View clinical trials related to Acute Lung Injury.
Filter by:The American European Consensus Conference (AECC) 1994 defined acute respiratory distress syndrome (ARDS) as an acute inflammatory syndrome manifesting as diffuse pulmonary edema and respiratory failure that cannot be explained by, but may co-exist with, left-sided heart failure. During the sequel Conference of the European Society of Intensive Care Medicine, in 2012 minor changes were made, and since that so-called Berlin definition of ARDS is used worldwide for the description of this severe disease. Three grades of severity were proposed to distinguish ARDS according to the level of hypoxemia with a mortality of 24% in patients with mild ARDS, rising to 48% in those with severe ones. Systemic inflammation is considered to be the main reason of ARDS. Activated neutrophils interact with the alveolar-capillary membrane causing the increasing permeability with the sequence lung edema's development. Inflammatory exudate inactivates surfactant leading to collapse and consolidation of distal airspaces with progressive loss of the lung's gas exchange surface area. Unfortunately, systemic inflammatory response syndrome (SIRS) simultaneously inhibits the mechanism of active pulmonary vasoconstriction and allows deoxygenated blood to pass through unventilated areas of the lung boosting the right-to-left shunt. Both mechanisms lead to hypoxemia, which is the main and obligatory feature of ARDS. Actually, endothelial dysfunction and transcapillary leakage seem to be one of the main steps in the development of respiratory failure during ARDS. Last decades it was found out that glycocalyx is also participating in this process too. Thus, it became clear that substances preserving endothelium and glycocalyx from SIRS-causing damage may have a beneficial effect in ARDS treatment. It seems to be crucially important so as the majority of drugs failed to demonstrate any positive effects in terms of ARDS treatment. To the moment we have some evidence, which came from experimental studies, that halogenated anesthetics can preserve glycocalyx against ischemia-reperfusion injury. The primary objective for the multicentral INVERSE Trial will be to determine the effects of inhalational (sevoflurane) versus intravenous (propofol) sedation on P/F ratio on the second day, hospital mortality and ICU (intensive care unit), and in-hospital length of stay in adults with a moderate form of ARDS.
During moderate to severe ARDS, sessions of prone positioning lead to lung and chest wall mechanics changes that modify regional ventilation, with a final redistribution of tidal volume and PEEP towards dependent lung regions: this limits ventilator-induced lung injury, increases oxygenation and convincingly improves clinical outcome. Physiological data indicate that the increase in chest wall elastance is crucial in determining the benefit by prone positioning on oxygenation. In some patients, however, prone positioning may not be feasible or safe due to particular comorbidities and/or technical issues. In the present pilot-feasibility study enrolling 15 subjects with moderate to severe ARDS in whom prone positioning is contraindicated or unfeasible, we aim at assessing whether and to what extent an artificial increase in chest wall elastance while the patient is in the supine position may yield a significant benefit to oxygenation. The increase in chest wall elastance will be achieved placing 100g/kg weight on the anterior chest wall of the patient while he/she is in the supine position: this approach previoulsy appeared safe and effective in case reports and small case series. Patient's position will be standardized (30 degrees head-up, semi seated position). This one-arm sequential study will evaluate the effects of the procedure on gas exchange, haemodynamics, lung and chest wall mechanics, alveolar recruitment (measured with the nitrogen washout-technique and multiple PV curves) and tidal volume and PEEP distribution (assessed with electrical impedance tomography).