Abstract
Cerebrovascular injury is one of the major detrimental consequences of preterm birth. Recent studies have focused their attention on factors that contribute to the development of brain lesions immediately after birth. Among those factors, hypothermia and lower cerebral oxygen saturation during delivery room resuscitation and high tidal volumes delivered during respiratory support are associated with increased risk of severe neurologic injury. In preterm infants, knowledge about causes and prevention of brain injury must be applied before and at birth. Preventive and therapeutic approaches, including correct timing of cord clamping, monitoring of physiological changes during delivery room resuscitation using pulse oximetry, respiratory function monitoring, near infrared spectroscopy, and alpha EEG, may minimize brain injury, Furthermore, postnatal administration of caffeine or other potential novel treatments (e.g., proangiogenic therapies, antioxidants, hormones, or stem cells) might improve long-term neurodevelopmental outcomes in preterm infants.
Highlights
Cerebrovascular lesions including hemorrhagic and ischemic injuries are major detrimental consequences of preterm birth resulting in adverse neurodevelopmental outcomes
We describe what is known about the factors involved in the development of brain injury during fetal-to-neonatal transition at birth
This is important as a recent individual patient analysis of eight trials demonstrated that 46% of preterm infants resuscitated with an initial low oxygen concentration did not reach Oxygen saturation (SpO2) of 80% at 5 min, which was associated with increased risk of major intraventricular hemorrhage (IVH) [19]
Summary
Cerebrovascular lesions including hemorrhagic and ischemic injuries are major detrimental consequences of preterm birth resulting in adverse neurodevelopmental outcomes. Rook et al compared 30 vs 65% oxygen and reported a significantly faster time to reach an SpO2 of 88% [median (IQR) 3:14 (2:08–5:24) vs 5:45 (3:49–7:51) min] [18] This is important as a recent individual patient analysis of eight trials demonstrated that 46% of preterm infants resuscitated with an initial low oxygen concentration did not reach SpO2 of 80% at 5 min, which was associated with increased risk of major IVH [19]. Severe IVH (grade III or IV) developed in 33/124 (27%) infants in the high VT group and 2/41 (6%) in the normal VT group (P = 0.01) These results are supported by animal studies in preterm lambs who reported an increase in brain inflammation, oxidative stress, vascular extravasation, and brain inflammation when using VT > 8 mL/kg during initial resuscitation. While these therapies seem promising, their application to reduce VIBI during the initial resuscitation in the DR is questionable and clinical trials are needed to confirm their feasibility, safety, and effectiveness
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