Intraumbilical Amino Acids and Glucose Supplementation Via Subcutaneously Implanted Port System by Severe IUGR Human Fetuses
Description:
Placental insufficiency is the main source of the development of intrauterine growth
restriction (IUGR) caused by one of a variety of factors including chronic placental
infections, many maternal diseases, abnormal genome and intravascular trophoblast invasion
impairment. Placental insufficiency is responsible for fetal loss in about 40% of all
stillbirths and long term neurological deficits. The reduction of blood flow resistance of
cerebral arteries in severe IUGR conditions with reduced pulsatility index (PI) in the medial
cerebral artery predicts the 11 fold increased risk of intraventricular hemorrhage,
periventricular leukomalacia, hypoxic ischemic encephalopathy, necrotizing enterocolitis,
bronchopulmonary dysplasia, sepsis, and death. The mean interval from diagnosis of brain
sparing of severe IUGR fetuses to delivery has been recently identified by only seven days
(ranging 2-15 days).
The amino acids (AA) concentration of fetal plasma is many times higher than in mother
because of active transplacental transport of AA and additional AA synthesis in the placenta.
The critical placental player in the active AA transport from the mother to the fetus is the
trophoblast, which is irreversibly changed in severe IUGR fetuses caused by placental
insufficiency. Thus, a logical partial solution of IUGR could be the direct supply of AAs and
glucose to the fetus, in order to improve the fetal growth, normalize the IUGR changed fetal
programming and to prolong the pregnancy. Additional oxygen supply of fetal tissues could
also be important in improving the uptake of injected nutritional supplements and may avoid
the development of lactate acidosis in IUGR fetuses.
The aim of this prospective pilot study was to further test the efficacy of the
administration of AAs and glucose supplementation with hyperbaric oxygenation (HBO), via a
subcutaneously implanted intraumbilical perinatal port system, as a treatment option for
severe IUGR human fetuses with brain sparing.
Study design – IUGR was defined in this study as an estimated fetal weight of < 5%, combined
with increased resistance in both uterine arteries with pulsatility index (PI) > 95%. Fetuses
with morphological and/or chromosomal abnormalities were not included in the final analysis.
Condition:
Intrauterine Growth Restriction
Treatment:
fetal nutrition port system
Start Date:
January 2010
Sponsor:
Martin-Luther-Universität Halle-Wittenberg
For More Information:
https://clinicaltrials.gov/show/NCT02596594