Oxygen Use in Neonatal Care: A Two-edged Sword

Abstract

In the neonatal period, the clinical use of oxygen should be taken into consideration for its beneficial and toxicity effects. Oxygen toxicity is due to the development of reactive oxygen species (ROS) such as OH• that is one of the strongest oxidants in nature. Of note, generation of ROS is a normal occurrence in human and it is involved in a myriad of physiological reactions. Anyway an imbalance between production of oxidant species and antioxidant defenses, called oxidative stress, could affect various aspect of organisms’ physiology and it could determine pathological consequences to living beings. Neonatal oxidative stress is essentially due to decreased antioxidants, increased ROS, or both. Studies have demonstrated that antioxidant capacity is lower in preterm newborns than term babies. This well-known deficiency of antioxidant factors is only a piece of a cohort of factors, which can be involved in the neonatal oxidative stress and the increased production of ROS may be a main factor. Mechanisms of ROS generation are: mitochondrial respiratory chain, free iron and Fenton reaction, inflammation, hypoxia and/or ischemia, reperfusion, and hyperoxia. Oxidative stress following hyperoxia has been recognized to be responsible for lung, central nervous system, retina, red blood cell injuries, and possibly generalized tissue damage. When supplemental oxygen is needed for care, it would be prudent to avoid changes and fluctuations in SpO2. The definition of the safest level of oxygen saturations in the neonate remains an area of active research. Currently, on the basis of the published evidences, the most suitable approach would be to set alarm limits between 90 and 95%. It should allow to avoid SpO2 values associated with potential hypoxia and/or hyperoxia. Although the usefulness of antioxidant protection in the neonatal period is still under investigation, the risk of tissue damage due to oxidative stress in perinatal period should not be underestimated.

Combined fetal inflammation and postnatal hypoxia causes myelin deficits and autism‐like behavior in a rat model of diffuse white matter injury

“…Yet, due to immature and often diseased respiratory, vascular and immune systems, preterm infants are often exposed to unstable oxygen saturation levels (Van Tilborg et al, ). Although optimal oxygen saturation levels in preterm infants are still an important topic of debate (Castillo et al, ; Lakshminrusimha, Manja, Mathew, & Suresh, ), in case of hypoxia infants are often treated with ventilation therapy, receiving supplemental oxygen which further contributes to large fluctuations in oxygen levels and which has been associated with increased levels of harmful oxidative stress (Perrone, Bracciali, Di Virgilio, & Buonocore, ). Oxygen instability has been used in a variety of neonatal rodent models to mimic preterm birth‐related brain injury.…”

Postępowanie w niespodziewanych trudnych drogach oddechowych u dzieci — stanowisko Sekcji Anestezjologii i Intensywnej Terapii Dziecięcej, Sekcji Przyrządowego Udrażniania Dróg Oddechowych Polskiego Towarzystwa Anestezjologii i Intensywnej Terapii oraz Po

“…This problem may be overcome with oxygen being delivered via nasal cannulae. Neonates require special attention, and premature babies in particular, as they are sensitive to excessive oxygen therapy/delivery while, on the other hand, being prone to hypoxia related to hypoventilation [13,44]. Cautious pre-oxygenation is recommended in this group of patients, although there are no clear guidelines regarding either the technique or its the length [33,36].…”

Decreased oxygen exposure during transportation of newborns

“…Oxygen can cause tissue injury through reactive oxygen species formation, especially in premature infants with reduced antioxidant defences, and may result in short-term and long-term toxic effects 1. Inappropriate oxygen use is associated with retinopathy of prematurity (ROP), periventricular leukomalacia or bronchopulmonary dysplasia (BPD) and with increased risk of infection, ageing, DNA damage and cancer 1 2.…”