). The trial demonstrated an increase in ventilator-free days with a fluid-conservative protocol. Finally, there was a discussion of recent experimental studies that show promise for cell-based therapy with mesenchymal stem cells for the treatment of endotoxin-induced ALI in mice. There were three objectives for this presentation at the 2007 Lung...
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Biomarkers in Acute Lung Injury: Insights into the Pathogenesis of Acute Lung Injury
Critical Care Clinics, 2011Co-Authors: Lj Mark Cross, Michael A. MatthayAbstract:Studies of potential biomarkers in experimental models of acute Lung Injury (ALI) and from clinical samples from patients with ALI have provided extensive information relating to the pathophysiology of the mechanisms of Lung Injury and repair. The utility of biomarkers remains still solely part of the research tools to investigate Lung Injury and repair mechanisms and due to lack of sensitivity and specificity cannot yet be used as a clinical decision tool in patients with either acute Lung Injury or ARDS. We have reviewed known biomarkers in context of their major biological activity such as inflammatory mediators, coagulation/fibrinolytic mediators, growth factors and the emerging use of proteomics. The continued interest in identifying and studying biomarkers is relevant as it continues to provide important information regarding the mechanisms involved in Lung Injury and repair and how this may be helpful in the identification and design of future therapeutic targets and strategies as well as hopefully to identify a sensitive and specific biomarker that would be of clinical relevance.
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Alveolar edema fluid clearance and acute Lung Injury
Respiratory Physiology & Neurobiology, 2007Co-Authors: Yves Berthiaume, Michael A. MatthayAbstract:Although Lung-protective ventilation strategies have substantially reduced mortality of acute Lung Injury patients there is still a need for new therapies that can further decrease mortality in patients with acute Lung Injury. Studies of epithelial ion and fluid transport across the distal pulmonary epithelia have provided important new concepts regarding potential new therapies for acute Lung Injury. Overall, there is convincing evidence that the alveolar epithelium is not only a tight epithelial barrier that resists the movement of edema fluid into the alveoli, but it is also actively involved in the transport of ions and solutes, a process that is essential for edema fluid clearance and the resolution of acute Lung Injury. The objective of this article is to consider some areas of recent progress in the field of alveolar fluid transport under normal and pathologic conditions. Vectorial ion transport across the alveolar and distal airway epithelia is the primary determinant of alveolar fluid clearance. The general paradigm is that active Na+ and Cl− transport drives net alveolar fluid clearance, as demonstrated in several different species, including the human Lung. Although these transport processes can be impaired in severe Lung Injury, multiple experimental studies suggest that upregulation of Na+ and Cl− transport might be an effective therapy in acute Lung Injury. We will review mechanisms involved in pharmacological modulation of ion transport in Lung Injury with a special focus on the use of β-adrenergic agonists which has generated considerable interest and is a promising therapy for clinical acute Lung Injury.
Mark Ballard - One of the best experts on this subject based on the ideXlab platform.
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Primary blast Lung Injury
American Journal of Respiratory and Critical Care Medicine, 2015Co-Authors: Andrew Mc Donald Johnston, Mark BallardAbstract:A soldier was injured by a vehicle-borne suicide bomb, sustaining injuries to his upper body, with flash burns, superficial fragmentation wounds, ruptured eardrums, facial sinus fractures, and a fractured forearm. A chest radiograph (Figure 1) and computed tomographic (CT) trauma series from his circle of Willis to proximal femurs (Figures 2 and 3) were carried out. The appearances are suggestive of the pulmonary contusion and hemorrhage seen in blast Lung Injury. figure Figure 1. Chest radiograph demonstrating patchy bilateral opacification in both Lungs, predominating in the middle and lower zones with a perihilar distribution consistent with hemorrhage. No frank air bronchograms were seen. There was no radiologic evidence of hemothorax or pneumothorax, no rib fractures, and no free subdiaphragmatic gas. [More] figure Figure 2. A coronal reconstruction of a thoracic computed tomography scan with iodinated contrast medium demonstrated patchy diffuse ground-glass opacities in a predominantly perihilar distribution consistent with hemorrhage. There was no endobronchial lesion or obstruction. The heart and thoracic great vessels were normal, and there was no evidence of pulmonary embolism. There were no rib fractures. No fragments from the explosion were seen within the thorax. [More] figure Figure 3. Axial reconstruction of a thoracic computed tomography scan showing diffuse patchy infiltrates consistent with hemorrhage. [More] Some 7 to 11% of military patients injured by explosions develop blast Lung Injury, often in association with extrathoracic trauma (1, 2). Injury from blast is due to compression and disruption of tissues by a shock wave that lasts for milliseconds, with damage occurring where one tissue is more compressible than another, especially at interfaces between air and fluid within tissues such as the middle ear, bowel, or Lung. Compression and shearing forces lead to disruption of the affected tissue, with subsequent hemorrhage and edema (3, 4). Histological studies of patients with blast Lung Injury show ruptured alveoli and hemorrhage around pulmonary vessels (5). Patients with blast Lung Injury who die typically do so from thoracic injuries, including hemothorax and pneumothorax, or from extrathoracic injuries (2). Treatment should include careful attention to the patient’s extrathoracic injuries. Invasive respiratory support should be used if required for hypoxia or ventilatory failure (6). Initial management may be complicated by hemorrhage into the airways (7). Some patients require advanced ventilatory management including extracorporeal support, which may be performed during evacuation to a tertiary center by specialized teams (8). In one published series from a bus bombing, most survivors of blast Lung Injury showed resolution of chest radiograph abnormalities within 5 months, and Lung function had returned to normal in the majority of patients at 1-year follow up (9). The patient described was treated with noninvasive ventilation for 3 days and discharged to a rehabilitation facility on Day 25. He made a good recovery, with normal Lung function 5 months later. One year later, he had returned to high-intensity cycling.
Andrew Mc Donald Johnston - One of the best experts on this subject based on the ideXlab platform.
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Primary blast Lung Injury
American Journal of Respiratory and Critical Care Medicine, 2015Co-Authors: Andrew Mc Donald Johnston, Mark BallardAbstract:A soldier was injured by a vehicle-borne suicide bomb, sustaining injuries to his upper body, with flash burns, superficial fragmentation wounds, ruptured eardrums, facial sinus fractures, and a fractured forearm. A chest radiograph (Figure 1) and computed tomographic (CT) trauma series from his circle of Willis to proximal femurs (Figures 2 and 3) were carried out. The appearances are suggestive of the pulmonary contusion and hemorrhage seen in blast Lung Injury. figure Figure 1. Chest radiograph demonstrating patchy bilateral opacification in both Lungs, predominating in the middle and lower zones with a perihilar distribution consistent with hemorrhage. No frank air bronchograms were seen. There was no radiologic evidence of hemothorax or pneumothorax, no rib fractures, and no free subdiaphragmatic gas. [More] figure Figure 2. A coronal reconstruction of a thoracic computed tomography scan with iodinated contrast medium demonstrated patchy diffuse ground-glass opacities in a predominantly perihilar distribution consistent with hemorrhage. There was no endobronchial lesion or obstruction. The heart and thoracic great vessels were normal, and there was no evidence of pulmonary embolism. There were no rib fractures. No fragments from the explosion were seen within the thorax. [More] figure Figure 3. Axial reconstruction of a thoracic computed tomography scan showing diffuse patchy infiltrates consistent with hemorrhage. [More] Some 7 to 11% of military patients injured by explosions develop blast Lung Injury, often in association with extrathoracic trauma (1, 2). Injury from blast is due to compression and disruption of tissues by a shock wave that lasts for milliseconds, with damage occurring where one tissue is more compressible than another, especially at interfaces between air and fluid within tissues such as the middle ear, bowel, or Lung. Compression and shearing forces lead to disruption of the affected tissue, with subsequent hemorrhage and edema (3, 4). Histological studies of patients with blast Lung Injury show ruptured alveoli and hemorrhage around pulmonary vessels (5). Patients with blast Lung Injury who die typically do so from thoracic injuries, including hemothorax and pneumothorax, or from extrathoracic injuries (2). Treatment should include careful attention to the patient’s extrathoracic injuries. Invasive respiratory support should be used if required for hypoxia or ventilatory failure (6). Initial management may be complicated by hemorrhage into the airways (7). Some patients require advanced ventilatory management including extracorporeal support, which may be performed during evacuation to a tertiary center by specialized teams (8). In one published series from a bus bombing, most survivors of blast Lung Injury showed resolution of chest radiograph abnormalities within 5 months, and Lung function had returned to normal in the majority of patients at 1-year follow up (9). The patient described was treated with noninvasive ventilation for 3 days and discharged to a rehabilitation facility on Day 25. He made a good recovery, with normal Lung function 5 months later. One year later, he had returned to high-intensity cycling.
Shaf Keshavjee - One of the best experts on this subject based on the ideXlab platform.
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ischemia reperfusion induced Lung Injury
American Journal of Respiratory and Critical Care Medicine, 2003Co-Authors: Marc De Perrot, Thomas K Waddell, Shaf KeshavjeeAbstract:Ischemia-reperfusion-induced Lung Injury is characterized by nonspecific alveolar damage, Lung edema, and hypoxemia occurring within 72 hours after Lung transplantation. The most severe form may lead to primary graft failure and remains a significant cause of morbidity and mortality after Lung transplantation. Over the past decade, better understanding of the mechanisms of ischemia-reperfusion Injury, improvements in the technique of Lung preservation, and the development of a new preservation solution specifically for the Lung have been associated with a reduction in the incidence of primary graft failure from approximately 30 to 15% or less. Several strategies have also been introduced into clinical practice for the prevention and treatment of ischemia-reperfusion-induced Lung Injury with various degrees of success. However, only three randomized, double-blinded, placebo-controlled trials on ischemia-reperfusion-induced Lung Injury have been reported in the literature. In the future, the development of new agents and their application in prospective clinical trials are to be expected to prevent the occurrence of this potentially devastating complication and to further improve the success of Lung transplantation.
Randolph H. Hastings - One of the best experts on this subject based on the ideXlab platform.
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Monitoring alveolar epithelial function in acute Lung Injury.
Journal of clinical monitoring and computing, 2020Co-Authors: Randolph H. HastingsAbstract:Identification of humoral markers of acute Lung Injury may lead to insights into pathologic mechanisms. In addition, specific markers may be useful for predicting development of acute respiratory distress syndrome (ARDS) or for assessing prognosis. Ultimately, studies of Lung Injury markers may help define interventions that prevent or moderate ARDS. The alveolar epithelium is important both for the integrity of the blood-gas barrier and for repair of the barrier after Lung Injury. This article reviews markers that derive from or relate to the alveolar epithelium and that might be used for monitoring alveolar epithelial function in acute Lung Injury. Surfactant apoproteins may be important markers of Injury or for prognosis. Levels of surfactant apoprotein A (SP-A) fall 50-75% in patients with severe Lung Injury compared to normal patients. Serum levels of SP-A in patients dying of acute respiratory distress syndrome are double serum levels of survivors.
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Monitoring alveolar epithelial function in acute Lung Injury.
Journal of Clinical Monitoring and Computing, 2000Co-Authors: Randolph H. HastingsAbstract:Objective.Identification of humoral markers of acute Lung Injury may lead to insights into pathologic mechanisms. In addition, specific markers may be useful for predicting development of acute respiratory distress syndrome (ARDS) or for assessing prognosis. Ultimately, studies of Lung Injury markers may help define interventions that prevent or moderate ARDS. The alveolar epithelium is important both for the integrity of the blood-gas barrier and for repair of the barrier after Lung Injury. This article reviews markers that derive from or relate to the alveolar epithelium and that might be used for monitoring alveolar epithelial function in acute Lung Injury. Surfactant apoproteins may be important markers of Injury or for prognosis. Levels of surfactant apoprotein A (SP-A) fall 50–75% in patients with severe Lung Injury compared to normal patients. Serum levels of SP-A in patients dying of acute respiratory distress syndrome are double serum levels of survivors.
