Tiffany A Moore1, Rita H Pickler2. 1. Assistant Professor, College of Nursing, University of Nebraska Medical Center (UNMC), Omaha. 2. The FloAnn Sours Easton Professor of Child and Adolescent Health; Director, PhD & MS in Nursing Science Programs; The Ohio State University College of Nursing; pickler.1@osu.edu.
Abstract
PURPOSE: Identifying relationships between feeding intolerance (FI), inflammation, and early measures of neurodevelopment may provide the basis for clinically relevant assessments for NICU clinicians and staff. The purpose of this secondary analysis was to examine the relationship of FI to inflammatory markers and/or neurobehaviors in the first week of life. METHODS: This was a retrospective, matched case-control design with data drawn from 114 infants born at ≤32 weeks gestation. RESULTS: Eight infants developed FI prior to full enteral feedings. These infants were more likely to have dysregulated levels of cytokines, specifically IL6, and lower neurodevelopmental scores compared to infants without FI. CONCLUSIONS: Results suggest physiologic dysregulation and an immature nervous system may contribute to the phenomenon of FI in preterm infants. Further research to identify the role of the brain-gut-immune axis on FI and other GI complications in this population is warranted.
PURPOSE: Identifying relationships between feeding intolerance (FI), inflammation, and early measures of neurodevelopment may provide the basis for clinically relevant assessments for NICU clinicians and staff. The purpose of this secondary analysis was to examine the relationship of FI to inflammatory markers and/or neurobehaviors in the first week of life. METHODS: This was a retrospective, matched case-control design with data drawn from 114 infants born at ≤32 weeks gestation. RESULTS: Eight infants developed FI prior to full enteral feedings. These infants were more likely to have dysregulated levels of cytokines, specifically IL6, and lower neurodevelopmental scores compared to infants without FI. CONCLUSIONS: Results suggest physiologic dysregulation and an immature nervous system may contribute to the phenomenon of FI in preterm infants. Further research to identify the role of the brain-gut-immune axis on FI and other GI complications in this population is warranted.
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