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Organizational culture is considered a protective factor against burnout among ICU professionals. The aim of this study is to study the association between organizational culture as a potential antecedent to previously found mediating risk factors for burnout, namely, work-life balance and moral distress. Multicenter cross sectional study in eleven Dutch ICUs. The primary outcome measure was the core symptom of burnout, emotional exhaustion, measured using the validated Dutch version of the Maslach Burnout Inventory. Organizational culture was assessed using the Culture of Care Barometer, which measures five aspects of organizational culture. Moral distress and work-life balance were measured with validated questionnaires. 696 ICU professionals (39.7 %) responded. All aspects of the CoCB were negatively associated with the emotional exhaustion component of burnout, both in univariable and multivariable models. Four aspects of organizational culture were significantly associated to the serial association between moral distress, work-to-home spillovers, and emotional exhaustion. For these aspects, the total indirect association was equal or larger than the total direct association. Multiple aspects of organizational culture reduce burnout among ICU professionals in a largely indirect manner, via moral distress and work-life balance. Improving organizational culture can mitigate burnout symptoms among ICU clinicians. •There are large difference in burnout prevalence across hospitals.•ICU organizational culture is undervalued as a factor that protects against burnout.•Organizational culture may contribute to moral distress and negative work-home balance.•strong collegial relations may, from the top down, help ICU professionals make sense of morally distressing situations.•Improving organizational culture can mitigate burnout symptoms among ICU clinicians.

Pulmonary coagulopathy may play a pathogenetic role in acute respiratory distress syndrome (ARDS), by contributing to alveolocapillary inflammation and increased permeability. Recombinant human activated protein C (rh-APC) may inhibit this process and thereby improve patient outcome. A prospective randomized, saline-controlled, single-blinded clinical trial was performed in the intensive care units of two university hospitals, and patients with ARDS were included within 24 h after meeting inclusion criteria. A 4-day course of intravenous rh-APC (24 mcg/kg/h) (n = 33) versus saline (n = 38). The primary outcome parameter was the pulmonary leak index (PLI) of 67Gallium-transferrin as a measure of alveolocapillary permeability and secondary outcomes were disease severity scores and ventilator-free days, among others. Baseline characteristics were similar; in 87% of patients the PLI was above normal and in 90% mechanical or non-invasive ventilation was instituted at a median lung injury score of 2.5. There was no evidence that Rh-APC treatment affected the PLI or attenuated lung injury and sequential organ failure assessment scores. Mean ventilator-free days amounted to 14 (rh-APC) and 12 days (saline, P = 0.35). 28-day mortality was 6% in rh-APC- and 18% in saline-treated patients (P = 0.12). There was no difference in bleeding events. The study was prematurely discontinued because rh-APC was withdrawn from the market. There is no evidence that treatment with intravenous rh-APC during 4 days for infectious or inflammatory ARDS ameliorates increased alveolocapillary permeability or the clinical course of ARDS patients. We cannot exclude underpowering. Nederlands Trial Register ISRCTN 52566874.

AI holds the potential to transform healthcare, promising improvements in patient care. Yet, realizing this potential is hampered by over-reliance on limited datasets and a lack of transparency in validation processes. To overcome these obstacles, we advocate the creation of a detailed registry for AI algorithms. This registry would document the development, training, and validation of AI models, ensuring scientific integrity and transparency. Additionally, it would serve as a platform for peer review and ethical oversight. By bridging the gap between scientific validation and regulatory approval, such as by the FDA, we aim to enhance the integrity and trustworthiness of AI applications in healthcare.

Critically ill patients frequently develop acute lung injury (ALI). Disturbed alveolar fibrin turnover, a characteristic feature of ALI, is the result of both activation of coagulation and inhibition of fibrinolysis. Nebulized fibrinolytic agents could exert lung-protective effects, via promotion of fibrinolysis as well as anti-inflammation. Rats were challenged intratracheally with Pseudomonas aeruginosa, resulting in pneumonia as a model for direct ALI, or received an intravenous bolus infusion of lipopolysaccharide, as a model for indirect ALI. Rats were randomized to nebulization of normal saline (placebo), recombinant tissue plasminogen activator (rtPA), or monoclonal antibodies against plasminogen activator inhibitor-type 1 (anti-PAI-1). Nebulized rtPA or anti-PA1-1 enhanced the bronchoalveolar fibrinolytic system, as reflected by a significant reduction of PAI-1 activity levels in bronchoalveolar lavage fluid, and a consequent increase in plasminogen activator activity (PAA) levels to supranormal values. Both treatments also significantly affected systemic fibrinolysis as reflected by a significant increase in PAA levels in plasma to supranormal levels. Neither nebulized rtPA nor anti-PA1-1 affected pulmonary inflammation. Neither treatment affected bacterial clearance of P. aeruginosa from the lungs in case of pneumonia. Local treatment with rtPA or anti-PA1-1 affects pulmonary fibrinolysis but not inflammation in models of direct or indirect ALI in rats.

Caponigro and colleagues5 have speculated that plasma concentrations of EBV DNA can be used as a biomarker for case-finding in high-risk populations. [...] when EBV serology and cytology do not provide an adequate explanation for cervical lymphadenopathy, quantitative PCR for EBV should be considered.

Bilateral re-expansion pulmonary edema (RPE) is an extremely rare entity. We report the unique case of bilateral RPE following a traumatic, unilateral hemopneumothorax in a young healthy male. Bilateral RPE occurred only one hour after drainage of a unilateral hemopneumothorax. The patient was treated with diuretics and supplemental oxygen. Diagnosis was confirmed by excluding other causes, using laboratory findings, chest radiography, pulmonary and cardiac ultrasound and high resolution computed tomography. His recovery was uneventful. The pathophysiology of bilateral RPE is not well known. Treatment is mainly supportive and consists of diuretics, mechanical ventilation, inotropes and steroids. In case of a pulmonary deterioration after the drainage of a traumatic pneumothorax, bilateral RPE should be considered after exclusion of more common causes of dyspnea.

Objective Pulmonary hypertension is a characteristic feature of acute respiratory distress syndrome (ARDS) and contributes to mortality. Administration of sildenafil in ambulatory patients with pulmonary hypertension improves oxygenation and ameliorates pulmonary hypertension. Our aim was to determine whether sildenafil is beneficial for patients with ARDS. Design Prospective, open-label, multicenter, interventional cohort study. Setting Medical-surgical ICU of two university hospitals. Patients Ten consecutive patients meeting the NAECC criteria for ARDS. Interventions A single dose of 50 mg sildenafil citrate administered via a nasogastric tube. Main results Administration of sildenafil in patients with ARDS decreased mean pulmonary arterial pressure from 25 to 22 mmHg ( P  = 0.022) and pulmonary artery occlusion pressure from 16 to 13 mmHg ( P  = 0.049). Systemic mean arterial pressures were markedly decreased from 81 to 75 mmHg ( P  = 0.005). Sildenafil did not improve pulmonary arterial oxygen tension, but resulted in a further increase in the shunt fraction. Conclusion Although sildenafil reduced pulmonary arterial pressures during ARDS, the increased shunt fraction and decreased arterial oxygenation render it unsuitable for the treatment of patients with ARDS.

Abstract Background: Pulmonary coagulopathy may contribute to an adverse outcome in lung injury. We assessed the effects of local anticoagulant therapy on bronchoalveolar and systemic haemostasis in a rat model of endotoxemia-induced lung injury. Methods: Male Sprague–Dawley rats were intravenously challenged with lipopolysaccharide (LPS) and treated with nebulized normal saline (placebo), recombinant human-activated protein C (APC), plasma-derived antithrombin (AT), heparin, or danaparoid. Results: Intravenous administration of LPS resulted in lung injury associated with elevated bronchoalveolar levels of thrombin–antithrombin complex (TATc), 6.9 ± 0.8 ng/mL (placebo) versus 0.5 ± 0.2 ng/mL (healthy control) (p < 0.01), and elevated bronchoalveolar levels of fibrin degradation products (FDP), 555 ± 74 ng/mL versus 27 ± 12 ng/mL (p < 0.01). Nebulized APC, AT, and danaparoid all significantly limited the rise of bronchoalveolar levels of TATc, 2.4 ± 0.7 ng/mL), 1.5 ± 0.2, 3.8 ± 0.7, and 3.2 ± 0.9 ng/mL, respectively (all p < 0.01 vs. placebo), and fibrin degradation products, 243 ± 77, 113 ± 20, 317 ± 74, and 300 ± 42 ng/mL (all p < 0.01 vs. placebo). Heparin and danaparoid also significantly affected systemic coagulopathy. However, pulmonary inflammatory responses [neutrophil influx into the lungs, bronchoalveolar levels of myeloperoxidase, and bronchoalveolar levels of tumor necrosis factor (TNF), interleukin (IL)-6 and CINC-3], and histopathology of lungs were not affected by nebulization of anticoagulants. Conclusions: In conclusion, local treatment with APC, AT, heparin, or danaparoid attenuate pulmonary coagulopathy, but not inflammation, in rats with endotoxemia-induced lung injury.