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Science-based strategies for providing nutrition for high-risk neonates
Key points
- 1.
Optimization of the delivery of nutrition to the high-risk infant is essential for ideal growth and development.
- 2.
Standardizing nutrition guidelines based on the current best evidence leads to reduced risk of infection and necrotizing enterocolitis (NEC), fewer parenteral nutrition–associated morbidities, improved postnatal growth, and earlier attainment of full enteral feeds.
- 3.
Mother’s own milk (MoM) is considered the preferred enteral dietary choice for the preterm infant. Provision of MoM has been associated with fewer morbidities, such as sepsis, NEC, and retinopathy of prematurity, in the high-risk infant.
- 4.
Human donor milk (HDM) is the preferred alternative to MoM when MoM is unavailable. However, the pasteurization process results in decreased protein and immunomodulatory factors.
- 5.
Prolonged fasting is detrimental to the high-risk infant. The current evidence suggests that volume increases of up to 30 mL/kg/d of enteral feeds may be safe and beneficial to the neonate. Delaying the advancement of enteral nutrition does not decrease the risk for NEC.
- 6.
Fortification of feeds is imperative in the optimization of neonatal nutrition. Unfortified feeds increase the risk of osteopenia, poor growth, and nutrient deficiency. Earlier initiation of fortification increases protein intake and has not been shown to increase the risk for feeding intolerance and intestinal catastrophes.
- 7.
More studies are needed to determine the superiority of human milk–based fortification versus bovine milk–based fortification. The routine use of human milk–based fortification is still controversial and comes with concerns of poor growth and high costs.
- 8.
Both standardized and individualized fortification are methods to add multicomponent fortifiers to MoM and HDM.
- 9.
The routine evaluation of gastric residuals is not beneficial in preventing NEC and may lead to delays in achieving complete enteral nutrition.
- 10.
Parenteral nutrition (PN) is needed to provide adequate nutrients until the neonate’s gastrointestinal tract can accept sufficient enteral load. However, PN has potential complications such as central line–associated bloodstream infections, parenteral nutrition–associated liver disease (PNALD), and other metabolic disturbances.
- 11.
Glucose, lipids, and proteins are carefully titrated to optimize PN delivery.
Introduction
Providing adequate and appropriate nutrition is vital for ideal development and growth of preterm infants. The nutrition goal for a premature infant is to approximate the rate of growth and body composition of the average healthy fetus of the same age. , Clinicians often target growth velocities of approximately 15 g/kg/d or 10 to 30 g/d for weight and 1 cm/week for head circumference and length. Correlations between anthropometric measurements and improved outcomes later in life have been reported. However, they do not fully account for body composition. Most infants fail to keep up with this intrauterine growth rate and are relatively growth restricted. Growth failure ensues when there is a failure to provide adequate amounts of essential nutrients to the infant. Neurodevelopmental limitations and increased morbidity also accompany this. ,
Delivering nutrition to a very premature infant is compounded by issues unrelated to nutritional support. Many premature infants are critically ill with pathologic stresses such as necrotizing enterocolitis (NEC), bronchopulmonary dysplasia (BPD), hypoxic-ischemic conditions, sepsis, and anemia of prematurity that reduce the infant’s capacity for growth. Growth is also negatively affected by common medications used in the NICU, such as corticosteroids, diuretics, and catecholamines.
The premature infant’s intestinal tract is predisposed to vulnerabilities and difficulties in providing suitable enteral nutrition. Gastric acid production is limited in this population, impairing host defenses against harmful organisms predisposing to NEC. The developing premature infant has increased gut permeability, reduced immunoglobulins, immature intestinal epithelia, and a decreased mucin barrier. These infants are widely known to have issues with dysmotility and decreased gastric emptying. All these factors play a role in the undernutrition of the premature infant, which has been shown to have cumulative protein and energy deficits. This leads to delays in providing adequate enteral nutrition; interruptions in initiating, advancing, and fortifying enteral feeds; and regular withholding of feeds.
If provided in adequate quantity, nutrition via parenteral and enteral routes promotes positive energy and protein balance, resulting in improved outcomes. Stephens et al. showed that first-week protein and caloric intake was associated with an improved 18-month mental developmental index. Appropriate premature infant growth is also associated with fewer morbidities, such as severe retinopathy of prematurity and chronic diseases. , Evidence-based standardization of care and optimization of nutritional intervention is an essential component of the medical management of the premature infant. Standardization of feeding protocols minimizes variation in nutritional practices and has been shown to improve postnatal growth, shorten the time to attain full feeds, and decrease days on PN. Moreover, standardized feeding regimens are a method to reduce the incidence of NEC.
Enteral nutrition
Mother’s own milk and human donor milk
Mother’s own milk (MoM) is the preferred dietary choice for preterm infants due to its protective benefits. , These benefits are related to the composition of human milk, which contains many growth factors, micro- and macronutrients, hormones, antimicrobial agents, oligosaccharides, enzymes, hormones, and stem cells. For more than 30 years breast milk has been accepted as superior to preterm formula in preventing NEC. Provision of human milk to the premature infant has been associated with reduced rates of sepsis, NEC, and retinopathy of prematurity. Analysis by Miller et al. of 6 randomized trials and 43 observational studies in very-low-birth-weight (<1500 g) infants, or those <28 weeks gestational age, revealed a 5% reduction in late-onset sepsis (LOS) and a 7.6% reduction in retinopathy of prematurity. Sisk et al. showed that MoM is dose dependent with an 83% reduction in NEC if infant feeds comprise more than 50% MoM in the first 14 days. The likelihood of NEC or death decreased by a factor of 0.83 for each 10% increase in the proportion of MoM of the total intake. In the event the mother does not produce sufficient amounts of MoM, human donor milk (HDM) has emerged as an accepted alternative. The recent Cochrane database review concluded that HDM conferred a protective effect for NEC compared to infants who were fed formula; however, HDM does not affect LOS incidence. Yet, as with most meta-analyses, the conclusions can be misleading because they are only as good as the review studies. There is still a need for large prospective studies on this issue. Human milk also seems to confer a more appropriate intestinal microbiome with greater diversity and is better tolerated by the infant. , Compared to formula-fed infants, those fed with MoM have improved neurodevelopmental outcomes, although the influence of pasteurized HDM on neurodevelopment is controversial. , The Donor Milk for Improved Neurodevelopmental Outcomes (DoMINO) study analyzed neurodevelopmental outcomes of infants randomized to HDM versus preterm formula and did not find a significant benefit at 18 months. HDM is pooled and pasteurized from donors who undergo medical screening. The pasteurization process affects some milk components, resulting in lower protein and lipase content, diminished immunomodulatory factors such as lactoferrin and IgA, and removal of potentially beneficial bacteria. , Studies comparing an exclusive human milk–based diet versus those with some bovine components (bovine formula, bovine fortifier) have revealed mixed results in NEC prevention. One of the most extensive recently conducted randomized trials did not find a significant advantage in morbidity, mortality, growth, or 18-month neurodevelopmental outcomes. ,
Initiation and advancement of feeds
The initiation and advancement of enteral feeding has been a challenge in preterm infants where there is vulnerability and susceptibility of the immature gastrointestinal tract to injury and insult. Therefore enteral feeding has been met with resistance due to fear of a catastrophic gastrointestinal insult. However, human and animal studies have shown that both withholding enteral feeds and prolonged fasting are detrimental to the premature tract. Prolonged fasting has been shown to increase proinflammatory cytokines, resulting in villus atrophy, decreased mesenteric blood flow, enzyme activity digestive capability, and functional adaptation of the immature gastrointestinal tract. Furthermore, delayed introduction of enteral nutrition has been linked with fewer days on full feeds and increased morbidities such as retinopathy of prematurity, BPD, and intestinal inflammation. A meta-analysis of 14 randomized trials of 1551 infants found no evidence that delaying initiation of enteral feeds beyond 4 days of life affects the risk of NEC development. The provision of early and minimal enteral nutrition is now widely accepted in clinical practice.
The optimal enteral feed volume advancement rate remains controversial and is variable among clinicians. Raban et al. compared daily feeding advancements of 36 mL/kg/d versus 24 mL/kg/d and found that rapid advancement was well tolerated and improved weight gain. The recent Cochrane review of 13 randomized trials analyzed the slow advancement of enteral feeds in NEC prevention. Slow advancement was defined as a daily increment of 15 to 20 mL/kg of enteral feeding volume and faster advancement as a daily increment of 30 to 40 mL/kg. No difference in NEC risk or all-cause mortality was found between the groups. Advancing at a slower rate may slightly increase the risk for infection. The Speed of Increasing milk Feeds Trial (SIFT) randomized more than 2800 infants to 18 mL/kg/d versus 30 mL/kg/d volume advancement until reaching full feeding volumes. There was no significant difference in survival or morbidity between the groups at 24 months. , Extremely premature infants may tolerate faster (30–40 mL/kg/d) feeding advancement to optimize their enteral nutrition. Some caution should be heeded for unstable infants and high-risk infants, where slower advancement may initially be needed. Slower rates of feeding advancement and delays in attaining full feeds are associated with neurodevelopmental impairment and complications related to prolonged PN and central line–associated bloodstream infections. ,
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