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Quality indicators are registered to monitor and improve the quality of care. However, the number and effectiveness of quality indicators is under debate, and may influence the joy in work of physicians and nurses. Empirical data on the nature and consequences of the registration burden are lacking. The aim of this study was to identify and explore healthcare professionals' perceived burden due to quality registrations in hospitals, and the effect of this burden on their joy in work. A mixed methods observational study, including participative observations, a survey and semi-structured interviews in two academic hospitals and one teaching hospital in the Netherlands. Study participants were 371 healthcare professionals from an intensive care unit (ICU), a haematology department and others involved in the care of elderly patients and patients with prostate or gastrointestinal cancer. On average, healthcare professionals spend 52.3 minutes per working day on quality registrations. The average number of quality measures per department is 91, with 1380 underlying variables. Overall, 57% are primarily registered for accountability purposes, 19% for institutional governance and 25% for quality improvement objectives. Only 36% were perceived as useful for improving quality in everyday practice. Eight types of registration burden were identified, such as an excessive number of quality registrations, and the lack of usefulness for improving quality and inefficiencies in the registration process. The time healthcare professionals spent on quality registrations was not correlated with any measure of joy in work. Perceived unreasonable registrations were negatively associated with healthcare professionals' joy in work (intrinsic motivation and autonomy). Healthcare professionals experienced quality registrations as diverting time from patient care and from actually improving quality. Registering fewer quality indicators, but more of what really matters to healthcare professionals, is key to increasing the effectiveness of registrations for quality improvement and governance. Also the efficiency of quality registrations should be increased through staffing and information and communications technology solutions to reduce the registration burden experienced by nurses and physicians.

Artificial intelligence (AI) has the potential to revolutionize critical care medicine by enhancing patient care, improving resource allocation and reducing clinician workload. Despite this promise, many AI applications remain confined to scientific research rather than being integrated into everyday clinical practice. This manuscript aims to help intensivists prepare themselves and their intensive care units (ICUs) for AI implementation. It provides a comprehensive yet practical roadmap, detailing AI methods, applications, responsible AI principles, common roadblocks and implementation strategies. We propose a three-tiered risk-based approach to AI implementation, starting with low-risk low-complexity administrative AI, progressing to logistical AI, and finally integrating medical AI as clinical decision support systems. This ensures a gradual build-up of AI skills, technical AI readiness of the ICU, incremental value demonstration and alignment with evolving regulatory standards. For each AI project, responsible AI principles should be incorporated and adequately addressed throughout the entire AI lifecycle, from development to validation to implementation and scaling. Common roadblocks for AI implementation including technical issues (such as data quality and interoperability issues), organizational challenges (such as lack of a clear vision and strategy), and clinical concerns (such as limited AI literacy among staff), should be addressed proactively. By following this roadmap, ICUs can achieve sustainable AI integration, ultimately improving patient outcomes and clinician experience. The future of critical care lies in the responsible and strategic adoption of AI, with intensivists playing a central role in shaping its implementation. [Display omitted] •A three-tiered, risk-based approach is advised for successful AI implementation in ICUs.•Responsible AI principles should be integrated throughout the entire AI lifecycle, from development to validation to implementation and scaling.•Common roadblocks to AI implementation include technical, organizational, and clinical challenges.•A practical roadmap for AI readiness in ICUs includes defining strategic vision, starting with low-risk high-value applications, focusing on foundational readiness, selecting the appropriate use case aligned with readiness level and goals, establishing monitoring and governance systems and incorporating lessons learned from early adopters.

Infection is a major cause of death in the intensive care unit (ICU). Strategies to reduce rates of infection in ICUs include selective digestive tract decontamination (SDD), in which cefotaxime and topical antimicrobial agents are administered for 4 days, and selective oropharyngeal decontamination (SOD), in which only topical antimicrobial agents are administered. In this cluster-randomization study involving 13 ICUs in the Netherlands, SOD and SDD did not affect crude mortality but did appear to reduce mortality slightly at day 28, with adjustment for covariates. Strategies to reduce rates of infection in ICUs include selective digestive tract decontamination (SDD) and selective oropharyngeal decontamination (SOD). In this study involving 13 ICUs in the Netherlands, SOD and SDD did not affect crude mortality but did appear to reduce mortality slightly at day 28. Infections acquired in the intensive care unit (ICU) are important complications of the treatment of critically ill patients, increasing morbidity, mortality, and health care costs. 1 Reductions in the incidence of respiratory tract infections have been achieved with the use of prophylactic antibiotic regimens, such as selective decontamination of the digestive tract (SDD) 2 , 3 and selective oropharyngeal decontamination (SOD). 4 , 5 The SDD approach 6 , 7 consists of prevention of secondary colonization with gram-negative bacteria, Staphylococcus aureus, and yeasts through application of nonabsorbable antimicrobial agents in the oropharynx and gastrointestinal tract, preemptive treatment of possible infections with commensal respiratory tract bacteria through systemic . . .

Excessive or persistent proinflammatory cytokine production plays a central role in autoimmune diseases. Acute activation of the sympathetic nervous system attenuates the innate immune response. However, both the autonomic nervous system and innate immune system are regarded as systems that cannot be voluntarily influenced. Herein, we evaluated the effects of a training program on the autonomic nervous system and innate immune response. Healthy volunteers were randomized to either the intervention (n = 12) or control group (n = 12). Subjects in the intervention group were trained for 10 d in meditation (third eye meditation), breathing techniques (i.a., cyclic hyperventilation followed by breath retention), and exposure to cold (i.a., immersions in ice cold water). The control group was not trained. Subsequently, all subjects underwent experimental endotoxemia (i.v. administration of 2 ng/kg Escherichia coli endotoxin). In the intervention group, practicing the learned techniques resulted in intermittent respiratory alkalosis and hypoxia resulting in profoundly increased plasma epinephrine levels. In the intervention group, plasma levels of the anti-inflammatory cytokine IL-10 increased more rapidly after endotoxin administration, correlated strongly with preceding epinephrine levels, and were higher. Levels of proinflammatory mediators TNF-α, IL-6, and IL-8 were lower in the intervention group and correlated negatively with IL-10 levels. Finally, flu-like symptoms were lower in the intervention group. In conclusion, we demonstrate that voluntary activation of the sympathetic nervous system results in epinephrine release and subsequent suppression of the innate immune response in humans in vivo. These results could have important implications for the treatment of conditions associated with excessive or persistent inflammation, such as autoimmune diseases.

Abstract Sepsis is the leading cause of death in the intensive care unit and ranks in the top 10 causes of death in general worldwide. Proinflammatory mediators are related to symptoms observed early in patients with sepsis, such as fever and hemodynamic instability. However, in recent years it has become clear that most septic patients do not die from an overwhelming proinflammatory immune response but in an immunosuppressive state, which can last for days or even weeks, and that results in increased susceptibility to secondary (opportunistic) infections. Although infection control and supportive therapies will remain the cornerstone of treatment, especially in the early phase of sepsis, the identification of this so-called “immunoparalysis” is currently causing a paradigm shift in the adjunctive treatment of sepsis from therapies that suppress the immune system toward immunostimulation. In this Critical Care Perspective we give an overview of the pathophysiology of sepsis, with a focus on immunosuppressive mechanisms that play an important role in outcome. In addition, we present an appraisal of the recent advances in immunotherapy as an adjunctive treatment for sepsis.

While most influenza patients have a self-limited respiratory illness, 5–10% of hospitalized patients develop severe disease requiring ICU admission. The aim of this study was to identify influenza-specific factors associated with ICU admission and mortality. Furthermore, influenza-specific pulmonary bacterial, fungal and viral co-infections were investigated. 199 influenza patients, admitted to two academic hospitals in the Netherlands between 01-10-2015 and 01-04-2016 were investigated of which 45/199 were admitted to the ICU. A history of Obstructive/Central Sleep Apnea Syndrome, myocardial infarction, dyspnea, influenza type A, BMI > 30, the development of renal failure and bacterial and fungal co-infections, were observed more frequently in patients who were admitted to the ICU, compared with patients at the normal ward. Co-infections were evident in 55.6% of ICU-admitted patients, compared with 20.1% of patients at the normal ward, mainly caused by Staphylococcus aureus, Streptococcus pneumoniae, and Aspergillus fumigatus. Non-survivors suffered from diabetes mellitus and (pre-existent) renal failure more often. The current study indicates that a history of OSAS/CSAS, myocardial infarction and BMI > 30 might be related to ICU admission in influenza patients. Second, ICU patients develop more pulmonary co-infections. Last, (pre-existent) renal failure and diabetes mellitus are more often observed in non-survivors. •A history of OSAS/CSAS, myocardial infarction and BMI > 30 are risk factors for ICU admission.•Non-survivors suffer more often from diabetes mellitus and (pre-existent) renal failure.•ICU patients develop renal failure and bacterial/fungal co-infections more often.

Abstract Rationale Reversal of sepsis-induced immunoparalysis may reduce the incidence of secondary infections and improve outcome. Although IFN-γ and granulocyte-macrophage colony–stimulating factor (GM-CSF) restore immune competence of ex vivo stimulated leukocytes of patients with sepsis, effects on immunoparalysis in vivo are not known. Objectives To investigate the effects of IFN-γ and GM-CSF on immunoparalysis in vivo in humans. Methods We performed a double-blind, placebo-controlled, randomized study in 18 healthy male volunteers that received Escherichia coli endotoxin (LPS; 2 ng/kg, intravenously) on days 1 and 7 (visits 1 and 2). On days 2, 4, and 6, subjects received subcutaneous injections of IFN-γ (100 μg/day; n = 6), GM-CSF (4 μg/kg/day; n = 6), or placebo (NaCl 0.9%; n = 6). Measurements and Main Results In the placebo group, immunoparalysis was illustrated by a 60% (48–71%) reduction of LPS-induced tumor necrosis factor (TNF)-α plasma concentrations during visit 2 (P = 0.03), whereas the antiinflammatory IL-10 response was not significantly attenuated (39% [2–65%]; P = 0.15). In contrast, in the IFN-γ group, TNF-α concentrations during visit 2 were not significantly attenuated (28% [1–47%]; P = 0.09), whereas the IL-10 response was significantly lower (reduction of 54% [47–66%]; P = 0.03). Compared with the placebo group, the reduction in the LPS-induced TNF-α response during visit 2 was significantly less pronounced in the IFN-γ group (P = 0.01). Moreover, compared with placebo, treatment with IFN-γ increased monocyte HLA-DR expression (P = 0.02). The effects of GM-CSF tended in the same direction as IFN-γ, but were not statistically significant compared with placebo. Conclusions IFN-γ partially reverses immunoparalysis in vivo in humans. These results suggest that IFN-γ is a promising treatment option to reverse sepsis-induced immunoparalysis. Clinical trial registered with www.clinicaltrials.gov (NCT 01374711).

Evidence has accumulated that respiratory muscle dysfunction develops in critically ill patients and contributes to prolonged weaning from mechanical ventilation. Accordingly, it seems highly appropriate to monitor the respiratory muscles in these patients. Today, we are only at the beginning of routinely monitoring respiratory muscle function. Indeed, most clinicians do not evaluate respiratory muscle function in critically ill patients at all. In our opinion, however, practical issues and the absence of sound scientific data for clinical benefit should not discourage clinicians from having a closer look at respiratory muscle function in critically ill patients. This perspective discusses the latest developments in the field of respiratory muscle monitoring and possible implications of monitoring respiratory muscle function in critically ill patients.