Name (Synonyms) | Correlation | |
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drug1217 | Sampling (EDTA blood, pharyngeal and nose swabs, bronchoalveolar lavage ,urine) Wiki | 0.71 |
drug518 | FilmArray Pneumonia Wiki | 0.71 |
drug438 | Dornase Alfa Wiki | 0.71 |
drug439 | Dornase Alfa Inhalation Solution Wiki | 0.71 |
Name (Synonyms) | Correlation | |
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D045169 | Severe Acute Respiratory Syndrome NIH | 0.04 |
D018352 | Coronavirus Infections NIH | 0.03 |
Name (Synonyms) | Correlation |
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There are 2 clinical trials
International guidelines suggest the administration of empirical broad-spectrum antibiotics for suspected bacterial co-infection in COVID-19 critically ill. However, data on associated respiratory infections is rare and antimicrobial stewardship interventions promoting antibiotic savings are non-existent in this context. The main objectives of the trial are: to evaluate the rate of co-infections among COVID-19 critically ill to evaluate the added value of a a rapid molecular diagnostic tool (FA-PNEU) to detect the presence of co-infecting pathogens in order to rapidly tailor the patient's antibiotic treatment
Description: COVID-19 infections with additional bacteria/viruses identified through FA-PNEU testing
Measure: % of COVID-19 co-infections Time: through study completion, an average of 1 monthDescription: The rapid FA results could allow a fast modification of the empirical antibiotherapy. This percentage will be measured.
Measure: % of antibiotic switches following FA results Time: through study completion, an average of 1 monthIn light of the rapidly emerging pandemic of SARS-CoV-2 infections, the global population and health care systems are facing unprecedented challenges through the combination of transmission and the potential for severe disease. Acute respiratory distress syndrome (ARDS) has been found with unusual clinical features dominated by substantial alveolar fluid load. It is unknown whether this is primarily caused by endothelial dysfunction leading to capillary leakage or direct virus induced damage. This knowledge gap is significant because the initial balance between fluid management and circulatory support appear to be decisive. On progression of the disease, bacterial superinfection facilitated by inflammation and virus related damage, has been identified as the main factor for patient outcome, but the role of the host versus the environment microbiome remains unclear. The overarching aim of the present research proposal is to improve therapeutic strategies in critically ill patients with ARDS due to SARS-CoV-2 infection by advancing the pathophysiological understanding of this novel disease. This research thus focuses on inflammation, microcirculatory dysfunction and superinfection, aiming to elucidate risk factors (RF) for the development of severe ARDS in SARS-CoV-2 infected patients and contribute to the rationale for therapeutic strategies. The hypotheses are that (I) the primary damage to the lung in SARS-CoV-2 ARDS is mediated through an exaggerated pro-inflammatory response causing primary endothelial dysfunction, and subsequently acting two-fold on the degradation of the lung parenchyma - through the primary cytokine response, and through recruitment of the inflammatory-monocyte-lymphocyte-neutrophil axis. The pronounced inflammation and primary damage to the lung disrupts the pulmonary microbiome, leading secondarily to pulmonary superinfections. (II) Pulmonary bacterial superinfections are a significant cause of morbidity and mortality in COVID-19 patients. Pathogen colonization main Risk Factor for lower respiratory tract infections. To establish colonization, pathogens have to interact with the local microbiota (a.k.a. microbiome) and certain microbiome profiles will be more resistant to pathogen invasion. Finally, (III) Handheld devices used in clinical routine are a potential reservoir and carrier of both, SARS-CoV-2, as well as bacteria causing nosocomial pneumonia.
Description: Daily recorded Vitals and Inflammatory Response will be analyzed by means of multivariable mixed effect models analysis and generalized linear models, with corrections for time and randomness. To account for the different units of measure we will standardize all values to an absolute measure by means of the z-score. The following variables will be considered: Respiratory values, Vital signs, Haemodynamic monitoring, Microcirculation, Inflammatory values, Hematology: T-cells CD3, 4 and 6 Chemistry: Inflammatory Cytokines and Biomarkers:CRP, PCT, MR-ProADM, IFN-1, IFN-γ, TNF-α/β, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, MIG, RANTES, MCP-1, IP-10, PD1, PD-L1 Lipid-pannel3: LDL, HDL, Cholesterol, Triglyceride Other: HLA DR/DQ TBS, Swabs, sublingual nonnvasive microscopy
Measure: Change of pro-inflammatory response over the ICU stay as a causative for primary endothelial dysfunction Time: Admission, on day 0, day 1, day 2 , day 3, day 5, every 5 days up to 1 yearDescription: COX proportional hazards model and generalized mixed effect models assessing the effect of positive bacterial infection on mortality. Correction for time and randomness (multiple sampling). Super infection will be defined as a positive bacterial/ fungal sample (Bood cultures, BAL, TBS, Swabs, Urine)
Measure: Time-to-event "pulmonary bacterial superinfection or death" Time: Through study completion, an average of 30 daysDescription: Mobile devices will be swabed for bacterial and viral contamination, simultaneously adherence of the user to disinfection protocols will be assessed.
Measure: Positive bacteria and/ or SARS-CoV-2 cultures on handheld devices used in clinical routine and correlation to the adherence to disinfection protocols Time: Through study completion, an average of 30 daysDescription: SF 36 questionnaire
Measure: Life Quality after COVID-19 Infection Time: follow up 30 + 90 days and 1 year after discharge