Objective: To discover the potential association between diminished intraoperative average SctO levels and postoperative neurodevelopmental delays among patients after pediatric living-donor liver transplantation.
Study Design: Patients undergoing living-donor liver transplantation were recruited for this trial. The neurodevelopment status of patients was assessed using the Ages Stages Questionnaires. The primary outcome was the occurrence of neurodevelopmental delay among patients at different intervals following pediatric liver transplantation. Secondary outcomes included the duration of mechanical ventilation, rates of re-intubation, length of ICU stay, postoperative hospitalization, and intraoperative comparisons of mean arterial pressure (MAP), arterial partial pressure of oxygen (PaO), arterial partial pressure of carbon dioxide (PaCO), and hemoglobin (Hb) concentration.
Results: A total of 119 patients were included in the statistical analysis and assigned to high saturation group (HS) and low saturation group (LS) according to the average intraoperative cerebral tissue oxygen saturation values. Following adjustment for PELD scores, significant differences between the two groups were observed for the incidence of neurodevelopmental delay in communication at 1 and 3 months follow-up ( = 0.019 and = 0.020, respectively), fine motor at six months follow-up ( = 0.014), and problem-solving abilities at one year follow-up ( = 0.047). Moverover, the length of ICU stay ( = 0.009) and postoperative hospitalization ( = 0.029) in LS group were also significant prolonged.
Conclusion: This prospective observational study revealed that the patients with low average SctO values were more predisposed to experiencing postoperative neurodevelopment delays, suggesting a potential association between decreased average SctO and neurodevelopmental delay.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11747418 | PMC |
http://dx.doi.org/10.3389/fped.2024.1416020 | DOI Listing |
Front Pediatr
January 2025
Department of Anesthesiology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Objective: To discover the potential association between diminished intraoperative average SctO levels and postoperative neurodevelopmental delays among patients after pediatric living-donor liver transplantation.
Study Design: Patients undergoing living-donor liver transplantation were recruited for this trial. The neurodevelopment status of patients was assessed using the Ages Stages Questionnaires.
Case Rep Genet
January 2025
Medical Investigation of Neurodevelopmental Disorders (MIND) Institute, University of California, 2825 50th Street, Davis, Sacramento 95817, California, USA.
Fragile X syndrome (FXS) presents with autism spectrum disorder (ASD), intellectual disability, developmental delay, seizures, hypotonia during infancy, joint laxity, behavioral issues, and characteristic facial features. The predominant mechanism is due to CGG trinucleotide repeat expansion of more than 200 repeats in the 5'UTR (untranslated region) of (Fragile X Messenger Ribonucleoprotein 1) causing promoter methylation and transcriptional silencing. However, not all patients presenting with the characteristic phenotype and point/frameshift mutations with deletions in have been described in the literature.
View Article and Find Full Text PDFEnviron Health (Wash)
January 2025
Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, 2699 Gaoke Road, Shanghai 201204, China.
Previous toxicological research has suggested the potential neurotoxicity of ultrafine particulate matter (UFP, particles ≤0.1 μm in diameter). However, evidence from human beings, particularly regarding the neurodevelopmental impacts of UFP, is still limited.
View Article and Find Full Text PDFHGG Adv
January 2025
GeneDx LLC, Gaithersburg, Maryland, 20877.
The ARHGEF40 gene, also known as SOLO, encodes a RhoA-targeting guanine nucleotide exchange factor (GEF) and is currently considered a candidate gene with a potential relationship to disease. Our laboratory has confirmed variants at position p.Arg225 of the ARHGEF40 protein in multiple unrelated individuals with a phenotype including dysmorphic features, congenital anomalies and neurodevelopmental abnormalities.
View Article and Find Full Text PDFClin Genet
December 2024
Univ. Lille, CHU Lille, ULR7364 - RADEME - Maladies RAres du DEveloppement embryonnaire et du Métabolisme, CRMR Déficiences Intellectuelles de Causes Rares, Lille, France.
Intellectual Developmental Disorder with Dysmorphic Facies and Ptosis (IDDDFP) is a rare autosomal dominant syndrome caused by pathogenic variants in the BRPF1 gene, which is critical for chromatin regulation. This study expands the clinical and molecular spectrum of IDDDFP by analysing 29 new patients from 20 families with confirmed BRPF1 variants. Our cohort presented with a wide range of clinical features including developmental delay, intellectual disability (ID) and characteristic dysmorphic facial features such as ptosis, blepharophimosis and a broad nasal bridge.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!