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Background: Protective ventilation seems crucial during early Acute Respiratory Distress Syndrome (ARDS), but the optimal duration of lung protection remains undefined. High driving pressures (ΔP) and excessive patient ventilatory drive may hinder lung recovery, resulting in self-inflicted lung injury. The hidden nature of the ΔP generated by patient effort complicates the situation further. Our study aimed to assess the feasibility of an extended lung protection strategy that includes a stepwise protocol to control the patient ventilatory drive, assessing its impact on lung recovery. Methods: We conducted a single-center randomized study on patients with moderate/severe COVID-19-ARDS with low respiratory system compliance (CRS < 0.6 (mL/Kg)/cmH2O). The intervention group received a ventilation strategy guided by Electrical Impedance Tomography aimed at minimizing ΔP and patient ventilatory drive. The control group received the ARDSNet low-PEEP strategy. The primary outcome was the modified lung injury score (mLIS), a composite measure that integrated daily measurements of CRS, along with oxygen requirements, oxygenation, and X-rays up to day 28. The mLIS score was also hierarchically adjusted for survival and extubation rates. Results: The study ended prematurely after three consecutive months without patient enrollment, attributed to the pandemic subsiding. The intention-to-treat analysis included 76 patients, with 37 randomized to the intervention group. The average mLIS score up to 28 days was not different between groups (P = 0.95, primary outcome). However, the intervention group showed a faster improvement in the mLIS (1.4 vs. 7.2 days to reach 63% of maximum improvement; P < 0.001), driven by oxygenation and sustained improvement of X-ray (P = 0.001). The intervention group demonstrated a sustained increase in CRS up to day 28 (P = 0.009) and also experienced a shorter time from randomization to room-air breathing (P = 0.02). Survival at 28 days and time until liberation from the ventilator were not different between groups. Conclusions: The implementation of an individualized PEEP strategy alongside extended lung protection appears viable. Promising secondary outcomes suggested a faster lung recovery, endorsing further examination of this strategy in a larger trial. Clinical trial registration This trial was registered with ClinicalTrials.gov (number NCT04497454) on August 04, 2020. [ABSTRACT FROM AUTHOR]

Currently there is a lack of randomized trial data examining the use of the antiviral nirmatrelvir/ritonavir in paediatric patients with SARS-CoV-2 infection. This target trial emulation study aims to address this gap by evaluating the use of nirmatrelvir/ritonavir in non-hospitalized paediatric patients aged 12–17 years with SARS-CoV-2 Omicron variant infection. Among paediatric patients diagnosed between 16th March 2022 and 5th February 2023, exposure was defined as outpatient nirmatrelvir/ritonavir treatment within 5 days of symptom onset or COVID-19 diagnosis. Primary outcome was 28 day all-cause mortality or all-cause hospitalization, while secondary outcomes were 28 day in-hospital disease progression, 28 day COVID-19-specific hospitalization, multisystem inflammatory syndrome in children (MIS-C), acute liver injury, acute renal failure, and acute respiratory distress syndrome. Overall, 49,378 eligible paediatric patients were included. Nirmatrelvir/ritonavir treatment was associated with reduced 28 day all-cause hospitalization (absolute risk reduction = 0.23%, 95%CI = 0.19%–0.31%; relative risk = 0.66, 95%CI = 0.56–0.71). No events of mortality, in-hospital disease progression, or adverse clinical outcomes were observed among nirmatrelvir/ritonavir users. The findings confirmed the effectiveness of nirmatrelvir/ritonavir in reducing all-cause hospitalization risk among non-hospitalized pediatric patients with SARS-CoV-2 Omicron variant infection. In this target trial emulation study, the authors evaluate effectiveness of nirmatrelvir/ritonavir in non-hospitalized paediatric patients aged 12–17 years with SARS-CoV-2 Omicron infection and show reduced risks of 28 day all-cause mortality or hospitalization associated with the treatment. [ABSTRACT FROM AUTHOR]

Background: Limited evidence exists regarding the link between platelet count and 30-day in-hospital mortality in acute respiratory failure (ARF) patients. Thus, this study aims to investigate this association among ICU patients experiencing acute respiratory failure. Methods: We conducted a retrospective cohort study across multiple centers, utilizing data from the US eICU-CRD v2.0 database covering 22,262 patients with ARF in the ICU from 2014 to 2015. Our aim was to investigate the correlation between platelet count and 30-day in-hospital mortality using binary logistic regression, subgroup analyses, and smooth curve fitting. Results: The 30-day in-hospital mortality rate was 19.73% (4393 out of 22,262), with a median platelet count of 213 × 109/L. After adjusting for covariates, our analysis revealed an inverse association between platelet count and 30-day in-hospital mortality (OR = 0.99, 95% CI 0.99, 0.99). Subgroup analyses supported the robustness of these findings. Furthermore, a nonlinear relationship was identified between platelet count and 30-day in-hospital mortality, with the inflection point at 120 × 109/L. Below the inflection point, the effect size (OR) was 0.89 (0.87, 0.91), indicating a significant association. However, beyond this point, the relationship was not statistically significant. Conclusion: This study establishes a clear negative association between platelet count and 30-day in-hospital mortality among ICU patients with ARF. Furthermore, we have identified a nonlinear relationship with saturation effects, indicating that among ICU patients with acute respiratory failure, the lowest 30-day in-hospital mortality rate occurs when the baseline platelet count is approximately 120 × 109/L. [ABSTRACT FROM AUTHOR]

Patients with acute exacerbation of lung fibrosis with usual interstitial pneumonia (EUIP) pattern are at increased risk for ventilator-induced lung injury (VILI) and mortality when exposed to mechanical ventilation (MV). Yet, lack of a mechanical model describing UIP-lung deformation during MV represents a research gap. Aim of this study was to develop a constitutive mathematical model for UIP-lung deformation during lung protective MV based on the stress–strain behavior and the specific elastance of patients with EUIP as compared to that of acute respiratory distress syndrome (ARDS) and healthy lung. Partitioned lung and chest wall mechanics were assessed for patients with EUIP and primary ARDS (1:1 matched based on body mass index and PaO2/FiO2 ratio) during a PEEP trial performed within 24 h from intubation. Patient's stress–strain curve and the lung specific elastance were computed and compared with those of healthy lungs, derived from literature. Respiratory mechanics were used to fit a novel mathematical model of the lung describing mechanical-inflation-induced lung parenchyma deformation, differentiating the contributions of elastin and collagen, the main components of lung extracellular matrix. Five patients with EUIP and 5 matched with primary ARDS were included and analyzed. Global strain was not different at low PEEP between the groups. Overall specific elastance was significantly higher in EUIP as compared to ARDS (28.9 [22.8–33.2] cmH2O versus 11.4 [10.3–14.6] cmH2O, respectively). Compared to ARDS and healthy lung, the stress/strain curve of EUIP showed a steeper increase, crossing the VILI threshold stress risk for strain values greater than 0.55. The contribution of elastin was prevalent at lower strains, while the contribution of collagen was prevalent at large strains. The stress/strain curve for collagen showed an upward shift passing from ARDS and healthy lungs to EUIP lungs. During MV, patients with EUIP showed different respiratory mechanics, stress–strain curve and specific elastance as compared to ARDS patients and healthy subjects and may experience VILI even when protective MV is applied. According to our mathematical model of lung deformation during mechanical inflation, the elastic response of UIP-lung is peculiar and different from ARDS. Our data suggest that patients with EUIP experience VILI with ventilatory setting that are lung-protective for patients with ARDS. [ABSTRACT FROM AUTHOR]

Acute Respiratory Distress Syndrome (ARDS) is a critical form of Acute Lung Injury (ALI), challenging clinical diagnosis and severity assessment. This study evaluates the potential utility of various hematological markers in burn-mediated ARDS, including Neutrophil-to-Lymphocyte Ratio (NLR), Mean Platelet Volume (MPV), MPV-to-Lymphocyte Ratio (MPVLR), Platelet count, and Platelet Distribution Width (PDW). Employing a retrospective analysis of data collected over 12 years, this study focuses on the relationship between these hematological markers and ARDS diagnosis and severity in hospitalized patients. The study establishes NLR as a reliable systemic inflammation marker associated with ARDS severity. Elevated MPV and MPVLR also emerged as significant markers correlating with adverse outcomes. These findings suggest these economical, routinely measured markers can enhance traditional clinical criteria, offering a more objective approach to ARDS diagnosis and severity assessment. Hematological markers such as NLR, MPV, MPVLR, Platelet count, and PDW could be invaluable in clinical settings for diagnosing and assessing ARDS severity. They offer a cost-effective, accessible means to improve diagnostic accuracy and patient stratification in ARDS. However, further prospective studies are necessary to confirm these findings and investigate their integration with other diagnostic tools in diverse clinical settings. [ABSTRACT FROM AUTHOR]

Background: Inflammation and endothelial barrier dysfunction are the major pathophysiological changes in acute respiratory distress syndrome (ARDS). Sphingosine-1-phosphate receptor 3 (S1PR3), a G protein-coupled receptor, has been found to mediate inflammation and endothelial cell (EC) integrity. However, the function of S1PR3 in ARDS has not been fully elucidated. Methods: We used a murine lipopolysaccharide (LPS)-induced ARDS model and an LPS- stimulated ECs model to investigate the role of S1PR3 in anti-inflammatory effects and endothelial barrier protection during ARDS. Results: We found that S1PR3 expression was increased in the lung tissues of mice with LPS-induced ARDS. TY-52156, a selective S1PR3 inhibitor, effectively attenuated LPS-induced inflammation by suppressing the expression of proinflammatory cytokines and restored the endothelial barrier by repairing adherens junctions and reducing vascular leakage. S1PR3 inhibition was achieved by an adeno-associated virus in vivo and a small interfering RNA in vitro. Both the in vivo and in vitro studies demonstrated that pharmacological or genetic inhibition of S1PR3 protected against ARDS by inhibiting the NF-κB pathway and improving mitochondrial oxidative phosphorylation. Conclusions: S1PR3 inhibition protects against LPS-induced ARDS via suppression of pulmonary inflammation and promotion of the endothelial barrier by inhibiting NF-κB and improving mitochondrial oxidative phosphorylation, indicating that S1PR3 is a potential therapeutic target for ARDS. [ABSTRACT FROM AUTHOR]

Cytokine-mediated systemic inflammation after open thoracoabdominal aortic aneurysm (TAAA) repairs plays a pivotal role in disrupting circulatory homeostasis, potentially leading to organ dysfunction. The bioactive form of adrenomedullin (bio-ADM) is a peptide hormone with immunomodulatory and vasomotor effects, making it a potential diagnostic agent in these cases. This retrospective, bicentric study, conducted between January 2019 and December 2022, recruited 36 elective open TAAA repair patients in two German centres. Serum and plasma samples were collected at multiple time points to measure bio-ADM levels. The primary objective was to evaluate the association of bio-ADM levels with the onset of acute respiratory distress syndrome (ARDS), with secondary endpoints focusing on mortality and SIRS-related morbidity. Results showed a significant association between postoperative bio-ADM levels (12–48 h after surgery) and the onset of ARDS (p <.001), prolonged ventilation (p =.015 at 12h after surgery), atrial fibrillation (p <.001), and mortality (p =.05 at 24h). The biomarker was also strongly associated with sepsis (p =.01 at 12 h) and multi-organ dysfunction syndrome (MODS) (p =.02 at 24 h after surgery). The study underscores the potential utility of bio-ADM as a diagnostic tool for identifying patients at risk of postoperative complications following open TAAA repairs. [ABSTRACT FROM AUTHOR]

Background: ARDS is a heterogeneous syndrome with distinct clinical phenotypes. Here we investigate whether the presence or absence of large pulmonary ultrasonographic consolidations can categorize COVID-19 ARDS patients requiring mechanical ventilation into distinct clinical phenotypes. Methods: This is a retrospective study performed in a tertiary-level intensive care unit in Israel between April and September 2020. Data collected included lung ultrasound (LUS) findings, respiratory parameters, and treatment interventions. The primary outcome was a composite of three ARDS interventions: prone positioning, high PEEP, or a high dose of inhaled nitric oxide. Results: A total of 128 LUS scans were conducted among 23 patients. The mean age was 65 and about two-thirds were males. 81 scans identified large consolidation and were classified as "C-type", and 47 scans showed multiple B-lines with no or small consolidation and were classified as "B-type". The presence of a "C-type" study had 2.5 times increased chance of receiving the composite primary outcome of advanced ARDS interventions despite similar SOFA scores, Pao2/FiO2 ratio, and markers of disease severity (OR = 2.49, %95CI 1.40–4.44). Conclusion: The presence of a "C-type" profile with LUS consolidation potentially represents a distinct COVID-19 ARDS subphenotype that is more likely to require aggressive ARDS interventions. Further studies are required to validate this phenotype in a larger cohort and determine causality, diagnostic, and treatment responses. [ABSTRACT FROM AUTHOR]

Aim: Acute respiratory distress syndrome or ARDS is an acute, severe form of respiratory failure characterised by poor oxygenation and bilateral pulmonary infiltrates. Advancements in signal processing and machine learning have led to promising solutions for classification, event detection and predictive models in the management of ARDS. Method: In this review, we provide systematic description of different studies in the application of Machine Learning (ML) and artificial intelligence for management, prediction, and classification of ARDS. We searched the following databases: Google Scholar, PubMed, and EBSCO from 2009 to 2023. A total of 243 studies was screened, in which, 52 studies were included for review and analysis. We integrated knowledge of previous work providing the state of art and overview of explainable decision models in machine learning and have identified areas for future research. Results: Gradient boosting is the most common and successful method utilised in 12 (23.1%) of the studies. Due to limitation of data size available, neural network and its variation is used by only 8 (15.4%) studies. Whilst all studies used cross validating technique or separated database for validation, only 1 study validated the model with clinician input. Explainability methods were presented in 15 (28.8%) of studies with the most common method is feature importance which used 14 times. Conclusion: For databases of 5000 or fewer samples, extreme gradient boosting has the highest probability of success. A large, multi-region, multi centre database is required to reduce bias and take advantage of neural network method. A framework for validating with and explaining ML model to clinicians involved in the management of ARDS would be very helpful for development and deployment of the ML model. [ABSTRACT FROM AUTHOR]

Super‐enhancers play prominent roles in driving robust pathological gene expression, but they are hidden in human genome at noncoding regions, making them difficult to explore. Leukemia inhibitory factor (LIF) is a multifunctional cytokine crucially involved in acute respiratory distress syndrome (ARDS) and lung cancer progression. However, the mechanisms governing LIF regulation in disease contexts remain largely unexplored. In this study, we observed elevated levels of LIF in the bronchoalveolar lavage fluid (BALF) of patients with sepsis‐related ARDS compared to those with nonsepsis‐related ARDS. Furthermore, both basal and LPS‐induced LIF expression were under the control of super‐enhancers. Through analysis of H3K27Ac ChIP‐seq data, we pinpointed three potential super‐enhancers (LIF‐SE1, LIF‐SE2, and LIF‐SE3) located proximal to the LIF gene in cells. Notably, genetic deletion of any of these three super‐enhancers using CRISPR‐Cas9 technology led to a significant reduction in LIF expression. Moreover, in cells lacking these super‐enhancers, both cell growth and invasion capabilities were substantially impaired. Our findings highlight the critical role of three specific super‐enhancers in regulating LIF expression and offer new insights into the transcriptional regulation of LIF in ARDS and lung cancer. Significance statement: Leukemia inhibitory factor (LIF) is a multifunctional cytokine with diverse functions, playing crucial roles in both acute respiratory distress syndrome (ARDS) and lung cancer development. However, the mechanisms underlying the elevation of LIF in diseases remain largely unclear. In our study, we discovered that basal and LPS‐induced expression of LIF is governed by super‐enhancers. This finding offers novel insights into the transcriptional regulation of LIF expression in the context of ARDS and lung cancer. [ABSTRACT FROM AUTHOR]

Administering sodium bicarbonate (NaHCO3) to patients with respiratory acidosis breathing spontaneously is contraindicated because it increases carbon dioxide load and depresses pulmonary ventilation. Nonetheless, several studies have reported salutary effects of NaHCO3 in patients with respiratory acidosis but the underlying mechanism remains uncertain. Considering that such reports have been ignored, we examined the ventilatory response of unanesthetized dogs with respiratory acidosis to hypertonic NaHCO3 infusion (1 N, 5 mmol/kg) and compared it with that of animals with normal acid-base status or one of the remaining acid-base disorders. Ventilatory response to NaHCO3 infusion was evaluated by examining the ensuing change in PaCO2 and the linear regression of the PaCO2 vs. pH relationship. Strikingly, PaCO2 failed to increase and the ΔPaCO2 vs. ΔpH slope was negative in respiratory acidosis, whereas PaCO2 increased consistently and the ΔPaCO2 vs. ΔpH slope was positive in the remaining study groups. These results cannot be explained by differences in buffering-induced decomposition of infused bicarbonate or baseline levels of blood pH, PaCO2, and pulmonary ventilation. We propose that NaHCO3 infusion improved the ventilatory efficiency of animals with respiratory acidosis, i.e., it decreased their ratio of total pulmonary ventilation to carbon dioxide excretion (VE/VCO2). Such exclusive effect of NaHCO3 infusion in animals with respiratory acidosis might emanate from baseline increased VD/VT (dead space/tidal volume) caused by bronchoconstriction and likely reduced pulmonary blood flow, defects that are reversed by alkali infusion. Our observations might explain the beneficial effects of NaHCO3 reported in patients with acute respiratory acidosis. [ABSTRACT FROM AUTHOR]

Purpose: Oxidative stress is proposed to be critical in acute lung disease, but methods to monitor radicals in lungs are lacking. Our goal is to develop low-frequency electron paramagnetic resonance (EPR) methods to monitor radicals that contribute to the disease. Procedures: Free radicals generated in a lipopolysaccharide-induced mouse model of acute respiratory distress syndrome reacted with cyclic hydroxylamines CPH (1-hydroxy-3-carboxy-2,2,5,5-tetramethylpyrrolidine hydrochloride) and DCP-AM-H (4-acetoxymethoxycarbonyl-1-hydroxy-2,2,5,5-tetramethylpyrrolidine-3-carboxylic acid), which were converted into the corresponding nitroxide radicals, CP• and DCP•. The EPR signals of the nitroxide radicals in excised lungs were imaged with a 1 GHz EPR spectrometer/imager that employs rapid scan technology. Results: The small numbers of nitroxides formed by reaction of the hydroxylamine with superoxide result in low signal-to-noise in the spectra and images. However, since the spectral properties of the nitroxides are known, we can use prior knowledge of the line shape and hyperfine splitting to fit the noisy data, yielding well-defined spectra and images. Two-dimensional spectral-spatial images are shown for lung samples containing (4.5 ± 0.5) ×1014 CP• and (9.9 ± 1.0) ×1014 DCP• nitroxide spins. These results suggest that a probe that accumulates in cells gives a stronger nitroxide signal than a probe that is more easily washed out of cells. Conclusion: The nitroxide radicals in excised mouse lungs formed by reaction with hydroxylamine probes CPH and DCP-AM-H can be imaged at 1 GHz. [ABSTRACT FROM AUTHOR]

Purpose: Patients with hyper- vs. hypo-inflammatory subphenotypes of acute respiratory distress syndrome (ARDS) exhibit different clinical outcomes. Inflammation increases the production of reactive oxygen species (ROS) and increased ROS contributes to the severity of illness. Our long-term goal is to develop electron paramagnetic resonance (EPR) imaging of lungs in vivo to precisely measure superoxide production in ARDS in real time. As a first step, this requires the development of in vivo EPR methods for quantifying superoxide generation in the lung during injury, and testing if such superoxide measurements can differentiate between susceptible and protected mouse strains. Procedures: In WT mice, mice lacking total body extracellular superoxide dismutase (EC-SOD) (KO), or mice overexpressing lung EC-SOD (Tg), lung injury was induced with intraperitoneal (IP) lipopolysaccharide (LPS) (10 mg/kg). At 24 h after LPS treatment, mice were injected with the cyclic hydroxylamines 1-hydroxy-3-carboxy-2,2,5,5-tetramethylpyrrolidine hydrochloride (CPH) or 4-acetoxymethoxycarbonyl-1-hydroxy-2,2,5,5-tetramethylpyrrolidine-3-carboxylic acid (DCP-AM-H) probes to detect, respectively, cellular and mitochondrial ROS – specifically superoxide. Several probe delivery strategies were tested. Lung tissue was collected up to one hour after probe administration and assayed by EPR. Results: As measured by X-band EPR, cellular and mitochondrial superoxide increased in the lungs of LPS-treated mice compared to control. Lung cellular superoxide was increased in EC-SOD KO mice and decreased in EC-SOD Tg mice compared to WT. We also validated an intratracheal (IT) delivery method, which enhanced the lung signal for both spin probes compared to IP administration. Conclusions: We have developed protocols for delivering EPR spin probes in vivo, allowing detection of cellular and mitochondrial superoxide in lung injury by EPR. Superoxide measurements by EPR could differentiate mice with and without lung injury, as well as mouse strains with different disease susceptibilities. We expect these protocols to capture real-time superoxide production and enable evaluation of lung EPR imaging as a potential clinical tool for subphenotyping ARDS patients based on redox status. [ABSTRACT FROM AUTHOR]

Aim: A pilot randomised controlled trial assessed the early application of nasal high‐flow (NHF) therapy compared with standard oxygen therapy (SOT), in children aged 0 to 16 years presenting to paediatric emergency departments with acute hypoxaemic respiratory failure (AHRF). The study estimated the need to escalate therapy and hospital length of stay in the NHF group compared with SOT. This sub‐study then assessed the subsequent cost‐effectiveness. Methods: A decision tree‐based model was developed, alongside the clinical study, to estimate cost‐effectiveness, from the healthcare sector perspective. The primary health economics outcome is measured as incremental cost per length of hospital stay avoided. Incremental cost effectiveness ratios (ICER) measuring change in cost per change in length of stay, were obtained for four samples, depending on responder status and obstructive airways disease. These were (1) obstructive and responder, (2) non‐obstructive and responder, (3) obstructive and non‐responder and (4) non obstructive and non‐responder. Bootstrapping of parameters accounted for uncertainty in estimates of cost and outcome. Results: The ICER for patients randomised to NHF, indicated an additional A$367.20 for a lower hospital length of stay (in days) in the non‐obstructive/non‐responder sample. In the bootstrap sample, this was found to be cost effective above a willingness to pay threshold of A$10 000. The ICER was A$440.86 in the obstructive/responder sample and A$469.56 in the non‐obstructive/responder sample – but both resulted in a longer length of stay. The ICER in the obstructive/non‐responder sample was A$52 167.76, also with a longer length of stay, mainly impacted by a small sample of severe cases. Conclusion: As first‐line treatment, NHF is unlikely to be cost‐effective compared with SOT, but for non‐obstructive patients who required escalation in care (non‐obstructive non‐responder), NHF is likely to be cost‐effective if willingness‐to‐pay per reduced hospital length of stay is more than A$10 000 per patient. [ABSTRACT FROM AUTHOR]

Background: During the COVID-19 pandemic, emergency departments were overcrowded with critically ill patients, and many providers were confronted with ethical dilemmas in assigning respiratory support to them due to scarce resources. Quick tools for evaluating patients upon admission were necessary, as many existing scores proved inaccurate in predicting outcomes. The ROX Index (RI), a rapid and straightforward scoring system reflecting respiratory status in acute respiratory failure patients, has shown promise in predicting outcomes for COVID-19 patients. The 24 h difference in the RI accurately gauges mortality and the need for invasive mechanical ventilation (IMV) among patients with COVID-19. Methods: Study design: Prospective cohort study. A total of 204 patients were admitted to the emergency department from May to August 2020. Data were collected from the clinical records. The RI was calculated at admission and 24 h later, and the difference was used to predict the association with mortality and the need for IMV, a logistic regression model was used to adjust for age, sex, presence of comorbidities, and disease severity. Finally, the data were analyzed using ROC. Results: The difference in respiratory RI between admission and 24 h is a good predictor for death (AUC 0.92) and for mechanic ventilation (AUC: 0.75). Each one-unit decrease in the RI difference at 24 h was associated with an odds ratio of 1.48 for the risk of death (95%CI: 1.31–1.67) and an odds ratio of 1.16 for IMV (95% IC: 1.1–1.23). Conclusions: The 24 h variation of RI is a good prediction tool to allow healthcare professionals to identify the patients who will benefit from invasive treatment, especially in low-resource settings. [ABSTRACT FROM AUTHOR]

Acute respiratory distress syndrome (ARDS) is an acute and severe clinical complication lacking effective therapeutic interventions. The disruption of the lung epithelial barrier plays a crucial role in ARDS pathogenesis. Recent studies have proposed the involvement of abnormal mitochondrial dynamics mediated by dynamin-related protein 1 (Drp1) in the mechanism of impaired epithelial barrier in ARDS. Hydrogen is an anti-oxidative stress molecule that regulates mitochondrial function via multiple signaling pathways. Our previous study confirmed that hydrogen modulated oxidative stress and attenuated acute pulmonary edema in ARDS by upregulating thioredoxin 1 (Trx1) expression, but the exact mechanism remains unclear. This study aimed to investigate the effects of hydrogen on mitochondrial dynamics both in vivo and in vitro. Our study revealed that hydrogen inhibited lipopolysaccharide (LPS)-induced phosphorylation of Drp1 (at Ser616), suppressed Drp1-mediated mitochondrial fission, alleviated epithelial tight junction damage and cell apoptosis, and improved the integrity of the epithelial barrier. This process was associated with the upregulation of Trx1 in lung epithelial tissues of ARDS mice by hydrogen. In addition, hydrogen treatment reduced the production of reactive oxygen species in LPS-induced airway epithelial cells (AECs) and increased the mitochondrial membrane potential, indicating that the mitochondrial dysfunction was restored. Then, the expression of tight junction proteins occludin and zonula occludens 1 was upregulated, and apoptosis in AECs was alleviated. Remarkably, the protective effects of hydrogen on the mitochondrial and epithelial barrier were eliminated after applying the Trx1 inhibitor PX-12. The results showed that hydrogen significantly inhibited the cell apoptosis and the disruption of epithelial tight junctions, maintaining the integrity of the epithelial barrier in mice of ARDS. This might be related to the inhibition of Drp1-mediated mitochondrial fission through the Trx1 pathway. The findings of this study provided a new theoretical basis for the application of hydrogen in the clinical treatment of ARDS. [Display omitted] • Hydrogen could alleviate impaired lung epithelial barrier in Acute Respiratory Distress Syndrome (ARDS). • Drp1-mediated mitochondrial fission in ARDS is a compensatory mechanism. • Hydrogen alleviates ARDS lung injury via inhibiting Drp1-mediated mitochondrial fission through the Trx1 pathway. [ABSTRACT FROM AUTHOR]

Background: The oxygenation index (OI) and oxygen saturation index (OSI) are proven mortality predictors in pediatric and adult patients, traditionally using mean airway pressure (Pmean). We introduce novel indices, replacing Pmean with DP (ΔPinsp), MPdyn, and MPtot, assessing their potential for predicting COVID-19 acute respiratory distress syndrome (ARDS) mortality, comparing them to traditional indices. Methods: We studied 361 adult COVID-19 ARDS patients for 7 days, collecting ΔPinsp, MPdyn, and MPtot, OI-ΔPinsp, OI-MPdyn, OI-MPtot, OSI-ΔPinsp, OSI-MPdyn, and OSI-MPtot. We compared these in surviving and non-surviving patients over the first 7 intensive care unit (ICU) days using Mann–Whitney U test. Logistic regression receiver operating characteristic (ROC) analysis assessed AUC and CI values for ICU mortality on day three. We determined cut-off values using Youden's method and conducted multivariate Cox regression on parameter limits. Results: All indices showed significant differences between surviving and non-surviving patients on the third day of ICU care. The AUC values of OI-ΔPinsp were significantly higher than those of P/F and OI-Pmean (P values.0002 and <.0001, respectively). Similarly, AUC and CI values of OSI-ΔPinsp and OSI-MPdyn were significantly higher than those of SpO2/FiO2 and OSI-Pmean values (OSI-ΔPinsp: P <.0001, OSI-MPdyn: P values.047 and.028, respectively). OI-ΔPinsp, OSI-ΔPinsp, OI-MPdyn, OSI-MPdyn, OI-MPtot, and OSI-MPtot had AUC values of 0.72, 0.71, 0.69, 0.68, 0.66, and 0.64, respectively, with cut-off values associated with hazard ratios and P values of 7.06 (HR = 1.84, P =.002), 8.04 (HR = 2.00, P ≤.0001), 7.12 (HR = 1.68, P =.001), 5.76 (HR = 1.70, P ≤.0001), 10.43 (HR = 1.52, P =.006), and 10.68 (HR = 1.66, P =.001), respectively. Conclusions: Critical values of all indices were associated to higher ICU mortality rates and extended mechanical ventilation durations. The OI-ΔPinsp, OSI-ΔPinsp, and OSI-MPdyn indices displayed the strongest predictive capabilities for ICU mortality. These novel indices offer valuable insights for intensivists in the clinical management and decision-making process for ARDS patients. [ABSTRACT FROM AUTHOR]

• Computer simulations and the Lipinski rule evaluate the pharmacokinetic and toxicological aspects of methyl eugenol as a drug candidate. • Treatment with methyl eugenol (ME) during and after the initiation of acute respiratory distress syndrome (ARDS) can prevent the progression of acute inflammation. • In vivo and in silico tests indicate that ME oil is an orally bioavailable drug that exerts multifunctional cytoprotective activities. • ME oil can treat and prevent intestinal I/R-induced ARDS in rats. Acute respiratory distress syndrome (ARDS) is an inflammatory disease that affects the lungs with rupture of the alveolar-capillary barrier and loss of lung compliance, orchestrated by an intense inflammatory process mediated by neutrophils that culminates in diffuse alveolar data and tissue hypoxia. In this context, no specific drug has yet been applied to treat the syndrome. Therefore, finding new therapeutic targets that can treat the syndrome has become a research study. In view of this, methyl-eugenol (ME) has become the target of this study. The aim of this work was to carry out an in silico pharmacological and toxicological analysis with ADMET, as well as to determine, by means of molecular docking, the interaction affinity of the 5-LOX and COX-2 enzymes with ME and then the in vivo tests; in which male rats were distributed into five groups with five rats each, in which some groups were subjected to the process of ischemia and reperfusion (I/R). Groups G4 and G5 were treated by inhalation with ME (10 %). After completing these procedures, statistical analysis and lung histology were carried out. In the ADMET prediction, ME showed high intestinal absorption and a medium-permeability blood-brain barrier. ME had no violations of Lipinski's rule, demonstrating high potential as a drug candidate. Molecular docking showed that ME had the highest binding affinity with the 5-LOX enzyme. Finally, the statistical and histological analyses of the in vivo test showed acute and accentuated lung damage in the G1 group, while in the G4 and G5 groups, ME showed pharmacological efficacy, reducing the number of inflammatory cells, free macrophages and free radicals. The results indicate that ME oil is a favorable therapeutic approach in the treatment of ARDS. [ABSTRACT FROM AUTHOR]

Acute respiratory distress syndrome (ARDS) is characterized by a redistribution of regional lung perfusion that impairs gas exchange. While speculative, experimental evidence suggests that perfusion redistribution may contribute to regional inflammation and modify disease progression. Unfortunately, tools to visualize and quantify lung perfusion in patients with ARDS are lacking. This review explores recent advances in perfusion imaging techniques that aim to understand the pulmonary circulation in ARDS. Dynamic contrast-enhanced computed tomography captures first-pass kinetics of intravenously injected dye during continuous scan acquisitions. Different contrast characteristics and kinetic modeling have improved its topographic measurement of pulmonary perfusion with high spatial and temporal resolution. Dual-energy computed tomography can map the pulmonary blood volume of the whole lung with limited radiation exposure, enabling its application in clinical research. Electrical impedance tomography can obtain serial topographic assessments of perfusion at the bedside in response to treatments such as inhaled nitric oxide and prone position. Ongoing technological improvements and emerging techniques will enhance lung perfusion imaging and aid its incorporation into the care of patients with ARDS. • Pulmonary perfusion in ARDS is highly variable and difficult to predict using existing clinical metrics. • Pulmonary perfusion impacts gas exchange and may modulate ARDS progression. • Several modalities exist to image and measure pulmonary perfusion in experimental and clinical ARDS. • Defining perfusion patterns using imaging will help advance precision medicine in ARDS. [ABSTRACT FROM AUTHOR]

Background: As the pandemic progressed, the use of extracorporeal membrane oxygenation (ECMO) for COVID‐19‐related acute respiratory distress syndrome increased, and patient triage and transfer to ECMO centers became important to optimize patient outcomes. Our objectives are to identify predictors of patient transfer for veno‐venous extracorporeal membrane oxygenation (V‐V ECMO) evaluation as well as to describe the outcomes of accepted patients. Methods: This is a single‐center, retrospective analysis of V‐V ECMO transfer requests for adult patients with known or suspected COVID‐19 and respiratory failure from March 2020 until March 2021. Data were collected prospectively during the triage process for transfer requests as part of clinical patient care at our institution. Results: Of 341 referred patients, 112 (33%) were accepted for transfer to our facility, whereas 229 (67%) patients were declined for transfer. The Classification and Regression Tree analysis showed that patients' high pressure during airway pressure release ventilation (APRV) and age were the variables most significantly associated with the decision to accept or decline patients for transfer. Conclusions: Our triage process enabled one‐third of referred patients to be transferred for evaluation, with nearly 70% of those patients ultimately receiving ECMO support. High ventilator settings on APRV and young age were associated with acceptance for transfer. Accepted patients also had a higher incidence of adjunctive therapies (proning and paralysis) prior to transfer request, less cardiac or renal dysfunction, and a shorter duration of mechanical ventilation. Further research is warranted to investigate the outcomes of nontransferred patients. [ABSTRACT FROM AUTHOR]

Background: Incorporating unfamiliar therapies into practice requires effective longitudinal learning and the optimal way to achieve this is debated. Though not a novel therapy, ketamine in critical care has a paucity of data and variable acceptance, with limited research describing intensivist perceptions and utilization. The Coronavirus-19 pandemic presented a particular crisis where providers rapidly adapted analgosedation strategies to achieve prolonged, deep sedation due to a surge of severe acute respiratory distress syndrome (ARDS). Question: How does clinical experience with ketamine impact the perception and attitude of clinicians toward this therapy? Methods: We conducted a mixed-methods study using quantitative ketamine prescription data and qualitative focus group data. We analyzed prescription patterns of ketamine in a tertiary academic ICU during two different time points: pre-COVID-19 (March 1–June 30, 2019) and during the COVID-19 surge (March 1–June 30, 2020). Two focus groups (FG) of critical care attendings were held, and data were analyzed using the Framework Method for content analysis. Results: Four-hundred forty-six medical ICU patients were mechanically ventilated (195 pre-COVID-19 and 251 during COVID-19). The COVID-19 population was more likely to receive ketamine (81[32.3%] vs 4 [2.1%], p < 0.001). Thirteen respondents participated across two FG sessions (Pre-COVID = 8, Post-COVID=5). The most prevalent attitude among our respondents was discomfort, with three key themes identified as follows: 1) lack of evidence regarding ketamine, 2) lack of personal experience, and 3) desire for more education and protocols. Conclusion: Despite a substantial increase in ketamine prescription during COVID-19, intensivists continued to feel discomfort with utilization. Factors contributing to this discomfort include a lack of evidence, a lack of experience, and a desire for more education and protocols. Increase in experience with ketamine alone was not sufficient to minimize provider discomfort. These findings should inform future curricula and call for process improvement to optimize continuing education. [ABSTRACT FROM AUTHOR]

Background: The COVID-19 pandemic served as a reminder of the limited treatments available for acute respiratory distress syndrome (ARDS). The pandemic has highlighted the need to identify different clinical phenotypes of ARDS and investigate various interventions and treatments, both new and old. Case Presentation: We present a patient with severe ARDS secondary to COVID-19 who rapidly deteriorated despite neuromuscular blockade and prone ventilation. He was aggressively managed using a combination of high frequency oscillatory ventilation (HFOV), high dose methylprednisolone, TPE, and direct instillation of liquid surfactant. He had an excellent clinical response and ultimately discharged to inpatient rehabilitation, then home, totally independent. Conclusion: Relatively few effective treatment options exist for ARDS. Our patient's response to a combination of interventions that have fallen out of clinical practice serves as a reminder that research is needed to help identify distinct phenotypes so that clinical trials can be designed to investigate interventions and treatments specific to the different phenotypes. [ABSTRACT FROM AUTHOR]

Objectives: Patients with severe stroke are at high risk of developing acute respiratory distress syndrome (ARDS), but this severe complication was often under-diagnosed and rarely explored in stroke patients. We aimed to investigate the prevalence, early predictors, and outcomes of ARDS in severe stroke. Methods: This prospective study included consecutive patients admitted to neurological intensive care unit (neuro-ICU) with severe stroke, including acute ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage. The incidence of ARDS was examined, and baseline characteristics and severity scores on admission were investigated as potential early predictors for ARDS. The in-hospital mortality, length of neuro-ICU stay, the total cost in neuro-ICU, and neurological functions at 90 days were explored. Results: Of 140 patients included, 35 (25.0%) developed ARDS. Over 90% of ARDS cases occurred within 1 week of admission. Procalcitonin (OR 1.310 95% CI 1.005–1.707, P = 0.046) and PaO2/FiO2 on admission (OR 0.986, 95% CI 0.979–0.993, P < 0.001) were independently associated with ARDS, and high brain natriuretic peptide (OR 0.994, 95% CI 0.989–0.998, P = 0.003) was a red flag biomarker warning that the respiratory symptoms may be caused by cardiac failure rather than ARDS. ARDS patients had longer stays and higher expenses in neuro-ICU. Among patients with ARDS, 25 (62.5%) were moderate or severe ARDS. All the patients with moderate to severe ARDS had an unfavorable outcome at 90 days. Conclusions: ARDS is common in patients with severe stroke, with most cases occurring in the first week of admission. Procalcitonin and PaO2/FiO2 on admission are early predictors of ARDS. ARDS worsens both short-term and long-term outcomes. The conflict in respiratory support strategies between ARDS and severe stroke needs to be further studied. [ABSTRACT FROM AUTHOR]

This article, published in the journal Respiratory Case Reports, discusses a case of respiratory distress caused by the consumption of a biscuit laced with liquid nitrogen. The case involves a teenage boy with allergic rhinitis who experienced coughing and difficulty breathing after eating the biscuit. Despite treatment, his symptoms persisted until he was given an inhaler containing corticosteroid and bronchodilator. The article highlights the need for awareness of the risks associated with liquid nitrogen-infused food and emphasizes the importance of proper handling and knowledge of potential health hazards. [Extracted from the article]

While considerable attention has been devoted to respiratory manifestations, such as pneumonia and acute respiratory distress syndrome (ARDS), emerging evidence underlines the significance of extrapulmonary involvement. In this study, we examined 15 hospitalized patients who succumbed to severe complications following SARS-CoV-2 infection. These patients were admitted to the Sibiu County Clinical Emergency Hospital in Sibiu, Romania, between March and October 2021. All patients were ethnic Romanians. Conducted within a COVID-19-restricted environment and adhering to national safety protocols, autopsies provided a comprehensive understanding of the disease's multisystemic impact. Detailed macroscopic evaluations and histopathological analyses of myocardial, renal, hepatic, splenic, and gastrointestinal tissues were performed. Additionally, reverse transcription-quantitative polymerase chain reaction (rt-qPCR) assays and immunohistochemical staining were employed to detect the viral genome and nucleocapsid within the tissues. Myocardial lesions, including ischemic microstructural changes and inflammatory infiltrates, were prevalent, indicative of COVID-19's cardiac implications, while renal pathology revealed the chronic alterations, acute tubular necrosis, and inflammatory infiltrates most evident. Hepatic examination identified hepatocellular necroinflammatory changes and hepatocytic cytopathy, highlighting the hepatic involvement of SARS-CoV-2 infection. Splenic parenchymal disorganization was prominent, indicating systemic immune dysregulation. Furthermore, gastrointestinal examinations unveiled nonspecific changes. Molecular analyses detected viral genes in various organs, with immunohistochemical assays confirming viral presence predominantly in macrophages and fibroblasts. These findings highlighted the systemic nature of SARS-CoV-2 infection, emphasizing the need for comprehensive clinical management strategies and targeted therapeutic approaches beyond respiratory systems. [ABSTRACT FROM AUTHOR]

Given the various clinical manifestations that characterize Coronavirus Disease 2019 (COVID-19), the scientific community is constantly searching for biomarkers with prognostic value. Surfactant proteins A (SP-A) and D (SP-D) are collectins that play a crucial role in ensuring proper alveolar function and an alteration of their serum levels was reported in several pulmonary diseases characterized by Acute Respiratory Distress Syndrome (ARDS) and pulmonary fibrosis. Considering that such clinical manifestations can also occur during Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection, we wondered if these collectins could act as prognostic markers. In this regard, serum levels of SP-A and SP-D were measured by enzyme immunoassay in patients with SARS-CoV-2 infection (n = 51) at admission (T0) and after seven days (T1) and compared with healthy donors (n = 11). SP-D increased in COVID-19 patients compared to healthy controls during the early phases of infection, while a significant reduction was observed at T1. Stratifying SARS-CoV-2 patients according to disease severity, increased serum SP-D levels were observed in severe compared to mild patients. In light of these results, SP-D, but not SP-A, seems to be an eligible marker of COVID-19 pneumonia, and the early detection of SP-D serum levels could be crucial for preventive clinical management. [ABSTRACT FROM AUTHOR]

Background: The most prevalent preventable reason of maternal sickness and death worldwide remains to be postpartum hemorrhage (PPH). Cohort investigations and randomized clinical trials that assess crucial strategies for anticipating, preventing and controlling PPH continue to be of the most importance given the rising frequency of the condition. One woman dies from PPH every 7 minutes globally, making it a clinically important cause of maternal morbidity and death. Therefore, it's crucial to quickly identify patients who are at risk for PPH, actively manage the 3rd stage of labor on a regular basis, quickly measure blood loss, monitor patients appropriately, and treat PPH. Epidemiology The prevalence of PPH varies greatly with age, being more prevalent in low socioeconomic status areas and between 1 and 5 percent of births, according to a realistic estimate. Numerous variables, including the aging of mothers at delivery, the increased frequency of multiple pregnancies as a result of assisted reproductive technologies and the increasing caesarean section rates, have been linked to the rise in PPH death rates. According to studies, early detection, more timely and effective treatment might reduce the number of PPH-related fatalities. This review's objective was to talk about PPH's causes, detection, treatment, prevention and prognosis. Conclusions: Postpartum hemorrhage (PPH) continues to be a major cause of maternal morbidity and mortality and a potentially life-threatening obstetric complication despite important advances in treatment over the past few decades. It is also linked to serious illnesses like hypovolemic shock, acute renal failure, disseminated intravascular coagulation, multiorgan failure, and acute respiratory distress syndrome. [ABSTRACT FROM AUTHOR]

Acute respiratory distress syndrome (ARDS) due to severe coronavirus disease 2019 (COVID-19) pneumonia is associated with a high incidence of ventilator-associated pneumonia (VAP). We aimed to evaluate the epidemiology of VAP associated with severe COVID-19 pneumonia. This retrospective observational study recruited patients with COVID-19-associated ARDS admitted to our center from April 1, 2020, to September 30, 2021. The primary outcome was the survival-to-discharge rate. The secondary outcomes were the VAP rate, time to VAP, length of ICU stay, length of ventilator support, and isolated bacteria. Sixty-eight patients were included in this study; 23 developed VAP. The survival-to-discharge rate was 60.9 % in the VAP group and 84.4 % in the non-VAP group. The median time to VAP onset was 16 days. The median duration of ventilator support and of ICU stay were higher in the VAP group than in the non-VAP group. The VAP rate was 33.8 %. The most common isolated species was Stenotrophomonas maltophilia. On admission, carbapenems were used in a maximum number of cases (75 %). Furthermore, the median body mass index (BMI) was lower and the median sequential organ failure assessment (SOFA) score on admission was higher in the VAP group than in the non-VAP group. The survival-to-discharge rate in VAP patients was low. Moreover, VAP patients tended to have long ICU stays, low BMI, and high SOFA scores on admission. Unusually, S. maltophilia was the most common isolated bacteria, which may be related to the frequent use of carbapenems. [ABSTRACT FROM AUTHOR]

Respiratory syncytial virus (RSV) infection represents one of the most common infections during childhood, with significant morbidity and mortality in newborns and in the early years of life. RSV is a common infection throughout all age groups, largely undetected and underestimated in adults, with a disproportionately high impact in older individuals. RSV infection has a wide range of clinical presentations, from asymptomatic conditions to acute pneumonia and severe life-threatening respiratory distress, including exacerbations of underlying chronic conditions. Overall, the incidence of RSV infections requiring medical attention increases with age, and it is highest among persons ≥ 70 years of age. As a consequence of a combination of an aging population, immunosenescence, and the related increased burden of comorbidities, high-income countries are at risk of developing RSV epidemics. The standard of care for RSV-infected patients remains supportive, including fluids, antipyretics, and oxygen support when needed. There is an urgent need for antivirals and preventive strategies in this population, particularly in individuals at higher risk of severe outcomes following RSV infection. In this review, we describe prevention and treatment strategies for RSV illnesses, with a deep focus on the novel data on vaccination that has become available (Arexvy, GSK, and Abrysvo, Pfizer) for older adults. [ABSTRACT FROM AUTHOR]

OBJECTIVES: Critically ill patients with tuberculosis carry high mortality. Identification of factors associated with mortality in critically ill tuberculosis patients may enable focused treatment. DATA SOURCES: An extensive literature search of PubMed (MEDLINE), Embase, the Cochrane Library, and Google Scholar was performed using Medical Subject Headings terms "tuberculosis," "critical care," "critical care outcome," and "ICU." We aimed to identify factors affecting mortality in critically ill tuberculosis patients. STUDY SELECTION: All the studies comparing factors affecting mortality between survivors and nonsurvivors in critically ill tuberculosis patients were included. The database search yielded a total of 3017 records, of which 17 studies were included in the meta-analysis. DATA EXTRACTION: Data were collected including the name of the author, year and country of publication, duration of the study, number of patients studied, type of tuberculosis, patient demography, smoking history, laboratory parameters, comorbidities, the requirement for mechanical ventilation, duration of ventilation, ICU and hospital length of stay (LOS), type of lung involvement, complications, and outcomes. DATA SYNTHESIS: The major factors that contributed to mortality in critically ill tuberculosis patients were age, platelet count, albumin, C-reactive protein (CRP), the requirement and duration of invasive mechanical ventilation, Pao2/Fio2 ratio, presence of acute respiratory distress syndrome, shock, hospital-acquired infections, renal replacement therapy, and ICU and hospital LOS. CONCLUSIONS: Patient age, platelet count, albumin and CRP levels, the requirement and duration of invasive mechanical ventilation, Pao2/Fio2 ratio, hospitalacquired infections, renal replacement therapy, and ICU LOS were variables associated with mortality. [ABSTRACT FROM AUTHOR]

OBJECTIVES: To examine trends in utilization and outcomes among patients with the acute respiratory distress syndrome (ARDS) requiring prolonged venovenous extracorporeal membrane oxygenation (VV ECMO) support. DESIGN: Retrospective observational cohort study. SETTING: Adult patients in the Extracorporeal Life Support Organization registry. PATIENTS: Thirteen thousand six hundred eighty-one patients that required ECMO for the support of ARDS between January 2012 and December 2022. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Mortality while supported with VV ECMO and survival to hospital discharge based on ECMO duration were examined utilizing multivariable logistic regression. Among the 13,681 patients supported with VV ECMO, 4,040 (29.5%) were supported for greater than or equal to 21 days and 975 (7.1%) for greater than or equal to 50 days. Patients supported with prolonged VV ECMO were less likely to be discharged alive from the hospital compared with those with short duration of support (46.5% vs. 59.7%; p < 0.001). However, among patients supported with VV ECMO greater than or equal to 21 days, duration of extracorporeal life support was not significantly associated with mortality (odds ratio [OR], 0.99; 95% CI, 0.98-1.01; p = 0.87 and adjusted OR, 0.99; 95% CI, 0.97-1.02; p = 0.48). Even in those supported with VV ECMO for at least 120 days (n = 113), 52 (46.0%) of these patients were ultimately discharged alive from the hospital. CONCLUSIONS: Prolonged VV ECMO support of ARDS has increased and accounts for a substantial portion of cases. Among patients that survive for greater than or equal to 21 days while receiving VV ECMO support, duration is not predictive of survival to hospital discharge and clinical recovery may occur even after very prolonged VV ECMO support. [ABSTRACT FROM AUTHOR]

Objective The aim of the study is to analyze the risk factors for neonatal acute respiratory distress syndrome (NARDS) development based on the Montreux definition among near- and full-term neonates with sepsis and received meropenem. Study Design This was a single-center, case–control, retrospective trial from January 2019 to June 2020. Newborns of gestational ages (GAs) ≥35 weeks, diagnosed with sepsis and received meropenem were included. Patients who developed NARDS subsequently were defined as the study group (NARDS group), while the others without NARDS were enrolled in the control group (non-NARDS group). Results Out of 213 eligible neonates, NARDS occurred in 52 (24.4%) cases. In univariate analysis, infants with NARDS had a lower GA and birth weight, but a higher rate of premature birth (p <0.05). The median onset times of sepsis were earlier among neonates with NARDS compared with those without NARDS (1 [1,1] vs. 6 [1,15] days, p <0.001). Neonates with NARDS were more likely to suffer from early-onset sepsis (EOS), persistent pulmonary hypertension of newborns, pulmonary hemorrhage, septic shock, and patent ductus arteriosus (p <0.05). During labor, women whose neonates experienced NARDS were more likely to have a cesarean delivery (67.3 vs. 46.6%, p = 0.009) and likely to receive at least one dose of corticosteroids (21.2 vs. 5.0%, p = 0.001). In multivariable analyses, factors remaining independently associated with NARDS were premature birth, cesarean delivery, EOS, and septic shock. Compared with conventional inflammatory markers for NARDS, procalcitonin (PCT) was correlated with septic neonates who developed NARDS (p = 0.012) but had a low diagnostic value (area under the curve [AUC] = 0.609). C-reactive protein, white blood cells, and PLT did not correlate with morbidity of NARDS (AUC <0.05 and p >0.05). Conclusion Premature birth, cesarean delivery, EOS, and septic shock were independently associated with NARDS among near- and full-term septic neonates. PCT showed limited predictive value for NARDS. Key Points NARDS is serious and sepsis is proved as a cause for it. But rare study suggests the risk factors of NARDS based on the Montreux definition. This study may first found the independent risk factors associated with NARDS in septic neonates. [ABSTRACT FROM AUTHOR]

Aim: Mitochondrial dysfunction causes oxidative stress, which triggers the release of proinflammatory cytokines, which play an important role in the immune response. One of these cytokines, fibroblast growth factor-21 (FGF-21), has demonstrated an increase in its level in severe coronavirus disease-2019 (COVID-19) infection. In this context, this study aimed to investigate whether FGF-21 can be used in the follow-up of COVID-19 infection. Methods: This study was conducted as a cross-sectional design between January 1, 2022, and December 31, 2022. This study included women and men over 18 years old who had recovered from the COVID-19 infection (n=27). The data regarding hospitalization place (internal medicine ward, internal medicine ward + intensive care unit), comorbidities, vital signs, acute respiratory distress syndrome development, and applied treatments were obtained from hospital records. Fibroblast growth factor-21 levels were specifically studied for this study. Results: The FGF-21 level was found to be 254 pg/mL at the beginning of the study and increased to 454 pg/mL at the end of the study. The difference was found to be statistically significant (p=0.004). Conclusion: Considering the increasing level of FGF-21 compared to the beginning of the infection, it is thought that FGF-21 plays a role in the healing process in the COVID-19 infection. [ABSTRACT FROM AUTHOR]

Venovenous extracorporeal membrane oxygenation is used for respiratory support in the most severe cases of acute respiratory distress syndrome. Blood is drained from the large veins, oxygenated in an artificial lung, and returned to the right atrium (RA). In this study, we have used large eddy simulations to simulate a single-stage "lighthouse" drainage cannula in a patient-averaged model of the large veins and RA, including the return cannula. We compared the results with previous experimental and numerical studies of these cannulas in idealized tube geometries. According to the simulations, wall proximity at the drainage holes and the presence of the return cannula greatly increased drainage through the tip (33% at 5 L/min). We then simulated a multi-stage device in the same patient-averaged model, showing similar recirculation performance across the range of extracorporeal membrane oxygenation (ECMO) flow rates compared to the lighthouse cannula. Mean and maximum time-averaged wall shear stress were slightly higher for the lighthouse design. At high ECMO flow rates, the multi-stage device developed a negative caval pressure, which may be a cause of drainage obstruction in a clinical environment. Finally, through calculation of the energy spectra and vorticity field, we observed ring-like vortices inside the cannula originating from the side holes, most prominent in the proximal position. Our work highlights the important differences between a patient-derived and simplified venous model, with the latter tending to underestimate tip drainage. We also draw attention to the different dynamics of single-stage and multistage drainage cannulas, which may guide clinical use. [ABSTRACT FROM AUTHOR]

Background Coronavirus disease 2019 (COVID-19)-related acute respiratory distress syndrome requiring veno-venous extracorporeal membrane oxygenation (vv-ECMO) is related with poor outcome, especially in Germany. We aimed to analyze whether changes in vv-ECMO therapy during the pandemic were observed and lead to changes in the outcome of vv-ECMO patients. Methods All patients undergoing vv-ECMO support for COVID-19 between 2020 and 2021 in a single center (n = 75) were retrospectively analyzed. Weaning from vv-ECMO and in-hospital mortality were defined as primary and peri-interventional adverse events as secondary endpoints of the study. Results During the study period, four infective waves were observed in Germany. Patients were assigned correspondingly to four study groups: ECMO implantation between March 2020 and September 2020: first wave (n = 11); October 2020 to February 2021: second wave (n = 23); March 2021 to July 2021: third wave (n = 25); and August 2021 to December 2021: fourth wave (n = 20). Preferred cannulation technique changed within the second wave from femoro-femoral to femoro-jugular access (p < 0.01) and awake ECMO was implemented. Mean ECMO run time increased by more than 300% from 10.9 ± 9.6 (first wave) to 44.9 ± 47.0 days (fourth wave). Weaning of patients was achieved in less than 20% in the first wave but increased to approximately 40% since the second one. Furthermore, we observed a continuous numerically decrease of in-hospital mortality from 81.8 to 57.9% (p = 0.61). Conclusion Preference for femoro-jugular cannulation and awake ECMO combined with preexisting expertise and patient selection are considered to be associated with increased duration of ECMO support and numerically improved ECMO weaning and in-hospital mortality. [ABSTRACT FROM AUTHOR]

Background: ALI/ARDS is a syndrome of acute onset characterized by progressive hypoxemia and noncardiogenic pulmonary edema as the primary clinical manifestations. Necroptosis is a form of programmed cell necrosis that is precisely regulated by molecular signals. This process is characterized by organelle swelling and membrane rupture, is highly immunogenic, involves extensive crosstalk with various cellular stress mechanisms, and is significantly implicated in the onset and progression of ALI/ARDS. Methods: The current body of literature on necroptosis and ALI/ARDS was thoroughly reviewed. Initially, an overview of the molecular mechanism of necroptosis was provided, followed by an examination of its interactions with apoptosis, pyroptosis, autophagy, ferroptosis, PANOptosis, and NETosis. Subsequently, the involvement of necroptosis in various stages of ALI/ARDS progression was delineated. Lastly, drugs targeting necroptosis, biomarkers, and current obstacles were presented. Conclusion: Necroptosis plays an important role in the progression of ALI/ARDS. However, since ALI/ARDS is a clinical syndrome caused by a variety of mechanisms, we emphasize that while focusing on necroptosis, it may be more beneficial to treat ALI/ARDS by collaborating with other mechanisms. [ABSTRACT FROM AUTHOR]

Introduction: Staphylococcus aureus (S. aureus) is an important pathogen in both community-acquired and hospital-acquired pneumonia. S. aureus pneumonia has a high mortality rate and serious complications. Resistance to multiple antibiotics is a major challenge in the treatment of S. aureus pneumonia. Understanding the antibiotic resistance profile of S. aureus and the risk factors for mortality can help optimize antibiotic regimens and improve patient outcomes in S. aureus pneumonia. Methods: A prospective cohort study of 118 patients diagnosed with S. aureus pneumonia between May 2021 and June 2023 was conducted, with a 30-day follow-up period. Demographic information, comorbidities, Charlson Comorbidity Index, clinical characteristics, outcomes, and complications were collected for each enrolled case. The data were processed and analyzed using R version 3.6.2. Results: S. aureus pneumonia has a 30-day mortality rate of approximately 50%, with complication rates of 22% for acute respiratory distress syndrome (ARDS), 26.3% for septic shock, and 14.4% for acute kidney injury (AKI). Among patients with methicillin-resistant S. aureus (MRSA) pneumonia treated with vancomycin (n = 40), those with a vancomycin minimum inhibitory concentration (MIC) ≤ 1 had significantly higher cumulative survival at day 30 compared to those with MIC ≥ 2 (log-rank test p = 0.04). The prevalence of MRSA among S. aureus isolates was 84.7%. Hemoptysis, methicillin resistance, acidosis (pH < 7.35), and meeting the Infectious Diseases Society of America/American Thoracic Society (IDSA/ATS) criteria for severe pneumonia were significantly associated with mortality in a multivariate Cox regression model based on the adaptive least absolute shrinkage and selection operator (LASSO). Conclusions: S. aureus pneumonia is a severe clinical condition with high mortality and complication rates. MRSA has a high prevalence in Can Tho City, Vietnam. Hemoptysis, methicillin resistance, acidosis (pH < 7.35), and meeting the IDSA/ATS criteria for severe pneumonia are risk factors for mortality in S. aureus pneumonia. [ABSTRACT FROM AUTHOR]

Purpose: Acute respiratory distress syndrome (ARDS) is a major cause of hypoxemic respiratory failure in adults. In ARDS extensive inflammation and leakage of fluid into the alveoli lead to dysregulation of pulmonary surfactant metabolism and function. Altered surfactant synthesis, secretion, and breakdown contribute to the clinical features of decreased lung compliance and alveolar collapse. Lung function in ARDS could potentially be restored with surfactant replacement therapy, and synthetic surfactants with modified peptide analogues may better withstand inactivation in ARDS alveoli than natural surfactants. Methods: This study aimed to investigate the activity in vitro and the bolus effect (200 mg phospholipids/kg) of synthetic surfactant CHF5633 with analogues of SP‐B and SP‐C, or natural surfactant Poractant alfa (Curosurf®, both preparations Chiesi Farmaceutici S.p.A.) in a severe ARDS model (the ratio of partial pressure arterial oxygen and fraction of inspired oxygen, P/F ratio ≤ 13.3 kPa) induced by hydrochloric acid instillation followed by injurious ventilation in adult New Zealand rabbits. The animals were ventilated for 4 h after surfactant treatment and the respiratory parameters, histological appearance of lung parenchyma and levels of inflammation, oxidative stress, surfactant dysfunction, and endothelial damage were evaluated. Results: Both surfactant preparations yielded comparable improvements in lung function parameters, reductions in lung injury score, pro-inflammatory cytokines levels, and lung edema formation compared to untreated controls. Conclusions: This study indicates that surfactant replacement therapy with CHF5633 improves lung function and lung architecture, and attenuates inflammation in severe ARDS in adult rabbits similarly to Poractant alfa. Clinical trials have so far not yielded conclusive results, but exogenous surfactant may be a valid supportive treatment for patients with ARDS given its anti-inflammatory and lung-protective effects. [ABSTRACT FROM AUTHOR]

The article discusses the differences between the American Thoracic Society (ATS) and the European Society of Intensive Care Medicine (ESICM) guidelines for the treatment of acute respiratory distress syndrome (ARDS). The ATS and ESICM published collaborative guidelines in 2017, but due to new evidence and the impact of COVID-19, they updated their guidelines independently. The updated ATS guidelines included recommendations for positive end-expiratory pressure (PEEP), venovenous extracorporeal membrane oxygenation (VV-ECMO), corticosteroids, and neuromuscular blocking agents (NMBA), while the ESICM guidelines focused on ECMO and NMBA. Despite some differences, there is more agreement than conflict between the guidelines, particularly regarding low tidal volume ventilation and prone positioning. The article emphasizes the need for collaboration and dialogue between scientific societies to ensure comprehensive and up-to-date guidelines for clinicians. [Extracted from the article]

Esophageal pressure (Peso) is a validated method for estimating pleural pressure (Ppl) and assessing intrathoracic pressure. Peso monitoring allows for the estimation of trans-pulmonary pressure (PL), which is important in understanding the risk of lung injuries. Peso measurements can also assess lung and chest wall elastance, quantify respiratory muscle effort, and monitor patient ventilator synchrony. Peso can be measured using a catheter with an air-filled balloon and can be displayed on an ICU ventilator or other devices. Peso measurements can be used to set positive end-expiratory pressure (PEEP) and tidal volume (VT) in patients with acute respiratory distress syndrome (ARDS) to individualize lung protective ventilation. However, the optimal values for PEEP and PL still need further study. Peso measurements can also help detect patient ventilator asynchronies and optimize ventilator settings during assisted ventilation. Overall, Peso is a useful tool for individualizing mechanical ventilation and optimizing patient care. [Extracted from the article]

Purpose: This is the first of three parts of the clinical practice guideline from the European Society of Intensive Care Medicine (ESICM) on resuscitation fluids in adult critically ill patients. This part addresses fluid choice and the other two will separately address fluid amount and fluid removal. Methods: This guideline was formulated by an international panel of clinical experts and methodologists. The Grading of Recommendations Assessment, Development, and Evaluation (GRADE) methodology was applied to evaluate the certainty of evidence and to move from evidence to decision. Results: For volume expansion, the guideline provides conditional recommendations for using crystalloids rather than albumin in critically ill patients in general (moderate certainty of evidence), in patients with sepsis (moderate certainty of evidence), in patients with acute respiratory failure (very low certainty of evidence) and in patients in the perioperative period and patients at risk for bleeding (very low certainty of evidence). There is a conditional recommendation for using isotonic saline rather than albumin in patients with traumatic brain injury (very low certainty of evidence). There is a conditional recommendation for using albumin rather than crystalloids in patients with cirrhosis (very low certainty of evidence). The guideline provides conditional recommendations for using balanced crystalloids rather than isotonic saline in critically ill patients in general (low certainty of evidence), in patients with sepsis (low certainty of evidence) and in patients with kidney injury (very low certainty of evidence). There is a conditional recommendation for using isotonic saline rather than balanced crystalloids in patients with traumatic brain injury (very low certainty of evidence). There is a conditional recommendation for using isotonic crystalloids rather than small-volume hypertonic crystalloids in critically ill patients in general (very low certainty of evidence). Conclusions: This guideline provides eleven recommendations to inform clinicians on resuscitation fluid choice in critically ill patients. [ABSTRACT FROM AUTHOR]

BACKGROUND: Thoracic endovascular aortic repair (TEVAR) is the standard of care for the treatment of blunt thoracic aortic injury (BTAI) requiring intervention. Data suggest that low-grade BTAI (grade I [intimal tears] or grade II [intramural hematoma]) will resolve spontaneously if treated with nonoperative management (NOM) alone. There has been no comparison specifically between the use of NOM vs TEVAR for low-grade BTAI. We hypothesize that these low-grade injuries can be safely managed with NOM alone. STUDY DESIGN: Retrospective analysis of all patients with a low-grade BTAI in the Aortic Trauma Foundation Registry from 2016 to 2021 was performed. The study population was 1 primary outcome was mortality. Secondary outcomes included complications, ICU length of stay, and ventilator days. RESULTS: A total of 880 patients with BTAI were enrolled. Of the 269 patients with low-grade BTAI, 218 (81%) were treated with NOM alone (81% grade I, 19% grade II), whereas 51 (19%) underwent a TEVAR (20% grade I, 80% grade II). There was no difference in demographic or mechanism of injury in patients with low-grade BTAI who underwent NOM vs TEVAR. There was a difference in mortality between NOM alone and TEVAR (8% vs 18%, p = 0.009). Aortic-related mortality was 0.5% in the NOM group and 4% in the TEVAR group (p = 0.06). Hospital and ICU length of stay and ventilator days were not different between the 2 groups. CONCLUSIONS: NOM alone is safe and appropriate management for low-grade BTAI, with lower mortality and decreased rates of complication when compared with routine initial TEVAR. [ABSTRACT FROM AUTHOR]

Background & Aims: During the coronavirus disease 2019 (COVID-19) pandemic a significant proportion of patients with severe acute respiratory distress syndrome (ARDS) due to COVID-19 infection developed secondary sclerosing cholangitis (SSC) as a hepatobiliary complication. Methods: 17 patients were endoscopically diagnosed and treated with COVID-19 SSC from February 2020 until October 2022 at our center. We retrospectively reviewed and analyzed the data to define risk factors, establish endoscopic treatment options, and to estimate incidence and outcomes. Results: 258 patients with COVID-19 infection were admitted to our tertiary center and mechanically ventilated. 10 patients developed COVID-19 SSC in-house, and 7 patients were transferred for further endoscopic treatment. All 17 patients were mechanically ventilated, received vasoactive substances and 12 of them were treated with extracorporeal membrane oxygenation therapy. Endoscopic retrograde cholangiography (ERC) was performed in all patients to establish the diagnosis of COVID-19 SSC and evaluate endoscopic treatment options. All ERCs revealed biliary casts. 9 patients had developed severe rarefication of the intrahepatic bile ducts and 4 showed biliary strictures. As endoscopic treatment approaches, casts were removed repeatedly, and strictures were dilated. During the study period, 14 patients died (82%). 3 patients are in follow-up to reassess the need for liver transplantation. Conclusions: COVID-19 SSC was observed in 2.6 % of the patients with severe COVID-19 in our center. We show that endoscopic approaches offer the opportunity to extract casts and to treat biliary strictures. As the mortality rate of COVID-19 SSC is high, endoscopic treatment can be of great clinical relevance as a bridge to liver transplantation. [ABSTRACT FROM AUTHOR]

Chronic cigarette smoke exposure decreases lung expression of WWOX which is known to protect the endothelial barrier during infectious models of acute respiratory distress syndrome (ARDS). Proteomic analysis of WWOX-silenced endothelial cells (ECs) was done using tandem mass tag mass spectrometry (TMT-MS). WWOX-silenced ECs as well as those isolated from endothelial cell Wwox knockout (EC Wwox KO) mice were subjected to cyclic stretch (18% elongation, 0.5 Hz, 4 h). Cellular lysates and media supernatant were harvested for assays of cellular signaling, protein expression, and cytokine release. These were repeated with dual silencing of WWOX and zyxin. Control and EC Wwox KO mice were subjected to high tidal volume ventilation. Bronchoalveolar lavage fluid and mouse lung tissue were harvested for cellular signaling, cytokine secretion, and histological assays. TMT-MS revealed upregulation of zyxin expression during WWOX knockdown which predicted a heightened inflammatory response to mechanical stretch. WWOX-silenced ECs and ECs isolated from EC Wwox mice displayed significantly increased cyclic stretch-mediated secretion of various cytokines (IL-6, KC/IL-8, IL-1β, and MCP-1) relative to controls. This was associated with increased ERK and JNK phosphorylation but decreased p38 mitogen-activated kinases (MAPK) phosphorylation. EC Wwox KO mice subjected to VILI sustained a greater degree of injury than corresponding controls. Silencing of zyxin during WWOX knockdown abrogated stretch-induced increases in IL-8 secretion but not in IL-6. Loss of WWOX function in ECs is associated with a heightened inflammatory response during mechanical stretch that is associated with increased MAPK phosphorylation and appears, in part, to be dependent on the upregulation of zyxin. NEW & NOTEWORTHY Prior tobacco smoke exposure is associated with an increased risk of acute respiratory distress syndrome (ARDS) during critical illness. Our laboratory is investigating one of the gene expression changes that occurs in the lung following smoke exposure: WWOX downregulation. Here we describe changes in protein expression associated with WWOX knockdown and its influence on ventilator-induced ARDS in a mouse model. [ABSTRACT FROM AUTHOR]

The purpose of this systematic review was to characterize the association between tobacco use and postoperative outcomes, complications, and revision rates following shoulder arthroplasty through a systematic review of the literature. The PubMed/MEDLINE and Embase databases were queried for studies published between January 1, 1985, and April 18, 2023, comparing outcomes following both anatomic and reverse total shoulder arthroplasty (TSA) between tobacco users and nontobacco users. Studies with a level of evidence IV or greater were included, while case reports, systematic reviews, basic science studies, and studies including revision arthroplasty were excluded. American Shoulder and Elbow Surgeons scores, simple shoulder test scores, visual analog scale for pain, complications, readmissions, and reoperations were reported. A total of 20 unique studies including 338,117 shoulder arthroplasties (38,225 [11.3%] performed on tobacco users) were included in this review. Patient-reported outcome measures, including American Shoulder and Elbow Surgeons, simple shoulder test, and visual analog scale, were overall superior in nontobacco users compared to tobacco users. Similarly, tobacco users had lower patient acceptable symptomatic state achievement, worse Single Assessment Numeric Evaluation scores (odds ratio 0.647; 95% confidence interval, 0.324-1.293; P =.0221), and worse constant scores (odds ratio, 0.478; 95% confidence interval, 0.251-0.909; P =.027). Tobacco users demonstrated a higher rate of complications in four of the eight included studies. Two included studies found higher rates of readmission in tobacco users (15.3% vs. 13.6%, P =.007 and 7.8% vs. 7.1%, P =.001), though six included studies found no significant difference in readmissions. Nine of 11 studies that included reoperation as a variable found higher rates of reoperation in tobacco users, with three reaching statistical significance (P <.05). Tobacco users experienced higher rates of gastrointestinal complications (0.07% vs. 0.01%, P =.021), acute renal failure (2.5% vs. 1.9%, P =.005), acute respiratory distress (1.3% vs. 0.9%, P =.002), need for ventilator assistance (1.2% vs. 0.7%, P <.001), instability of the prosthesis (P <.001), pneumonia (P <.001), sepsis (P =.001), and myocardial infarction (P <.001). Smokers also demonstrated increased postoperative opioid use (2643 mg oral morphine equivalents) compared to nonsmokers (2121 mg) and former smokers (2015 mg; P =.04). Tobacco use is associated with inferior outcomes after TSA, including lower patient-reported outcome measures, increased complications, and higher reoperation rates. Further high-level, prospective studies with long-term follow-up are required to further elucidate the impact of tobacco use on long-term postoperative outcomes following TSA. [ABSTRACT FROM AUTHOR]

Copyright of Biomédica: Revista del Instituto Nacional de Salud is the property of Instituto Nacional de Salud of Colombia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Critical illness can significantly alter the composition and function of the human microbiome, but few studies have examined these changes over time. Here, we conduct a comprehensive analysis of the oral, lung, and gut microbiota in 479 mechanically ventilated patients (223 females, 256 males) with acute respiratory failure. We use advanced DNA sequencing technologies, including Illumina amplicon sequencing (utilizing 16S and ITS rRNA genes for bacteria and fungi, respectively, in all sample types) and Nanopore metagenomics for lung microbiota. Our results reveal a progressive dysbiosis in all three body compartments, characterized by a reduction in microbial diversity, a decrease in beneficial anaerobes, and an increase in pathogens. We find that clinical factors, such as chronic obstructive pulmonary disease, immunosuppression, and antibiotic exposure, are associated with specific patterns of dysbiosis. Interestingly, unsupervised clustering of lung microbiota diversity and composition by 16S independently predicted survival and performed better than traditional clinical and host-response predictors. These observations are validated in two separate cohorts of COVID-19 patients, highlighting the potential of lung microbiota as valuable prognostic biomarkers in critical care. Understanding these microbiome changes during critical illness points to new opportunities for microbiota-targeted precision medicine interventions. Here, the authors profile the oral, lung, and gut microbiota of 479 patients with acute respiratory failure, revealing that reduced diversity and increased pathogen presence can predict survival outcomes, highlighting the potential for microbiota-based approaches in critical care. [ABSTRACT FROM AUTHOR]

Respiratory infection by Pseudomonas aeruginosa, common in hospitalized immunocompromised and immunocompetent ventilated patients, can be life-threatening because of antibiotic resistance. This raises the question of whether the host's immune system can be educated to combat this bacterium. Here we show that prior exposure to a single low dose of lipopolysaccharide (LPS) protects mice from a lethal infection by P. aeruginosa. LPS exposure trained the innate immune system by promoting expansion of neutrophil and interstitial macrophage populations distinguishable from other immune cells with enrichment of gene sets for phagocytosis- and cell-killing-associated genes. The cell-killing gene set in the neutrophil population uniquely expressed Lgals3, which encodes the multifunctional antibacterial protein, galectin-3. Intravital imaging for bacterial phagocytosis, assessment of bacterial killing and neutrophil-associated galectin-3 protein levels together with use of galectin-3-deficient mice collectively highlight neutrophils and galectin-3 as central players in LPS-mediated protection. Patients with acute respiratory failure revealed significantly higher galectin-3 levels in endotracheal aspirates (ETAs) of survivors compared to non-survivors, galectin-3 levels strongly correlating with a neutrophil signature in the ETAs and a prognostically favorable hypoinflammatory plasma biomarker subphenotype. Taken together, our study provides impetus for harnessing the potential of galectin-3-expressing neutrophils to protect from lethal infections and respiratory failure. This study reports training by lipopolysaccharide to expand neutrophils expressing the anti-bacterial galectin-3 protein defending mice from a lethal bacterial infection, a similar signature associated with survivors of respiratory failure in humans. [ABSTRACT FROM AUTHOR]

Copyright of Journal of University of Anbar for Pure Science is the property of Republic of Iraq Ministry of Higher Education & Scientific Research (MOHESR) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Acute respiratory distress syndrome (ARDS) is a severe complication that can lead to fatalities in multiple trauma patients. Nevertheless, the incidence rate and early prediction of ARDS among multiple trauma patients residing in high-altitude areas remain unknown. Methods: This study included a total of 168 multiple trauma patients who received treatment at Shigatse People's Hospital Intensive Care Unit (ICU) between January 1, 2019 and December 31, 2021. The clinical characteristics of the patients and the incidence rate of ARDS were assessed. Univariable and multivariable logistic regression models were employed to identify potential risk factors for ARDS, and the predictive effects of these risk factors were analyzed. Results: In the high-altitude area, the incidence of ARDS among multiple trauma patients was 37.5% (63/168), with a hospital mortality rate of 16.1% (27/168). Injury Severity Score (ISS) and thoracic injuries were identified as significant predictors for ARDS using the logistic regression model, with an area under the curve (AUC) of 0.75 and 0.75, respectively. Furthermore, a novel predictive risk score combining ISS and thoracic injuries demonstrated improved predictive ability, achieving an AUC of 0.82. Conclusions: This study presents the incidence of ARDS in multiple trauma patients residing in the Tibetan region, and identifies two critical predictive factors along with a risk score for early prediction of ARDS. These findings have the potential to enhance clinicians' ability to accurately assess the risk of ARDS and proactively prevent its onset. [ABSTRACT FROM AUTHOR]