View clinical trials related to Bronchoalveolar Lavage.
Filter by:Coronaviruses such as SARS-CoV2, MERS-CoV, and SARS-CoV can cause significant morbidity and mortality in infected persons. Lung is the most common site of infection for these viruses, which may manifest as acute respiratory distress syndrome and mortality. Pulmonary involvement is also responsible for the high viral transmission The aim of this study is to evaluate BAL in post-acute COVID-19 patients for:Cytological and cellular patterns. Microbial analysis for possibility of presence of bacterial, mycobacerial or fungal co-infection.PCR for corona virus
Introduction: Secondary pneumonia is frequently seen in COVID-19 cases followed up intubated, and high mortality rates can be observed. Isolation of the agent with bronchoalveolar lavage (BAL) culture or endotracheal aspirate (ETA) culture may increase the success of treatment. This study aimed to retrospectively analyze the results of BAL and ETA cultures in intubated COVID-19 cases. Methods: We routinely apply BAL culture with bronchoscopy or ETA culture within the first 48 hours after intubating. We retrospectively screened cases who underwent BAL and ETA. They were divided into two groups: Group B and E. Evaluated parameters were compared in both groups. Results: Demographic data and blood test results were similar in both groups. Intensive care unit (ICU) and intubation durations, and culture positivity were statistically significantly higher in Group B. Although not statistically significant, the mortality rate was higher in Group E. The most growth microorganisms were Candida species. Conclusion: Mortality rates were consistent with the literature. Since the microorganism isolation rate is higher with BAL and antimicrobial treatment is applied more effectively; early deaths were prevented and stay periods were prolonged. In contrast, these durations were shorter in the ETA group due to higher mortality. In intubated COVID-19 cases, a more effective treatment process can be carried out by clearing the airway with fiberoptic bronchoscopy and by specifically planning the treatment according to the BAL culture. This may have a positive effect on prognosis and mortality.
In order to improve the accuracy of the diagnosis of pulmonary pathogens and reduce the adverse impact of excessive BAL volume on patients, this study intends to explore the most optimal lavage volume in the middle lobe and the lower lobe of critical patients as well as seeking for the best way to manage BALF samples by means of detecting alveolar proteins and bacterial composition in BALF samples. The hypothesis is that the optimal lavage volume in the middle lobe and the lower lobe might be different. And to sample BALF separately through sequential lavage might be a better way to improve the accuracy of the diagnosis of pneumonia pathogens.
The execution of diagnostic-therapeutic investigations by bronchial endoscopy can expose the patient to acute respiratory failure (ARF). In particular, the risk of hypoxemia is greater during broncho-alveolar lavage (BAL). For this reason, oxygen therapy is administered at low or high flows during the course of bronchoscopic procedures, in order to avoid hypoxemia. Few clinical studies have demonstrated the efficacy and safety of high flow oxygen through nasal cannula (HFNC) during BAL procedures, and no study has evaluated, during bronchial endoscopy, the effects of HFNC on diaphragmatic effort (assessed with ultrasound) and aeration and ventilation of the different lung regions (assessed with electrical impedance tomography). Therefore, investigators conceived the present randomized controlled study to evaluate possible differences existing during bronchoscopy between oxygen therapy administered with HFNC and conventional (low-flow) oxygen therapy, delivered through nasal cannula.
Sepsis leads to a deregulated host response that can lead to organ failure. During sepsis, experimental and clinical data suggest the occurrence of mitochondrial dysfunctions, particularly in circulating muscle and monocytes, which may contribute to organ failure and death. Lower respiratory infection is the leading cause of death from infectious causes. Mechanical ventilation (MV) is required in 20% of cases of bacterial pneumopathy with Streptococcus pneumoniae (S.p.) , with mortality reaching 50%. There are then frequently criteria for acute respiratory distress syndrome (ARDS), combining bilateral lung involvement and marked hypoxemia. Cyclic stretching of lung cells induced by MV causes sterile inflammation and tissue damage (i.e. ventilator-induced lung injury [VILI]), which can cause cellular dysfunction that alter the immune response, particularly during ARDS. This is why the application of a so-called protective MV is then required. However, this does not prevent about one-third of patients from showing signs of alveolar overdistension, as evidenced by an increase in motor pressure (MP) (MP≥ 15 cmH2O), associated with an increase in mortality. The deleterious effects of MV could be explained by the occurrence of mitochondrial abnormalities. Indeed, the cyclic stretching of lung cells leads to dysfunction in the respiratory chain and the production of free oxygen radicals (FOS), altering membrane permeability. These phenomena could promote VILI, facilitate the translocation of bacteria from the lung to the systemic compartment and lead to alterations in immune response. In our model of S.p. pneumopathy in rabbits, animals on MV develop more severe lung disorders (lack of pulmonary clearance of bacteria, bacterial translocation in the blood, excess mortality), compared to animals on spontaneous ventilation (SV). Intracellular pulmonary mitochondrial DNA (mtDNA) concentrations, a reflection of the mitochondrial pool, are significantly decreased in ventilated rabbits compared to SV rabbits and in infected rabbits compared to uninfected rabbits. At the same time, the mitochondrial content of circulating cells decreased early (H8) in all infected rabbits, but was only restored in rabbits in SV, those who survived pneumonia (Blot et al, poster ECCMID 2015, submitted article). These data suggest an alteration in the mechanisms that restore mitochondrial homeostasis (mitochondrial biogenesis and mitophagy) during the dual infection/MV agression, which may explain the observed excess mortality. Other work by our team illustrates the importance of these phenomena by showing in a mouse model of polymicrobial infection that inhibition of mitophagia in macrophages promotes survival (Patoli et al, in preparation). Human data on this subject are non-existent. The phenomena of mitochondrial dysfunction nevertheless deserve to be explored in humans during the combined MV/pneumopathy aggression in order to understand its possible impact on the effectiveness of the host's immune response. In a personalized medicine approach, these data would open up prospects for targeted therapies, capable of activating mitochondrial biogenesis and/or modulating mitophagia, to prevent organ dysfunction and mortality during severe CALs treated with antibiotic therapy.