OBJECTIVE:To determine whether patient- and family-centered care interventions in the ICU improve outcomes.
DATA SOURCES:We searched MEDLINE, EMBASE, PsycINFO, CINAHL, and the Cochrane Library ...databases from inception until December 1, 2016.
STUDY SELECTION:We included articles involving patient- and family-centered care interventions and quantitative, patient- and family-important outcomes in adult ICUs.
DATA EXTRACTION:We extracted the author, year of publication, study design, population, setting, primary domain investigated, intervention, and outcomes.
DATA SYNTHESIS:There were 46 studies (35 observational pre/post, 11 randomized) included in the analysis. Seventy-eight percent of studies (n = 36) reported one or more positive outcome measures, whereas 22% of studies (n = 10) reported no significant changes in outcome measures. Random-effects meta-analysis of the highest quality randomized studies showed no significant difference in mortality (n = 5 studies; odds ratio = 1.07; 95% CI, 0.95–1.21; p = 0.27; I = 0%), but there was a mean decrease in ICU length of stay by 1.21 days (n = 3 studies; 95% CI, –2.25 to –0.16; p = 0.02; I = 26%). Improvements in ICU costs, family satisfaction, patient experience, medical goal achievement, and patient and family mental health outcomes were also observed with intervention; however, reported outcomes were heterogeneous precluding formal meta-analysis.
CONCLUSIONS:Patient- and family-centered care–focused interventions resulted in decreased ICU length of stay but not mortality. A wide range of interventions were also associated with improvements in many patient- and family-important outcomes. Additional high-quality interventional studies are needed to further evaluate the effectiveness of patient- and family-centered care in the intensive care setting.
Acute lung injury (ALI) remains a serious health issue with little improvement in our understanding of the pathophysiology and therapeutic approaches. We investigated the mechanism that ...lipopolysaccharide (LPS) induces early neutrophil recruitment to lungs and increases pulmonary vascular permeability during ALI. Intratracheal LPS induced release of pro-interleukin-1α (IL-1α) from necrotic alveolar macrophages (AM), which activated endothelial cells (EC) to induce vascular leakage via loss of vascular endothelial (VE)-cadherin. LPS triggered the AM purinergic receptor P2X7(R) to induce Ca2+ influx and ATP depletion, which led to necrosis. P2X7R deficiency significantly reduced necrotic death of AM and release of pro-IL-1α into the lung. CD14 was required for LPS binding to P2X7R, as CD14 neutralization significantly diminished LPS induced necrotic death of AM and pro-IL-1α release. These results demonstrate a key role for pro-IL-1α from necrotic alveolar macrophages in LPS-mediated ALI, as a critical initiator of increased vascular permeability and early neutrophil infiltration.
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•Intratracheal LPS induces alveolar macrophage necrosis and pro-IL-1α release•Pro-IL-1α activates EC via IL-1/MyD88 signaling leading to loss of VE-cadherin•VE-cadherin loss facilitates neutrophil recruitment and vascular leakage•LPS induces AM necrosis via Ca2+ influx triggered by CD14/P2X7R signaling
The mechanisms for early initiation of LPS-induced acute lung injury are not well understood. Arditi and colleagues show that LPS initiates pulmonary inflammation by inducing necrosis in alveolar macrophages via a CD14-P2x7R-Ca2+ pathway. Necrosis leads to pro-IL-1α release and subsequent EC activation allowing neutrophil recruitment into the lungs.
Mechanical ventilation is strongly associated with cognitive decline after critical illness. This finding is particularly evident among older individuals who have pre-existing cognitive impairment, ...most commonly characterized by varying degrees of cerebral amyloid-β accumulation, neuroinflammation, and blood-brain barrier dysfunction. We sought to test the hypothesis that short-term mechanical ventilation contributes to the neuropathology of cognitive impairment by (i) increasing cerebral amyloid-β accumulation in mice with pre-existing Alzheimer's disease pathology, (ii) increasing neurologic and systemic inflammation in wild-type mice and mice with pre-existing Alzheimer's disease pathology, and (iii) increasing hippocampal blood-brain barrier permeability in wild-type mice and mice with pre-existing Alzheimer's disease pathology.
We subjected double transgenic Alzheimer's disease (APP/PSEN1) and wild-type mice to mechanical ventilation for 4 h and compared to non-mechanically ventilated Alzheimer's disease model and wild-type mice. Cerebral soluble/insoluble amyloid-β
/amyloid-β
and neurological and systemic markers of inflammation were quantified. Hippocampal blood-brain barrier permeability was quantified using a novel methodology that enabled assessment of small and large molecule permeability across the blood-brain barrier.
Mechanical ventilation resulted in (i) a significant increase in cerebral soluble amyloid-β
(p = 0.007) and (ii) significant increases in neuroinflammatory cytokines in both wild-type and Alzheimer's disease mice which, in most cases, were not reflected in the plasma. There were (i) direct correlations between polymorphonuclear cells in the bronchoalveolar fluid and cerebral soluble amyloid-β
(p = 0.0033), and several Alzheimer's disease-relevant neuroinflammatory biomarkers including cerebral TNF-α and IL-6; (iii) significant decreases in blood-brain barrier permeability in mechanically ventilated Alzheimer's disease mice and a trend towards increased blood-brain barrier permeability in mechanically ventilated wild-type mice.
These results provide the first evidence that short-term mechanical ventilation independently promotes the neuropathology of Alzheimer's disease in subjects with and without pre-existing cerebral Alzheimer's disease pathology. Future studies are needed to further clarify the specific mechanisms by which this occurs and to develop neuroprotective mechanical ventilation strategies that mitigate the risk of cognitive decline after critical illness.
Objective
This article positions the special issue on telepsychology amidst the COVID‐19 pandemic, which has dramatically accelerated the adoption and dissemination of telepsychology.
Method
The ...article makes general observations about the themes emerging in the special issue with considerations for application, training, theory‐driven research, and policy. It then presents as a case example the rapid deployment during the pandemic of telepsychology doctoral training and services at the Virginia Commonwealth University (VCU) Primary Care Psychology Collaborative.
Results
Facilitators to VCU telepsychology deployment included trainee and supervisor resources, strong telepsychology training, and prior experience. Barriers to overcome included limited clinic capacity, scheduling, technology, and accessibility and diversity issues. Lessons learned involved presenting clinical issues, supervision, and working with children and adolescents.
Conclusions
Telepsychology is crucial for psychological service provision, during the COVID‐19 pandemic more than ever, and that is unlikely to change as psychologists and patients increasingly continue to appreciate its value.
Tumors often co-exist with T cells that recognize somatically mutated peptides presented by cancer cells on major histocompatibility complex I (MHC-I). However, it is unknown why the immune system ...fails to eliminate immune-recognizable neoplasms before they manifest as frank disease. To understand the determinants of MHC-I peptide immunogenicity in nascent tumors, we tested the ability of thousands of MHC-I ligands to cause tumor subclone rejection in immunocompetent mice by use of a new 'PresentER' antigen presentation platform. Surprisingly, we show that immunogenic tumor antigens do not lead to immune-mediated cell rejection when the fraction of cells bearing each antigen ('clonal fraction') is low. Moreover, the clonal fraction necessary to lead to rejection of immunogenic tumor subclones depends on the antigen. These data indicate that tumor neoantigen heterogeneity has an underappreciated impact on immune elimination of cancer cells and has implications for the design of immunotherapeutics such as cancer vaccines.
IL-1β is a potent proinflammatory cytokine that is implicated in the pathogenesis of acute respiratory distress syndrome. We hypothesized that LPS and mechanical ventilation (MV) together could lead ...to IL-1β secretion and the development of acute lung injury (ALI), and that this process would be dependent on caspase-1 and the nucleotide binding domain and leucine-rich repeat (NLR) pyrin domain containing 3 (NLRP3) inflammasome activation. The objectives of this study were to determine the specific role of IL-1β, caspase-1, and the NLRP3 inflammasome in a two-hit model of ALI due to LPS plus MV. We used a two-hit murine model of ALI in which both inhaled LPS and MV were required for the development of hypoxemia, pulmonary neutrophil infiltration, and alveolar leakage. Nlrp3-deficent and Casp1-deficient mice had significantly diminished IL-1β levels in bronchoalveolar lavage fluid, and were specifically protected from hypoxemia, despite similar alveolar neutrophil infiltration and leakage. The IL-1 receptor antagonist, Anakinra, significantly improved the specific development of hypoxemia without significant effects on neutrophil infiltration or alveolar leakage. MV resulted in increased bronchoalveolar lavage extracellular ATP and alveolar macrophage apoptosis as triggers of NLRP3 inflammasome activation. NLRP3 inflammasome activation and IL-1β production play a key role in ALI caused by the combination of LPS and MV, particularly in the hypoxemia associated with acute respiratory distress syndrome. Blocking IL-1 signaling in this model specifically ameliorates hypoxemia, without affecting neutrophil infiltration and alveolar leakage, disassociating these readouts of ALI. MV causes alveolar macrophage apoptosis, a key step in the activation of NLRP3 inflammasome and production of IL-1β.
Background A large portion of COVID-19 cases and deaths in the United States have occurred in nursing homes; however, current literature including the frontline perspective of staff working in ...nursing homes is limited. The objective of this qualitative assessment was to better understand what individual and facility level factors may have contributed to the impact of COVID-19 on Certified Nursing Assistants (CNAs) and Environmental Services (EVS) staff working in nursing homes. Methods Based on a simple random sample from the National Healthcare Safety Network (NHSN), 7,520 facilities were emailed invitations requesting one CNA and/or one EVS staff member for participation in a voluntary focus group over Zoom. Facility characteristics were obtained via NHSN and publicly available sources; participant demographics were collected via SurveyMonkey during registration and polling during focus groups. Qualitative information was coded using NVIVO and Excel. Results Throughout April 2021, 23 focus groups including 110 participants from 84 facilities were conducted homogenous by participant role. Staffing problems were a recurring theme reported. Participants often cited the toll the pandemic took on their emotional well-being, describing increased stress, responsibilities, and time needed to complete their jobs. The lack of consistent and systematic guidance resulting in frequently changing infection prevention protocols was also reported across focus groups. Conclusions Addressing concerns of low wages and lack of financial incentives may have the potential to attract and retain employees to help alleviate nursing home staff shortages. Additionally, access to mental health resources could help nursing home staff cope with the emotional burden of the COVID-19 pandemic. These frontline staff members provided invaluable insight and should be included in improvement efforts to support nursing homes recovering from the impact of COVID-19 as well as future pandemic planning.
Objective
In 2020, one study by Strait and colleagues raised awareness that the clinical images in rheumatology educational materials underrepresent people with skin of color (P‐SOC). Since then, ...publishers of rheumatology educational materials have focused on addressing this shortcoming. This study investigates the change in representation of P‐SOC following the review of Strait et al.
Methods
We used the methods of the aforementioned study to collect images from commonly referenced rheumatology educational materials and categorized the skin tones within them as “light” or “dark.” We calculated the proportional change in images depicting dark skin tones between 2020 and 2022 from the American College of Rheumatology (ACR) Image Library, the 10th edition of Kelley's Textbook of Rheumatology, and New England Journal of Medicine (NEJM) as well as between 2020 and 2024 from rheumatology articles within UpToDate. We compared results using one‐sided Z‐tests.
Results
Overall, the proportion of images depicting dark skin tones increased 40.6% (P < 0.0001). The 10th edition of Kelley's Textbook of Rheumatology most significantly increased inclusion of P‐SOC (90.1%; P = 0.0039), with ACR Image Library, UpToDate, and NEJM also enhancing representation (41.9%, P < 0.0001; 31.0%, P = 0.0083; 28.2%, P = 0.3046, respectively).
Conclusion
This study assesses the progress of rheumatology educational materials toward equitable representation of P‐SOC. It demonstrates that awareness coupled with focused efforts from educational publishers can enhance the proportion of images depicting dark skin tones, thereby enriching the quality of foundational knowledge relayed to rheumatology providers with the goal of improving health experiences and outcomes for P‐SOC with rheumatic diseases.
ObjectiveTo compare 2 years of radiographic sacroiliac joint (SIJ) changes in patients with recent onset axial spondyloarthritis (axSpA) receiving etanercept in a clinical trial (EMBARK) to similar ...patients not receiving biologics in a cohort study (DESIR).MethodsEndpoints were changes at week 104 per the modified New York (mNY) grading system in total SIJ score (primary endpoint) and net percentage of patients with progression defined three ways. Treatment effect was analysed with and without adjustment for baseline covariates.ResultsAt 104 weeks, total SIJ score improved in the etanercept group (n=154, adjusted least-squares mean change: –0.14) and worsened in the control group (n=182, change: 0.08). The adjusted difference between groups (etanercept minus control) was –0.22 (95% CI –0.38 to –0.06), p=0.008. The net percentage of patients with progression was significantly lower in the etanercept versus the control group for two of three binary endpoints: –1.9% versus 1.6% (adjusted difference for etanercept minus control: –4.7%,95% CI –9.9 to 0.5, p=0.07) for change in mNY criteria; –1.9% versus 7.8% (adjusted difference: –18.2%,95% CI –30.9 to –5.6, p=0.005) for change ≥1 grade in ≥1 SIJ; and –0.6% versus 6.7% (adjusted difference: –16.4%,95% CI –27.9 to –5.0, p=0.005) for change ≥1 grade in ≥1 SIJ, with shift from 0 to 1 or 1 to 0 considered no change.ConclusionDespite the slow radiographic SIJ progression rate over 2 years in axSpA, this study suggests a lower rate of progression in the SIJ with etanercept than without anti-tumour necrosis factor therapy.Trial registration numbersNCT01258738, NCT01648907; Post-results.
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