Effects of high maternal oxygen concentrations on the fetus

Published on 07/02/2015 by admin

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Effects of high maternal oxygen concentrations on the fetus

Inge Falk van Rooyen, MD

When necessary, 100% O₂ may be given to a parturient to improve fetal oxygenation; however, maternal hyperoxygenation may have a harmful effect on the developing fetal vascular beds. For more than a century, research has shown that, as a result of the harmful effects of free O₂ radicals and oxidative stress, O₂ can be toxic, particularly to the vascular beds of the central nervous system, the eye, and pulmonary circulation. It is also now clear that preterm infants are more susceptible to O₂ toxicity than are full-term infants. Several factors are known to affect severity of injury related to O₂ toxicity (Box 187-1).

Box 187-1 Factors Affecting the Severity of Fetal Injury Resulting from Exposure to High Maternal O₂ Concentrations

Duration of O₂ exposure

Steep gradient between maternal FIO₂ and fetal PaO₂

Extent of prematurity of the fetus

Preexisting fetal and maternal pathology

Within the fetomaternal circulation, the highest possible partial pressure gradient of O₂ that can be delivered to the fetus in utero is limited by the fetomaternal gas-exchange mechanisms (Figure 187-1). The placenta is 15 times less efficient at gas exchange than is the lung; however, the unloading of O₂ to the fetus is enhanced by several biochemical mechanisms.

Figure 187-1 Dissociation curves of fetal hemoglobin (HbF) and adult hemoglobin (HbA). In the placenta, the HbA frees up its O₂ in favor of the HbF, which possesses a higher affinity for O₂.

Placental transfer of O₂

Increasing maternal oxygenation will increase the partial pressure of O₂ (PO₂) in the fetal umbilical artery and umbilical vein. Because of limited flow exchange (placental), an increase in maternal PaO₂ does not produce an increase of equal magnitude in the fetus. Even with a maternal inspired O₂ concentration of 100%, fetal PO₂ in the umbilical vein will be less than 50 mm Hg. It has been shown in an animal model that, by increasing the maternal inspired O₂ concentration from 0.21 to 1.0, the PO₂ in the umbilical vein increases by only 10 mm Hg at 1 atm pressure.

Hyperbaric O₂ delivery to the mother will significantly increase fetal PO₂. It has been shown that hyperbaric O₂ delivery to a pregnant ewe to achieve an arterial PO₂ of 1300 mm Hg will raise umbilical vein PO₂ to nearly 600 mm Hg. No fall in uteroplacental or umbilical blood flow occurs.

Toxic effects of high maternal O₂ concentration

Three anatomic sites are considered to be most at risk for the toxic effects of hyperoxia: the lung, eye, and brain. Sequelae include bronchopulmonary dysplasia, retinopathy, and periventricular leukomalacia.

Bronchopulmonary dysplasia and O₂ toxicity

Chronic lung disease or bronchopulmonary dysplasia is a severe complication of prematurity. Pathologic mechanisms of tissue injury are complex. However, injury may be caused by direct reactive O₂ species production in response to hyperoxia or indirectly by reactive O₂ species due to phagocyte activation and inflammation. Recent studies in newborn mice exposed to 100% O₂ at normal atmospheric pressure for up to 6 weeks resulted in pulmonary changes comprising deposition of dense fibrous tissue, chronic bronchitis, bronchiolitis, and emphysema. Survival of the experimental animals also decreased with the duration of O₂ exposure.

Retinopathy of prematurity

Treatment with supplemental O₂ in premature infants who have incompletely vascularized retinas (a process that is usually completed at 36 weeks of gestation) may cause hyperoxia and vasoconstriction. This leads to local hypoxia, deposition of fibrous tissue, excessive tissue vascularization, and the further mechanisms of visual loss from retinopathy of prematurity.

O₂ and brain injury

Oxidative stress and damage to premyelinating oligodendrocytes in cerebral white matter has been proposed as a mechanism of periventricular leukomalacia, increasing the risk of cerebral palsy and cognitive deficit in preterm infants.

Fetal abnormalities

No fetal abnormalities have been found in human or animal models with administration to the parturient of up to 100% O₂ at 1 atm pressure. However, hyperbaric O₂ delivery has been shown to be teratogenic in animals. In one study, hamsters that received 100% O₂ delivered at 2 atm for 3 h or 3 atm for 2 h gave birth to offspring with a number of congenital anomalies, including spina bifida, exencephaly, and limb defects. In another experiment, hyperbaric O₂ administered to rabbits late in pregnancy resulted in retrolental fibroplasia, retinal detachment, microphthalmia, and stillbirth.

Optimal maternal O₂ concentration

To date, there is insufficient evidence available to suggest what the optimal O₂ saturation or PaO₂ values are in preterm infants (who receive supplemental O₂) to prevent O₂ toxicity while providing adequate O₂ delivery to tissues.

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