Objectives: To describe the characteristics of fluid accumulation in critically ill children and evaluate the association between the degree, timing, duration, and rate of fluid accumulation and patient outcomes.
Design: Retrospective cohort study.
Setting: PICUs in Alberta, Canada.
Patients: All children admitted to PICU in Alberta, Canada, between January 1, 2015, and December 31, 2015.
Interventions: None.
Measurements And Main Results: A total of 1,017 patients were included. Fluid overload % increased from median (interquartile range) 1.58% (0.23-3.56%; n = 1,017) on day 1 to 16.42% (7.53-27.34%; n = 111) on day 10 among those remaining in PICU. The proportion of patients (95% CI) with peak fluid overload % greater than 10% and greater than 20% was 32.7% (29.8-35.7%) and 9.1% (7.4-11.1%), respectively. Thirty-two children died (3.1%) in PICU. Peak fluid overload % was associated with greater PICU mortality (odds ratio, 1.05; 95% CI, 1.02-1.09; p = 0.001). Greater peak fluid overload % was associated with Major Adverse Kidney Events within 30 days (odds ratio, 1.05; 95% CI, 1.02-1.08; p = 0.001), length of mechanical ventilation (B coefficient, 0.66; 95% CI, 0.54-0.77; p < 0.001), and length of PICU stay (B coefficient, 0.52; 95% CI, 0.46-0.58; p < 0.001). The rate of fluid accumulation was associated with PICU mortality (odds ratio, 1.15; 95% CI, 1.01-1.31; p = 0.04), Major Adverse Kidney Events within 30 days (odds ratio, 1.16; 95% CI, 1.03-1.30; p = 0.02), length of mechanical ventilation (B coefficient, 0.80; 95% CI, 0.24-1.36; p = 0.005), and length of PICU stay (B coefficient, 0.38; 95% CI, 0.11-0.66; p = 0.007).
Conclusions: Fluid accumulation occurs commonly during PICU course and is associated with considerable mortality and morbidity. These findings highlight the need for the development and evaluation of interventional strategies to mitigate the potential harm associated with fluid accumulation.
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http://dx.doi.org/10.1097/CCM.0000000000004376 | DOI Listing |
Alzheimers Dement
December 2024
National Center for Neurological Disorders, Shanghai, Shanghai, China.
Background: The heart-brain connection has been proposed to correlate cardiac disorders with brain health. However, the associations between subclinical alterations in cardiac structure or function and Alzheimer's disease (AD) pathologies haven't been fully elucidated. This study aimed to delineate the interrelationships between the subclinical alterations in the left heart, cerebrospinal fluid (CSF) AD biomarkers, and cognition.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
The First Affiliated Hospital of Chongqing Medical University, Chongqing, Chongqing, China.
Background: The regulatory role of Trimethylamine-N-oxide (TMAO) for cognition from the perspective of microbiota-gut-brain (MGB) axis in AD remains unclear.
Method: In clinical cohort study for effects of 24-week computerized cognitive training (CCT), registered on clinicaltrials.gov (NCT06094452), plasma TMAO levels were quantified using ELISA in MCI (n=39) and mild AD patients (n=35).
Alzheimers Dement
December 2024
Barcelonaβeta Brain Research Center (BBRC), Pasqual Maragall Foundation, Barcelona, Spain.
Background: Alzheimer's disease (AD) blood biomarkers alone can detect amyloid-β (Aβ) pathology in cognitively unimpaired (CU) individuals. We assessed whether combining different plasma biomarkers improves the detection of Aβ-positivity and identifies rapid amyloid deposition in CU individuals.
Method: CU participants from the ALFA+ cohort were included.
Alzheimers Dement
December 2024
Huntington Medical Research Institutes, Pasadena, CA, USA.
Background: At the pre-clinical stages of Alzheimer's disease (AD) development, the accumulation of amyloid-β (Aβ) and tau induces neural toxicity, synaptic dysfunction, and excitation/inhibition instability of neural network activity, leading to cognitive decline. However, the effects of Aβ/tau accumulation on electroencephalography (EEG) functional connectivity (FC) in cognitively healthy (CH) individuals during a cognitive challenge have not been elucidated. Therefore, the main objective of this work is to evaluate the association between Aβ/tau level and brain FC during a cognitive challenge in CH individuals.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Wu Tsai Neurosciences Institute, Stanford University, Stanford, CA, USA.
Background: The buildup of brain amyloid-beta and tau protein aggregates do not sufficiently explain the heterogeneity in cognitive impairment in Alzheimer's disease (AD).
Method: To elucidate drivers of cognitive impairment, we measure the levels of 7,000 proteins, in addition to amyloid-beta-42 (Ab42) and phospho-tau-181 (PTau181), from the cerebrospinal fluid of 2,000 individuals from healthy to severe dementia.
Result: We identify synapse proteins as the strongest correlates of cognitive impairment.
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