TY - GEN
T1 - Timing the delivery of preterm fetus
T2 - 2009 AAAI FAll Symposium
AU - Yu, Tina
AU - Chiu, Tsung Hong
AU - Van Den Wijngaard, Jeroen
AU - Hsieh, T'sang T.ang
AU - Weserhof, Berend E.
AU - Tseng, Enson
PY - 2009
Y1 - 2009
N2 - The propagation of blood flow along the fetoplacental arterial system has been hypothesized to have a compensatory response to placental anomalies that may result in fetal stress. When the placenta generates increased resistance, the umbilical artery blood flow would decrease and in the worst scenario become absent, which will lead to fetal asphyxia and hypoxia. To compensate for the decreased oxygen supply from maternal placenta, the fetal middle cerebral arteries would become dilated leading to an increased diastolic flow, hence more oxygen. This compensatory phase, however, only lasts for a certain period of time, after which the hypoxia may lead to fetal demise or long term irreversible organ damages. In high-risk pregnancies, Doppler ultrasound technology is commonly used to monitor the fetoplacental arterial blood flow to assess fetal well being. If the anomalies occur prior to the end of the 40-week of gestation, surgical or aggressive medical intervention might be necessary to save the fetal life. Timing this intervention, however, is complex due to the fine balancing act to minimize potential risks from prematurity and organ damage vs. rescuing a fetal life through cesarean section or aggressive medical treatment or natural delivery at the earliest possible gestational age. A reasonable goal is to allow the pregnancy to continue to the point just before fetal damage occurs. To achieve that goal, various testing criteria, e.g. venous Doppler and fetal heart rate, have been used to identify de-compensation. In this work, we conducted computer simulation of the fetoplacental arterial blood flow of a Systemic Lupus Erythematosus (SLE) pregnancy based on Doppler blood flow readings taken during the 10-day period prior to the delivery. The simulation suggests that timing the delivery based on either Doppler waveform readings or fetal heart rates give similar pregnancy outcome.
AB - The propagation of blood flow along the fetoplacental arterial system has been hypothesized to have a compensatory response to placental anomalies that may result in fetal stress. When the placenta generates increased resistance, the umbilical artery blood flow would decrease and in the worst scenario become absent, which will lead to fetal asphyxia and hypoxia. To compensate for the decreased oxygen supply from maternal placenta, the fetal middle cerebral arteries would become dilated leading to an increased diastolic flow, hence more oxygen. This compensatory phase, however, only lasts for a certain period of time, after which the hypoxia may lead to fetal demise or long term irreversible organ damages. In high-risk pregnancies, Doppler ultrasound technology is commonly used to monitor the fetoplacental arterial blood flow to assess fetal well being. If the anomalies occur prior to the end of the 40-week of gestation, surgical or aggressive medical intervention might be necessary to save the fetal life. Timing this intervention, however, is complex due to the fine balancing act to minimize potential risks from prematurity and organ damage vs. rescuing a fetal life through cesarean section or aggressive medical treatment or natural delivery at the earliest possible gestational age. A reasonable goal is to allow the pregnancy to continue to the point just before fetal damage occurs. To achieve that goal, various testing criteria, e.g. venous Doppler and fetal heart rate, have been used to identify de-compensation. In this work, we conducted computer simulation of the fetoplacental arterial blood flow of a Systemic Lupus Erythematosus (SLE) pregnancy based on Doppler blood flow readings taken during the 10-day period prior to the delivery. The simulation suggests that timing the delivery based on either Doppler waveform readings or fetal heart rates give similar pregnancy outcome.
UR - http://www.scopus.com/inward/record.url?scp=77954234089&partnerID=8YFLogxK
M3 - 会议稿件
AN - SCOPUS:77954234089
SN - 9781577354376
T3 - AAAI Fall Symposium - Technical Report
SP - 131
EP - 139
BT - Complex Adaptive Systems and the Threshold Effect
Y2 - 5 November 2009 through 7 November 2009
ER -