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Acute respiratory distress syndrome (ARDS) and hospital-acquired pneumonia (HAP) are major problems of public health in intensive care units (ICUs), occurring in 15% of critically ill patients. Among the factors explaining ARDS development, sepsis is known as a frequent cause. Sepsis, ARDS, and HAP increase morbidity, mortality, length of stay in the ICU, and the overall costs of healthcare. The major challenge remains to identify accurately among critically ill patients those at risk of poor outcomes who could benefit from novel therapies. Endocan is released by the pulmonary endothelium in response to local or systemic injury. It inhibits mainly leukocyte diapedesis rather than leukocyte rolling or adhesion to the endothelial cells both in vitro and in vivo. Endocan was evaluated in 25 clinical reports, including 2454 critically ill patients and 452 healthy controls. The diagnostic value of endocan for sepsis or sepsis severity was equal to procalcitonin but its prognostic value was better. A predictive value for postoperative pneumonia was evidenced in two studies, and a predictive value for ARDS in four studies from three independent centers. This review presents an overview of the structure, expression, and functions of endocan. We also hereby summarize the potential applications of endocan in the prediction and prognosis of ARDS and HAP, as well as in the prognosis of sepsis.

Adsorption on the membrane may explain this progressive decrease in blood levels of endocan, as suggested by the likely influence of adsorptive properties of the membranes on the variations of endocan. [...]these results suggest major interference of hemodialysis with blood concentrations of endocan, especially when highly adsorptive membranes are used, making it unreliable as a prognostic biomarker of pulmonary and systemic inflammation in critically ill patients undergoing hemodialysis. A worldwide multicentre evaluation of the influence of deterioration or improvement of acute kidney injury on clinical outcome in critically ill patients with and without sepsis at ICU admission: results from The Intensive Care Over Nations audit.

Immunocompromised patients—including patients with cancer, hematological malignancies, solid organ transplants and individuals receiving immunosuppressive therapies for autoimmune diseases—account for an increasing proportion of critically-ill patients. While their prognosis has improved markedly in the last decades, they remain at increased risk of healthcare- and intensive care unit (ICU)-acquired infections. The most frequent of these are ventilator-associated lower respiratory tract infections (VA-LTRI), which include ventilator-associated pneumonia (VAP) and tracheobronchitis (VAT). Recent studies have shed light on some of the specific features of VAP and VAT in immunocompromised patients, which is the subject of this narrative review. Contrary to previous belief, the incidence of VAP and VAT might actually be lower in immunocompromised than non-immunocompromised patients. Further, the relationship between immunosuppression and the incidence of VAP and VAT related to multidrug-resistant (MDR) bacteria has also been challenged recently. Etiological diagnosis is essential to select the most appropriate treatment, and the role of invasive sampling, specifically bronchoscopy with bronchoalveolar lavage, as well as new molecular syndromic diagnostic tools will be discussed. While bacteria—especially gram negative bacteria—are the most commonly isolated pathogens in VAP and VAT, several opportunistic pathogens are a special concern among immunocompromised patients, and must be included in the diagnostic workup. Finally, the impact of immunosuppression on VAP and VAT outcomes will be examined in view of recent papers using improved statistical methodologies and treatment options—more specifically empirical antibiotic regimens—will be discussed in light of recent findings on the epidemiology of MDR bacteria in this population.

A large proportion of ICU-acquired infections are related to multidrug-resistant bacteria (MDR). Infections caused by these bacteria are associated with increased mortality, and prolonged duration of mechanical ventilation and ICU stay. The aim of this narrative review is to report on the association between COVID-19 and ICU-acquired colonization or infection related to MDR bacteria. Although a huge amount of literature is available on COVID-19 and MDR bacteria, only a few clinical trials have properly evaluated the association between them using a non-COVID-19 control group and accurate design and statistical methods. The results of these studies suggest that COVID-19 patients are at a similar risk of ICU-acquired MDR colonization compared to non-COVID-19 controls. However, a higher risk of ICU-acquired infection related to MDR bacteria has been reported in several studies, mainly ventilator-associated pneumonia and bloodstream infection. Several potential explanations could be provided for the high incidence of ICU-acquired infections related to MDR. Immunomodulatory treatments, such as corticosteroids, JAK2 inhibitors, and IL-6 receptor antagonist, might play a role in the pathogenesis of these infections. Additionally, a longer stay in the ICU was reported in COVID-19 patients, resulting in higher exposure to well-known risk factors for ICU-acquired MDR infections, such as invasive procedures and antimicrobial treatment. Another possible explanation is the surge during successive COVID-19 waves, with excessive workload and low compliance with preventive measures. Further studies should evaluate the evolution of the incidence of ICU-acquired infections related to MDR bacteria, given the change in COVID-19 patient profiles. A better understanding of the immune status of critically ill COVID-19 patients is required to move to personalized treatment and reduce the risk of ICU-acquired infections. The role of specific preventive measures, such as targeted immunomodulation, should be investigated.

Background: Veno-venous ECMO (VV ECMO) is a life-sustaining technique indicated in the most severe forms of acute respiratory distress syndrome (ARDS). VV ECMO remains associated with significant morbidity and mortality. In this context, the identification of prognostic factors during the first week following ECMO implantation seems of high interest. However, little is known about the prognostic values of the kinetics of clinical and biological parameters in this timeframe. Methods: Observational, retrospective, multicenter study conducted in three centers in France and Belgium. We enrolled patients aged 18 years or older who underwent VV ECMO for severe ARDS between March 2020 and January 2023, with at least one endocan assay within 7 days of VV ECMO implantation. Kinetics of endocan and of a panel of clinical and biological markers were compared between surviving and deceased patients. Results: Forty-nine patients were included in our study among whom 30 patients (61%) were deceased on discharge from intensive care. Compared with patients who died, surviving patients had lower membrane fraction of oxygen at D3, lower fresh gas flow at D7, higher tidal volumes at D1 and D7, higher lung compliance and mechanical power at D7, and lower SOFA score at D7. Compared with deceased patients, survivors had a higher pH and lower endocan concentration on D3, and lower fibrinogen on D3 and D7. Conclusion: One week after initiation of VV ECMO support for severe ARDS, there was a significant decrease in the level of support simultaneously with respiratory and overall improvement in surviving patients. Compared to patients discharged alive from ICU, non-survivors were characterized by lower concentrations of endocan concentration at D3.

Early distinguishing ventilator-associated tracheobronchitis (VAT) and ventilator-associated pneumonia (VAP) remains difficult in the daily practice. However, this question appears clinically relevant, as treatments of VAT and VAP currently differ. In this study, we assessed the accuracy of sepsis criteria according to the Sepsis-3 definition in the early distinction between VAT and VAP. Retrospective single-center cohort, including all consecutive patients with a diagnosis of VAT (n = 70) or VAP (n = 136), during a 2-year period. Accuracy of sepsis criteria according to Sepsis-3, total SOFA and respiratory SOFA, calculated at time of microbiological sampling were assessed in differentiating VAT from VAP, and in predicting mortality on ICU discharge. Sensitivity and specificity of sepsis criteria were found respectively at 0.4 and 0.91 to distinguish VAT from VAP, and at 0.38 and 0.75 for the prediction of mortality in VA-LRTI. A total SOFA ≥ 6 and a respiratory SOFA ≥ 3 were identified as the best cut-offs for these criteria in differentiating VAT from VAP, with sensitivity and specificity respectively found at 0.63 and 0.69 for total SOFA, and at 0.49 and 0.7 for respiratory SOFA. Additionally, for prediction of mortality, a total SOFA ≥ 7 and a respiratory SOFA = 4 were identified as the best-cut-offs, respectively yielding sensitivity and specificity at 0.56 and 0.61 for total SOFA, and at 0.22 and 0.95 for respiratory SOFA. Sepsis criteria according to the Sepsis-3 definition show a high specificity but a low sensitivity for the diagnosis of VAP. Our results do not support the use of these criteria for the early diagnosis of VAP in patients with VA-LRTI.

Drug poisoning frequently leads to admission to intensive care units, often resulting in aspiration, a potentially life-threatening condition if not properly managed. Aspiration can manifest as either bacterial aspiration pneumonia (BAP) or aspiration pneumonitis (AP), which are challenging to distinguish potentially leading to overprescription of antibiotics and the emergence of multidrug-resistant bacteria. This study aims to assess the accuracy of the Infectious Diseases Society of America (IDSA) and British Thoracic Society (BTS) criteria in differentiating BAP from AP in comatose ventilated patients following drug poisoning. This cross-sectional study included 95 patients admitted for drug poisoning at the Lille University Hospital intensive care department, between 2013 and 2017, requiring mechanical ventilation and receiving antibiotics for aspiration. Patients were categorized as having bacterial complications if tracheal sampling yielded positive culture results, and if they were otherwise considered to have chemical complications. The sensitivity, specificity, positive predictive value, and negative predictive value of IDSA and BTS criteria in identifying patients with bacterial complications were evaluated. Among the patients, 34 (36%) experienced BAP. The IDSA criteria demonstrated a sensitivity of 62% and specificity of 33%, while the BTS criteria showed a sensitivity of 50% and specificity of 38%. Both the IDSA and BTS criteria exhibited poor sensitivity and specificity in identifying microbiologically confirmed pneumonia in comatose ventilated patients following drug poisoning.

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Background and Aims Endocan is a marker of endothelial damage. Data regarding the association of this proteoglycan and acute respiratory distress syndrome (ARDS) is discrepant. Hence, this study sought to investigate the possible correlation between serum/plasma endocan concentration and ARDS. Methods A systematic review and meta‐analysis of international online databases was conducted following PRISMA guidelines. PubMed, SCOPUS, Embase, and Web of Science were searched in March 2023, with the leading search terms being “ARDS” OR “respiratory distress” AND “endocan” and other associated terms. Studies that measured endocan levels in patients with ARDS and compared it with non‐ARDS controls or within different severities of ARDS were included. We performed a random‐effect meta‐analysis for pooling the differences using standardized mean difference (SMD) and 95% confidence interval (CI). Results We included 14 studies involving 1,058 patients. Those developing ARDS had significantly higher levels of endocan compared to those without ARDS (SMD: 0.47, 95% CI: 0.10–0.84, p = 0.01). Our meta‐analysis of three studies found that endocan levels in ARDS nonsurvivors were significantly higher than in survivors (SMD: 0.31, 95% CI: 0.02–0.60, p = 0.03). Three studies investigated endocan levels in different severities of ARDS. Only one of these studies reported significantly higher endocan levels in patients with worsening acute respiratory failure at Day 15. The other two reported no significant association between ARDS severity and circulating endocan levels. Conclusion Blood endocan levels were significantly higher in patients with ARDS than those without. Additionally, among patients with ARDS, blood endocan values were significantly elevated in nonsurvivors compared to survivors. These findings could help researchers design future studies and solidify these findings and finally, clinicians to take advantage of measuring endocan in clinical settings for assessment of patients with ARDS.