Introduction: Critically injured pediatric burn patients require specialized management, yet few verified pediatric burn centers exist in the United States. Many pediatric hospitals have resources to care for severely burned patients but lack standardized care guidelines, which improve outcomes. To improve the morbidity and mortality of severely burned pediatric patients admitted to the pediatric intensive care unit, we created a specialized burn team. We implemented Pediatric Severe Burn Guidelines, focusing on improving fluid resuscitation accuracy and providing timely nutritional support.
Methods: This investigation is of a 9-year (2010-2019) retrospective preintervention and postintervention study of the effect of the formation of a multidisciplinary burn leadership committee and development and implementation of Pediatric Severe Burn Guidelines. The primary outcome measures are increasing the accuracy of fluid resuscitation and improving the timely administration of nutritional support. The process measure is the percentage of time the electronic health record power plan was used for burn admissions with burn leadership review of the cases. Balancing measures are pediatric intensive care unit and hospital length of stay.
Results: Preprotocol patients received acceptable fluid resuscitation 25% (5/20) of the time compared to 61.5% (8/13) of the time in postprotocol patients ( = 0.04). In postprotocol patients, there is an improvement in the timely placement of postpyloric feeding tube and initiation of feeds 48 hours after admission.
Conclusions: Extensive guidelines for standardized care require careful implementation and monitoring of adherence gaps. Creating a specialized burn team and implementing clinical guidelines standardize care leading to improvement in critical patient outcomes.
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http://dx.doi.org/10.1097/pq9.0000000000000388 | DOI Listing |
Cell Death Differ
December 2024
Georgetown University Medical Center, Lombardi Comprehensive Cancer Center, Washington, D.C., USA.
Germline inactivating mutations of the SLC25A1 gene contribute to various human disorders, including Velocardiofacial (VCFS), DiGeorge (DGS) syndromes and combined D/L-2-hydroxyglutaric aciduria (D/L-2HGA), a severe systemic disease characterized by the accumulation of 2-hydroxyglutaric acid (2HG). The mechanisms by which SLC25A1 loss leads to these syndromes remain largely unclear. Here, we describe a mouse model of SLC25A1 deficiency that mimics human VCFS/DGS and D/L-2HGA.
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December 2024
Health and Sports Medicine Department, Faculty of Sports Sciences and Health, University of Tehran, North Karegar St, P.O.B: 1439813117, Tehran, Iran.
Although the connection between muscular strength and flatfoot condition is well-established, the impact of corrective exercises on these muscles remains inadequately explored. This study aimed to assess the impact of intrinsic- versus extrinsic-first corrective exercise programs on muscle morphometry and navicular drop in boys with flexible flatfoot. Twenty-five boys aged 10-12 with flexible flatfoot participated, undergoing a 12-week corrective exercise program, with a shift in focus at six weeks.
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December 2024
Department of Obstetrics and Gynecology rehabilitation, West China Second Hospital, Sichuan University, Huaxi Technology Building, 16 Linjiang Middle Road, Wuhou District, Chengdu, 610000, Sichuan, China.
Rectus abdominis diastasis (RAD) is a key factor in the rehabilitation of postpartum women. This study aimed to evaluate the clinical efficacy of Kinesio Taping (KT) in RAD treatment and abdominal changes. The medical records of women with RAD who received KT treatment at the hospital were reviewed.
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December 2024
Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), Department of Chronic Diseases and Metabolism, KU Leuven, Leuven, Belgium.
The lungs of people with cystic fibrosis (PwCF) are characterized by recurrent bacterial infections and inflammation. Infections in cystic fibrosis (CF) are left unresolved despite excessive neutrophil infiltration. The role of CFTR in neutrophils is not fully understood.
View Article and Find Full Text PDFPediatr Rheumatol Online J
December 2024
Translational Genetics Research Group, La Fe Health Research Institute (IIS La Fe), Avenida Fernando Abril Martorell nº 106 Tower A, 7th Floor, Valencia, Spain.
Background: Aicardi-Goutières Syndrome is a monogenic type 1 interferonopathy with infantile onset, characterized by a variable degree of neurological damage. Approximately 7% of Aicardi-Goutières Syndrome cases are caused by pathogenic variants in the ADAR gene and are classified as Aicardi-Goutières Syndrome type 6. Here, we present a new homozygous pathogenic variant in the ADAR gene.
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