Introduction of oral feeding in premature infants on high flow nasal cannula in a level IV neonatal intensive care unit: a quality improvement initiative.

BACKGROUND: Failure to reach full oral feeding remains a significant barrier for premature infants to discharge home. Postmenstrual age (PMA) at first oral feeding is significantly associated with the length of hospital stay (LOS). METHODS: Single-center QI to introduce oral feeding to infants on high-flow nasal cannula (HFNC) by reducing the flow to 2 L during feeds. GLOBAL AIM: To reduce PMA at first oral feeding and reduce the LOS. SMART AIM: To introduce oral feeds in 40% of infants who are on ≤4 L HFNC by the end of 12 months. RESULTS: Over 12 months, SMART aim reached with 100% enrollment. PMA at first oral feeding decreased from a median of 42.4w ((IQR) (40,46.6) to 37.8w (35.8,43.2), PMA at discharge decreased from 47w (44.6,50.7) to 42.6w (41.3,48.8). CONCLUSION: Allowing oral feeding in infants while on HFNC is feasible. This approach can significantly reduce PMA at first and full oral feeding.

Use of surfactant beyond respiratory distress syndrome, what is the evidence?

Surfactant replacement therapy is currently approved by the United States Food and Drug Administration (FDA) for premature infants with respiratory distress syndrome (RDS) caused by surfactant deficiency due to immaturity. There is strong evidence that surfactant decreases mortality and air leak syndromes in premature infants with RDS. However, surfactant is also used "off-label" for respiratory failure beyond classic RDS. This review discusses current evidence for the use of off-label surfactant therapy for (1) term infants with lung disease such as meconium aspiration syndrome (MAS), pneumonia/sepsis, and congenital diaphragmatic hernia (2) premature infants after 72 h for acute respiratory failure, and (3) the use of surfactant lavage. At last, we briefly describe the use of surfactants for drug delivery and the current evidence on evaluating infants for surfactant deficiency.

Molecular Mechanisms of Maternal Diabetes Effects on Fetal and Neonatal Surfactant.

Respiratory distress is a significant contributor to newborn morbidity and mortality. An association between infants of diabetic mothers (IDMs) and respiratory distress syndrome (RDS) has been well recognized for decades. As obesity and diabetes prevalence have increased over the past several decades, more women are overweight and diabetic in the first trimester, and many more pregnant women are diagnosed with gestational diabetes. Glycemic control during pregnancy can be challenging due to the maternal need for higher caloric intake and higher insulin resistance. Surfactant is a complex molecule at the alveolar air-liquid interface that reduces surface tension. Impaired surfactant synthesis is the primary etiology of RDS. In vitro cell line studies, in vivo animal studies with diabetic rat offspring, and clinical studies suggest hyperglycemia and hyperinsulinemia can disrupt surfactant lipid and protein synthesis, causing delayed maturation in surfactant in IDMs. A better understanding of the molecular mechanisms responsible for surfactant dysfunction in IDMs may improve clinical strategies to prevent diabetes-related complications and improve neonatal outcomes.