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Clinical Trial Summary

Combined spinal-epidural (CSE) for labor analgesia has been used for many years and is practiced commonly at our institution, especially when the patient requests immediate pain relief. CSE is not only beneficial for its faster onset of analgesia, but also it is favorable in relation to the need for rescue analgesia, urinary retention, and rate of instrumental delivery compared to the traditional epidural. Despite its beneficial effects, there is a risk of about 15-30% of developing abnormal fetal heart rate following CSE. This is self-resolving with minimal or no intervention. Although the cause of fetal bradycardia is not fully elucidated, variations in uterine artery blood flow after epidural analgesia are thought to be due to the interaction of numerous events related to blockade of sympathetic innervations, fluid administration, maternal hypotension, uterine vascular effects of sympathetic block, fluctuations in circulating catecholamines, and possibly the effect of opioids. Similar mechanism is thought to be a cause of fetal bradycardia after the CSE with its faster onset and superior block. Maternal or fetal circulation during labor can be assessed using continuous-wave Doppler ultrasound to monitor maternal uterine artery (UtA) and fetal umbilical artery (UmA) velocity waveforms to detect changes in blood flow. The velocimetry indices mentioned above have been often used to assess the changes in the blood flow before and after the induction of epidural analgesia during labor in several studies. Although there are some studies regarding the effect of labor epidural analgesia using velocimetry indices, but there is currently no published study evaluating velocimetry indices of uterine and umbilical arteries before and after the induction of CSE. Thus, the aim of this study is to investigate the impact of CSE to maternal and fetal blood flow to evaluate the relationships. The investigators hypothesize that both uterine artery and umbilical artery blood flow are reduced after the induction of CSE, which may be responsible for the occurrence of fetal bradycardia.


Clinical Trial Description

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Study Design


Related Conditions & MeSH terms


NCT number NCT05512065
Study type Interventional
Source Samuel Lunenfeld Research Institute, Mount Sinai Hospital
Contact
Status Completed
Phase N/A
Start date September 14, 2022
Completion date March 30, 2024

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