View clinical trials related to Acute Lung Injury.
Filter by:Emergency study to test the safety of Descartes-30 cells in patients with moderate-to-severe acute respiratory distress syndrome (ARDS) AND COVID-19
PNEUMA is a preliminary safety and feasibility trial of a novel approach to the titration of neuromuscular blockade (NMB) to safe spontaneous breathing in patients with severe acute respiratory distress syndrome (ARDS) supported with veno-venous extracorporeal membrane oxygenation (VV-ECMO).
The first case of a person infected with SARS-Cov-2 virus can be tracked back on November the 17th, 2019, in China. On March 11, 2020, the World Health Organization (WHO) declared COVID-19 outbreak a pandemic. On April 13, COVID-19 is affecting 210 countries and territories worldwide, about 2 million positive cases have been officially declared along with 115.000 deaths. The real number of infected and deaths is scarily higher, considering that up to 65% people are asymptomatic and thus, not tested. The percentage of patients with COVID-19 needed for intensive care unit (ICU) varied from 5 to 32% in Wuhan, China. It was up to 9% in Lombardy, Italy. According to available data from Lombardy, 99% of patients admitted to the ICU needed respiratory support (88% invasive ventilation, 11% non invasive ventilation). The aim of the present investigation is to test the hypothesis whether transcutaneous partial O2 and CO2 pressures may be reliable predictive factors for acute respiratory distress syndrome (ARDS) development in hospitalized clinically stable COVID-19 positive patients and to clarify the role of the Angiotensin Converting Enzyme 2 (ACE2) and its final product, angiotensin 2 (Ang II) in the pathogenesis of this systemic disease. We also aim to test the hypothesis that plasma concentration of Clara Cell protein (CC16) and surfactant protein D (SPD), which are a biomarkers of acute lung injury, are severely decreased in COVID-19 positive patients and the plasma concentration is related to the severity of lung injury.
Spontaneous Breathing (SB) can be potentially harmful in patient with Acute Respiratory Distress Syndrome (ARDS) during the transition phase of passive ventilation to partial ventilatory support. The application of high Positive End Expiratory Pressure (PEEP) during SB has shown to ameliorate the progression of lung injury by decreasing the TP and esophageal pressure (EP) swings and the stress / strain applied to the lung. The mechanisms proposed to be responsible for these effects are the activation of Hering Breuer reflex, the recruitment of previously collapsed tissue, the homogenization of lung and the improvement of respiratory system compliance and the impairment in the length - tension relationship of the diaphragm. If all the previously explained mechanisms have an effect on the control of inspiratory effort, a decrease in the intensity of effort is expected during an end-inspiratory occlusion in patients who will respond to high PEEP application. Based on this rationale, the investigators developed an index called "Inspiratory Ratio" (IR) to predict the response of patient's inspiratory effort to the application of high PEEP without need of esophageal manometry.
Acute respiratory distress (ARD) is one of the most frequent reasons for consultation and hospitalization in emergency medicine. The use of ultrasound methods as a diagnostic and clinical assessment tool in emergency medicine is increasingly important. As such, ultrasound is a simple, non-invasive means of assessing diaphragmatic function in the patient's bed. Several methods of ultrasound assessment of diaphragm function have been described. Among these different methods, the diaphragmatic excursion seems to have a better intra and interobserver reproducibility as well as a greater feasibility, in particular because of its speed of realization and its learning curve seeming faster in comparison with the measurement. of the thickening fraction. Measuring the diaphragmatic excursion could therefore ultimately represent a simple means of assessing respiratory function, both diagnostic and prognostic, in patients with acute respiratory distress in the emergency departments. The etiologies of acute respiratory distress in very elderly patients (i.e.> 75 years) admitted to the emergency reception service are multiple. To our knowledge, there is no data available in the literature on the prevalence of diaphragmatic dysfunction and its short- and long-term course in this category of patients. The main objective of this study is therefore to assess the prevalence of diaphragmatic dysfunction and its evolutionary kinetics in patients over the age of 75 admitted for acute respiratory distress in the emergency medicine department.
In patients with SARS-CoV-2 or bacterial infection admitted to the intensive care unit (ICU), the state of the intravascular volume, the characteristics of the blood volume components, and the development of a vascular leak is currently unknown. The relationship of these parameters with parameters of cardiac performance, lung edema and sublingual microcirculatory perfusion parameters have never been studied.
Pandemic SARS-CoV-2 (COVID-19) respiratory infection is responsible for more than 4,000 deaths, mainly (67%) secondary to acute respiratory distress syndromes (ARDS). ARDS is usually associated with a mortality of around 40%, but this rate reaches 61% in patients infected with SARS-CoV-2. Two endotypes have been described in patients with ARDS: one, hyper-inflammatory, associated with very high mortality (51%); the second, slightly inflammatory (immunoparalysis), associated with much lower mortality (19%). In COVID-19 patients, distinct immune response profiles have also been observed. Some patients present deep lymphopenia and/or prolonged viral excretions associated with more frequent occurrence of co-infections (+ 29% of virus, + 23% of bacteria, + 10% of fungi). The latter group may be at higher risk in terms of mortality. The intensity of the inflammatory response and/or microbial coinfections therefore appear as risk factors for severity and mortality in patients infected with SARS-CoV-2 which determine the course of the disease. To adapt early optimal therapeutic management to each forms of the disease, it is essential to be able to characterize these profiles on the microbiological and inflammatory level. With a committed network of 6 intensive-care units across eastern and northern Ile-de-France, 180 patients with ARDS and infected with SARS-CoV-2 are being enrolled. For these patients, a nasopharyngeal swab is collected at inclusion; followed by a new nasopharyngeal swab and a deep respiratory sample once a week, until D28, for an exploration of co-infections and for monitoring the viral load of SARS-CoV-2. The rest of each of these samples are collected for the study. In parallel, the clinical data usually collected in the context of intensive care will be collected on a CRF. They will allow to calculate risk scores such as SOFA.
The investigators present a randomised open label phase Ib/IIa trial of nebulised unfractionated heparin to evaluate the effect of nebulised unfractionated heparin on the procoagulant response in ICU patients with SARS-CoV-2 requiring advanced respiratory support. As this is one of the first studies of nebulised heparin in COVID 19 lung disease the investigators will assess safety as a co-primary outcome.
This was a Phase 2, randomized, double-blind, placebo-controlled, parallel-group, multicenter, dose escalation and proof-of-concept study to evaluate the safety and efficacy of razuprotafib, administered 3 times daily (TID) (every 8 hours [Q8H]), in hospitalized subjects with moderate to severe Coronavirus disease 2019 (COVID-19) receiving standard of care therapy. The study was planned to include 2 parts with Part 1 comprising the dose escalation period of the study and Part 2 comprising the proof-of-concept safety and efficacy period of the study.
Rationale: The renin-angiotensin-aldosterone system (RAAS) dysregulation may play a central role in the pathophysiology of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection associated acute lung injury (ALI) / acute respiratory distress syndrome (ARDS). In the RAAS, Angiotensin I (Ang I) is converted to angiotensin II (Ang II) by angiotensin converting enzyme (ACE). Ang II mediates vasoconstrictive, pro-inflammatory and pro-oxidative effects through agonism at Ang II type 1 receptor (AT1R). ACE2 converts Ang II to angiotensin 1-7 (Ang1-7), which finally binds to Mas receptor (MasR) and mediates many beneficial actions, including vasodilation and anti-inflammatory, anti-oxidant and antiapoptotic effects. ACE2, a homologue of ACE, is an integral cell membrane protein with a catalytic domain on the extracellular surface exposed to vasoactive peptides. SARS-CoV-2 penetrates the cell through ACE2, and the increase of this receptor (due to the use of ACE inhibitors or angiotensin receptor blockers [ARBs]) may facilitate SARS-CoV-2 infection, which might increase the risk of developing severe and fatal SARS-CoV-2 infection. However, through upregulation of ACE2, ACE inhibitors/ARBs can exert anti-inflammatory and antioxidative effects, which may be beneficial in preventing ALI and ARDS. Objective: To evaluate the effectiveness and safety of telmisartan in respiratory failure due to COVID-19. Study design: This is an open label, phase 2 clinical trial. Study population: Adult hospitalized SARS-CoV-2-infected patients (n=60). Intervention: The active-treatment arm will receive telmisartan 40 mg daily and the control arm will receive standard care. Treatment duration will be 14 days or up to hospital discharge <14 days or occurrence of the primary endpoint if <14 days. Main study endpoint: The primary study endpoint is the occurrence within 14 days of randomization of either: 1) Mechanical ventilation or 2) Death.