Transplacental Aspirin Therapy for Early Onset Fetal Growth Restriction

Fetal Growth Restriction, Fetal Growth Retardation, Intrauterine Growth Restriction, Intrauterine Growth Retardation

Maternal Aspirin Therapy

The purpose of this investigation is to evaluate the ability of maternal aspirin (ASA) therapy to prevent preterm birth for fetal indications prior to 32 weeks gestation in women with early onset Fetal Growth Restriction (FGR). Aspirin is a commonly used medication that blocks blood platelets from clumping. Aspirin crosses the placenta in a dose dependent mode. There is preliminary evidence in smaller studies that aspirin can block fetal platelet clumping and, therefore, slow down the progression of placental disease under specific circumstances. The optimal time for aspirin to work is when the fetus' placental dysfunction is still mild. The goal of this research study is to show if fetuses that receive aspirin through maternal intake at a dose shown to affect fetal platelet aggregation will be less likely to deliver before 32 weeks for fetal deterioration. The outcomes of patients that receive aspirin will be compared to women that receive standard FGR management but do not take any aspirin. The decision if a study participant receives aspirin or not will be randomly picked. Such a research study is called a randomized controlled trial.

Early onset FGR requiring preterm delivery by 32 weeks gestation complicates 1-5% of pregnancies and is an important health problem. Over 60% of children have long-term health consequences after being delivered for early onset FGR. There is no prenatal treatment for fetal growth restriction. The current management of FGR consists of fetal surveillance to detect a decline in the baby's health and deliver when this can be safely done. In a large number of early onset FGR, premature delivery is required to prevent the fetus from becoming more compromised or even dying in the womb. Placental dysfunction leading to early onset FGR is characterized by changes to the blood vessels of the placenta, leading to a decline in the amount of blood flow to the placenta. The arteries that run in the umbilical cord of the fetus (umbilical arteries) are important for nutrient exchange between the fetal and placental circulation. Many fetuses with early onset FGR have elevated resistance in the blood vessels entering the placenta. This results in decreased blood flow in the umbilical artery (UA). The blood flow in the umbilical artery is evaluated by a specialized ultrasound technique called Doppler ultrasound. Doppler ultrasound of the umbilical arteries examines the blood flow to see if there is evidence of abnormal blood flow into the placenta. When the amount of blood flow at the end of every pulse decreases, it is classified as elevated UA blood flow resistance. When the blood flow briefly pauses at the end of each pulse, this is called absent end-diastolic velocity (AEDV) or UA AEDV. When the blood flow reverses at the end of each pulse, this is called reversed end-diastolic velocity (UA REDV). In fetuses with elevated UA blood flow, the placenta can usually supply enough nutrients and oxygen for at least 9 weeks. After that time, delivery is typically required. The worsening of blood flow to UA AEDV, or even UA REDV, increases the risk for fetal deterioration and preterm birth within the next 2-6 weeks. Approximately, 80% of early onset FGR fetuses progress to UA AEDV, or even UA REDV, and then require delivery by 32 weeks. There is no treatment that can stop this progression which is of critical importance in determining how much time is left for the fetus before delivery will be necessary.

No related papers found yet.