This month's column will shed light on fetal monitoring theory that is unknown to most practicing clinicians, but recently has become popular in the legal arena.
It is likely not surprising that the assumptions underlying this theory lack supporting evidence in the literature. Specifically, the notion that uterine contractions can produce focal, "silent" hypoxic-ischemic brain injury has never been confirmed in any published scientific study. Descriptive studies have reported that fetal head pressures during labor can be more than twice as high as intra-amniotic pressures;3 however, no study has demonstrated that contraction-related pressure on the fetal head causes abnormal newborn brain function or clinically silent injury.
Other studies have demonstrated changes in fetal cerebral perfusion pressure, cerebral blood flow, and cerebral oxygen consumption during fetal head pressure.5,6 However, no published level I or level II evidence has linked such changes to any measure of clinical, subclinical, or histologic pathology. In fact, observations in fetal sheep suggest that the reflex Cushing response to head compression is protective against such injury.7,8
Maternal sFLT1 and EDN1 linked to late-onset preeclampsia
November 25th 2024A new study highlights the association of maternal soluble Fms-like tyrosine kinase 1 and endothelin 1 with preeclampsia severity, offering insights into the pathogenesis of early- and late-onset forms of the condition.
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