Introduction: Infants with single ventricle following stage I palliation are at risk for poor nutrition and growth failure. We hypothesise a standardised enteral feeding protocol for these infants that will result in a more rapid attainment of nutritional goals without an increased incidence of gastrointestinal co-morbidities. Materials and methods: Single-centre cardiac ICU, prospective case series with historical comparisons. Feeding cohort consisted of consecutive patients with a single ventricle admitted to cardiac ICU over 18 months following stage I palliation (n = 33). Data were compared with a control cohort and admitted to the cardiac ICU over 18 months before feeding protocol implementation (n = 30). Feeding protocol patients were randomised: (1) protocol with cerebro-somatic near-infrared spectroscopy feeding advancement criteria (n = 17) or (2) protocol without cerebro-somatic near-infrared spectroscopy feeding advancement criteria (n = 16). Results: Median time to achieve goal enteral volume was significantly higher in the control compared to feeding cohort. There were no significant differences in enteral feeds being held for feeding intolerance or necrotising enterocolitis between cohorts. Feeding cohort had significant improvements in discharge nutritional status (weight, difference admit to discharge weight, weight-for-age z score, volume, and caloric enteral nutrition) and late mortality compared to the control cohort. No infants in the feeding group with cerebro-somatic near-infrared spectroscopy developed necrotising enterocolitis versus 4/16 (25%) in the feeding cohort without cerebro-somatic near-infrared spectroscopy (p = 0.04). Conclusions: A feeding protocol is a safe and effective means of initiating and advancing enteral nutrition in infants following stage I palliation and resulted in improved nutrition delivery, weight gain, and nourishment status at discharge without increased incidence of gastrointestinal co-morbidities.
INTRODUCTION: Non-alcoholic fatty liver disease (NAFLD) is pandemic across the world and has a wide spectrum of presentations. Both NAFLD and its most severe histopathologic subtype, non-alcoholic steatohepatitis (NASH), can progress to cirrhosis, making early diagnosis pivotal. Liver histology is critical for the diagnosis of NASH, however little is known about the association of social and medical factors with its histologic features. We are conducting a retrospective analysis of a large single center database of over 2000 patients with fatty liver disease proven by biopsy. Here we focus on one year of data collected at our institution. METHODS: We reviewed 653 liver biopsies from a one-year period at Methodist Liver Institute to identify subjects with NAFLD and NASH based on the NAFLD Activity Score (NAS). NASH was defined as NAS score = >3. Patients under the age of 18, documented significant alcohol use, and without steatosis were excluded. We then collected data on demographics (age, race, insurance, and median income), comorbid disease (diabetes mellitus, hypertension, hyperlipidemia, metabolic syndrome), and medication use (antihypertensives, oral antihyperglycemics, insulin, statins, opioids), and used univariate statistical analysis to compare subjects with and without NASH. RESULTS: Of 253 biopsies included, 118 had steatosis without NASH and 145 had steatosis with NASH. Subjects with NASH were significantly younger, and more likely to be of Caucasian race than African American race, have Medicaid than commercial insurance, and have diabetes mellitus with use of oral antihyperglycemics. There was no significant difference between NASH and no NASH groups with regards to BMI, hypertension, hyperlipidemia, metabolic syndrome, or use of antihypertensives, statins, insulin, or opioids (Table 1). CONCLUSION: Though histologic confirmation is the gold standard to distinguish NAFLD from NASH, there is a lack of data establishing prognostic factors that may predict the degree of fibrosis. In our analysis having diabetes mellitus or Medicaid instead of commercial insurance correlated with more severe histopathologic disease, suggesting that more aggressive screening and treatment should be promoted in this population. There was no significant difference in socioeconomic factors such as median income or metabolic syndrome. Our study was limited by small size, and data collection is ongoing to determine other factors that may contribute to worsening fibrosis and validate or refute these early findings.
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