Abstract and Introduction
Abstract
Extrauterine growth restriction (EUGR) is commonly seen in small premature infants due to a lack of early aggressive nutrition that results in energy and protein deficits during the first few days of life. These deficits lead to early postnatal growth failure that continues at discharge resulting in growth parameters being below the 10th percentile, which is associated with poor neurodevelopmental outcomes. Strong evidence supports an early aggressive nutrition plan that includes early parenteral nutrition administration with 3–4 g kg−1 day−1 of protein and minimal enteral feedings. This article presents the current evidence surrounding early aggressive nutrition, minimal enteral feedings, use of human milk and human milk fortification and makes the argument for standardized practice to improve nutrition in small premature infants.
Introduction
Premature birth continues to occur despite medical advancement in the diagnosis, treatment and prevention of preterm labor. As a result, the need for neonatal intensive care remains in high demand. The demand for such care has led to major advances in technology and life support measures leading to an improvement in the survival of the smallest and most premature infants.[1] Although survival of small premature infants has increased, these infants still experience a number of morbidities at the time of hospital discharge. One of these morbidities is postnatal growth failure or extrauterine growth restriction (EUGR).
EUGR occurs when a premature infant's growth falls below the 10th percentile in comparison to a normal fetus of the same gestational age.[2] This type of postnatal growth failure is commonly seen in very low birth weight (VLBW) (< 1500 g) and extremely low birth weight (ELBW) (< 1000 g) infants. In fact, in 2001 the National Institute of Child and Human Development (NICHD) Neonatal Research Network[3] found that 97% of all VLBW and 99% of all ELBW infants included in the study experienced EUGR by 36 weeks corrected gestational age. In another study, Ehrenkranz and colleagues assessed growth in VLBW infants and found that at the time of discharge most of the infants born between 24 and 29 weeks gestation failed to reach the median birth weight of their fetal counterparts with the same postmenstrual age.[4]
These two studies were the first to identify EUGR as a new morbidity seen in premature infants. The study data suggest that the incidence of EUGR increases as gestational age and birth weight decrease. This finding is also consistent with Clark's and associates review of over 20,000 premature infants admitted to 124 neonatal intensive care units (NICU) across the nation.[2]
Extreme prematurity and the associated critical illness seen in such small premature infants often delay the initiation of early nutrition. Delaying early nutrition results in nutrient deficits, which Embelton et al. estimate to be over 12 g/kg of protein and over 300 kcal/kg of energy during the first few weeks of life.[5] These ongoing deficits were identified by Embelton et al., to be directly related to poor growth and subsequent development of EUGR.[5]
The development of EUGR is considered by many to be inevitable in small premature infants who do not receive early nutrition with adequate amounts of protein and energy during the first few weeks of life.[6–10] Most believe early nutrition should mimic the intrauterine environment where: 1) Amino acids are actively transported to the fetus via the placenta for protein accretion with half of the amino acids being oxidized and used for energy,[7,8] 2) Glucose is delivered at a rate that is equivalent to fetal utilization,[7] and 3) Fetal lipid uptake occurs at a rate that meets the needs for neuronal and central nervous system development and fat is not used for energy production until the third trimester.[9]
On the other hand, in the extrauterine environment: 1) Amino acids are held or limited due to fear of intolerance,[11] 2) Glucose is given as the sole source of energy administered at high rates resulting in hyperglycemia,[9] and 3) Fat, in the form of intralipids, is usually withheld due to hyperglycemia and fear of lung injury or kernicterus.[10]
The drastic change from a nutrient enriched environment as seen in utero to the nutrient sparse extrauterine environment puts additional stress on an already vulnerable sick premature infant.[8] During this time of transition is when optimal nutrition is necessary to prevent catabolism or metabolic shock from occurring. According to Hay, this type of nutrient deprivation early in life leads to permanent growth failure; which, Ehrenkranz et al. have linked to poor long-term neurodevelopmental outcomes.[9,12]
The identification of EUGR as a morbidity seen mostly in small premature infants has prompted a large amount of research to be conducted. A number of studies have focused on the initiation of early parenteral nutrition as a means to combat the early nutritional deficits that have been observed in small premature infants. Initiation of enteral nutrition and how quickly to advance enteral feedings has also been on the forefront. Human milk and the use of donor milk along with proper fortification have been highlighted in the literature more recently.
As neonatal nurses it is important that we practice according to current evidence so we are able to provide the best quality care to our neonatal patients. This article will review and discuss the current evidence in support of early aggressive nutrition to promote adequate postnatal growth in our tiniest of patients. Evidence to support the use of human milk and donor human milk as well as proper fortification will also be discussed. Lastly, evidence to support the use of standardized nutritional management guidelines will be provided.
NAINR. 2014;14(3):92-98. © 2014 Elsevier Science, Inc.
