Sentences with phrase «fetal hypoxia»

Instead, the report was used constantly in birth injury litigation by paid experts testifying on behalf of obstetricians and hospitals sued for ignoring the signs and symptoms of fetal distress and failing to treat fetal hypoxia.

In and of itself, fetal hypoxia is not a birth injury, but a number of factors can contribute to an increased risk.

The parents of children that are born with serious injuries as a result of fetal hypoxia may be able to file a lawsuit with a birth injury attorney against the medical facility and staff responsible.

Fetal hypoxia occurs when a a fetus is deprived of sufficient oxygen during the birthing process.

The implications of these data are that maternal treatment with antioxidants may provide possible therapy against the programming effects on vascular dysfunction in pregnancy complicated by fetal hypoxia, such as during placental insufficiency, preeclampsia, gestational diabetes or high altitude pregnancy.

A new study suggests that one risk factor may begin even before birth, showing how low oxygen in the womb — or fetal hypoxia — can impair the heart later in life.

Giussani says that the findings show that fetal hypoxia programs both the heart and the circulation in adult life through oxidative stress in the womb.

When fetal hypoxia is prolonged, the embryo's heart and vessels change: The walls of the heart and aorta grow thicker, and blood vessels may become less responsive to signals to relax, which makes it harder for blood to flow.

Fetal hypoxia can be caused by a variety of factors.

A leading researcher in developmental programming, Challis says this study opens the door to thinking about combating fetal hypoxia in humans with antioxidant therapy.

Fetal hypoxia is when the fetus is deprived of oxygen inside the womb and could lead to many complication for mom and baby.

A compressed umbilical cord can also lead to short episodes of fetal hypoxia, which involves the baby being deprived from oxygen in the womb and can lead to other health complications including death.

Not exact matches

Nor do they know that fetal readiness for labor (including protection against hypoxia and readiness for newborn transitions after birth) is coordinated with preparation of the mother's body for labor, breastfeeding and mother - infant attachment.

In animal models, exposure to cigarette smoke or nicotine during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDS.

They argue that fetal monitoring trials have focused on uncommon outcomes, such as cerebral palsy, which is rarely linked to hypoxia during labour, and say «we should be focusing on other forms of evidence relating to the more common outcome with serious long term implications — namely, neonatal encephalopathy.»

They acknowledge that electronic fetal monitoring increases the rate of instrumental delivery (such as use of forceps) and caesarean section, but argue that increased intervention «may not be entirely undesirable, given that appropriately timed intervention is likely to avoid neonatal hypoxia, seizures, and perinatal death.»

Electronic fetal monitoring is often used during labour to detect unborn babies at risk of brain damage (neonatal encephalopathy) from a lack of oxygen (hypoxia).

He points out that babies still die or are damaged because of intrapartum hypoxia and that focusing entirely on the fetal heart rate without taking account of other relevant risk factors «may create a lack of situational awareness and lead to adverse outcomes.»

For example, using new technologies to identify more reliable fetal biomarkers of hypoxia.

He argues that «most of the fetuses identified as being at risk of hypoxia are not» and highlights a review of trial data for nearly 37,000 women that found no difference in perinatal mortality between labours with electronic fetal monitoring versus intermittent auscultation.

Finally, alcohol and cigarette smoking were associated with a decreased risk of intrauterine passing of meconium, a sign of acute fetal stress and / or hypoxia; methamphetamine, with an increased risk.

In our study, developmental hypoxia throughout most of gestation did not affect maternal food intake or fetal growth, but it increased placental weight.

The effects of chronic prenatal hypoxia on the fetal and adult offspring cardiovascular system are prevented by maternal treatment with vitamin C during pregnancy.

Therefore, the primary novelty of the discoveries reported here is that programming by prenatal chronic hypoxia of cardiac and vascular dysfunction in adulthood follows the induction of oxidative stress in the fetal heart and vasculature, and that cardiac and endothelial dysfunction in adulthood can both be prevented by maternal treatment with antioxidants during pregnancy.

Here, we tested the hypothesis that oxidative stress in the fetal heart and vasculature underlies the molecular basis through which prenatal hypoxia contributes to the developmental programming of cardiac and endothelial dysfunction.

New models of perinatal hypoxia were developed in rats with emphasis on the potential protective effect of pre-conditioning by a previous fetal hypoxic period.

Furthermore, studies are performed on fetal cardiovascular adaptation to hypoxia and its short and long term consequences.

Mouse fetal development is perturbed by culture in low oxygen concentration that increases expression of oxygen - sensitive genes via hypoxia inducible factors: A non-epigenetic embryonic programming phenomenon?

VBAC complications from uterine rupture can cause an array of problems affecting your baby, including fetal distress, cerebral palsy, hypoxia and brain injury, paralysis, seizure disorders, developmental delays, and in the worst cases, stillbirth.

According to the plaintiff, during the latter part of the pregnancy and on the day the baby was born, the defendants failed to respond properly to obvious signs of fetal distress which caused serious hypoxia; this resulted in the infant suffering permanent brain damage.

Careful attention must be paid to the fetal heart monitor to ensure that any hypoxia event is noticed and acted upon.