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Surfactant delivery by aerosol inhalation – past, present, and future

Surfactant replacement therapy by nebulization to spontaneously breathing patients has been regarded as the Holy Grail since surfactant deficiency was first identified as the cause for neonatal respiratory distress syndrome. It avoids neonatal endotracheal intubation, a procedure that is often difficult and occasionally harmful. 

Unstable SpO2 in preterm infants: The key role of reduced ventilation to perfusion ratio

Instability of peripheral oxyhemoglobin saturation (SpO2) in preterm infants is correlated with late disability and is poorly understood. We hypothesised that a reduced ventilation to perfusion ratio (VA/Q) is the key predisposing factor for SpO2 instability.

Lung Recruitment Before Surfactant Administration in Extremely Preterm Neonates: 2-Year Follow-Up of a Randomized Clinical Trial

To examine follow-up outcomes at corrected postnatal age (cPNA) 2 years of preterm infants previously enrolled in an RCT and treated with IN-REC-SUR-E or IN-SUR-E in 35 tertiary neonatal intensive care units.

The Lancet Child & Adolescent Health Commission on the future of neonatology

Jane Pillow BMedSci (Dist) MBBS, PhD (Dist) FRACP Head, Developmental Chronobiology jane.pillow@thekids.org.au Head, Developmental Chronobiology

Comparison of "IN-REC-SUR-E" and LISA in preterm neonates with respiratory distress syndrome: a randomized controlled trial (IN-REC-LISA trial)

Surfactant is a well-established therapy for preterm neonates affected by respiratory distress syndrome (RDS). The goals of different methods of surfactant administration are to reduce the duration of mechanical ventilation and the severity of bronchopulmonary dysplasia (BPD); however, the optimal administration method remains unknown. 

Vitamin A and bronchopulmonary dysplasia: the next steps

Preterm infants are often vitamin A deficient, and vitamin A has functions that could mitigate the processes that lead to bronchopulmonary dysplasia. Therefore, supplementation of preterm infants with vitamin A to reduce the risk of bronchopulmonary dysplasia makes inherent sense.

Continuous Telemetric In Utero Tracheal Pressure Measurements in Fetal Lambs

Normal in utero lung development and growth rely upon the expansion of airspaces and the controlled efflux of lung liquid into the amniotic space. Infants with congenital diaphragmatic hernia (CDH) also have lung hypoplasia due to occupation of the chest cavity by the stomach and bowel and, in the most severe cases, the liver. Balloon tracheal occlusion reduces the severity of lung hypoplasia in fetuses with CDH but increases the risk of premature birth.

Vitamin A supplementation in very-preterm or very-low-birth-weight infants to prevent morbidity and mortality: A systematic review and meta-Analysis of randomized trials

A previous systematic review showed that intramuscular vitamin A supplementation reduced the risk of bronchopulmonary dysplasia (BPD) in very-low-birth-weight (VLBW) infants. However, more recent studies have questioned this finding.

Effect of Enteral Vitamin A on Fecal Calprotectin in Extremely Preterm Infants: A Nested Prospective Observational Study

Vitamin A has anti-inflammatory and immune-modulating properties. We aimed to assess whether enteral water-soluble vitamin A supplementation in extremely preterm infants decreases fecal calprotectin, a marker of intestinal inflammation.

Lung recruitment before surfactant administration in extremely preterm neonates with respiratory distress syndrome (IN-REC-SUR-E): a randomised, unblinded, controlled trial

The importance of lung recruitment before surfactant administration has been shown in animal studies. Well designed trials in preterm infants are absent. We aimed to examine whether the application of a recruitment manoeuvre just before surfactant administration, followed by rapid extubation (intubate-recruit-surfactant-extubate [IN-REC-SUR-E]), decreased the need for mechanical ventilation during the first 72 h of life compared with no recruitment manoeuvre (ie, intubate-surfactant-extubate [IN-SUR-E]).