Improving extrauterine growth: evaluation of an optimized, standardized neonatal parenteral nutrition protocol.

OBJECTIVE: Poor extrauterine growth in very low birth weight (VLBW) neonates is common and associated with worsened long-term outcomes. We aimed to decrease growth restriction, measured by the change in weight z-score from birth to 36 weeks post menstrual age, from - 1.13 (baseline) to < -1 within 12 months. STUDY DESIGN: The Model for Improvement was used in the design and implementation of an optimized, standardized parenteral nutrition protocol. Three Plan-Do-Study-Act cycles were completed and a [Formula: see text] and S control chart was created for the primary outcome. RESULT: Mean weight z-score change from birth to 36 weeks post menstrual age improved by 23% to - 0.87. Improvements in early weight gain and linear growth were seen as well. CONCLUSION: Use of the Model for Improvement to implement an optimized, standardized parenteral nutrition protocol can help improve extrauterine growth among VLBW infants.

Nutrition management for the promotion of growth in very low birth weight premature infants.

Premature infants are highly susceptible to extrauterine growth restriction. Without early and adequate nutrition support, nutrition deficits of energy and protein can quickly accrue. Growth failure has been implicated in poor neurodevelopmental outcomes and long-term morbidity, creating a major focus on neonatal nutrition alongside medical management. Optimal nutrition is paramount for optimal growth outcomes. The purpose of this article is to review the implications and long-term effects of growth failure in premature infants, specifically, those with very low birth weights. In addition, nutrition interventions and treatments will be presented to manage and improve growth outcomes of the neonate.

Oxidative metabolism: glucose versus ketones.

The coupling of upstream oxidative processes (glycolysis, beta-oxidation, CAC turnover) to mitochondrial oxidative phosphorylation (OXPHOS) under the driving conditions of energy demand by the cell results in the liberation of free energy as ATP. Perturbations in glycolytic CAC or OXPHOS can result in pathology or cell death. To better understand whole body energy expenditure during chronic ketosis, we used a diet-induced rat model of ketosis to determine if high-fat-carbohydrate-restricted "ketogenic" diet results in changes in total energy expenditure (TEE). Consistent with previous reports of increased energy expenditure in mice, we hypothesized that rats fed ketogenic diet for 3 weeks would result in increased resting energy expenditure due to alterations in metabolism associated with a "switch" in energy substrate from glucose to ketone bodies. The rationale is ketone bodies are a more efficient fuel than glucose. Indirect calorimetric analysis revealed a moderate increase in VO2 and decreased VCO2 and heat with ketosis. These results suggest ketosis induces a moderate uncoupling state and less oxidative efficiency compared to glucose oxidation.