Abstract
BackgroundIncreased uterine activity (UA) may not allow adequate recovery time for foetal oxygenation.MethodsThe aim of the study was to determine if increased UA during labour is associated with an increased risk of either short- or long-term neurological injury in term neonates, or with neonatal proxy measures of intrapartum hypoxia-ischemia. MEDLINE, CINAHL, and ClinicalTrials.gov were searched using the following terms: uterine activity, excessive uterine activity, XSUA, uterine hyperstimulation, and tachysystole. Any study that analysed the relationship between UA during term labour and neurological outcomes/selected proxy neurological outcomes was eligible for inclusion. Outcomes from individual studies were reported in tables and presented descriptively with odds ratios (OR) and 95% confidence intervals (CI) for dichotomous outcomes and means with standard deviations for continuous outcomes. Where group numbers were provided, ORs and their CIs were calculated according to Altman.Main resultsTwelve studies met the inclusion criteria. Seven studies featured umbilical artery pH as an individual outcome. Umbilical artery base excess and Apgar scores were both reported as individual outcomes in four studies. No study examined long term neurodevelopmental outcomes and only one study reported on encephalopathy as an outcome. The evidence for a relationship between UA and adverse infant outcomes was inconsistent. The reported estimated effect size varied from non-existent to clinically significant.ConclusionsThere is some evidence that increased UA may be a non-specific predictor of depressed neurological function in the newborn, but it is inconsistent and insufficient to support the conclusion that an association generally exists.
Highlights
Increased uterine activity (UA) may not allow adequate recovery time for foetal oxygenation
There is some evidence that increased UA may be a non-specific predictor of depressed neurological function in the newborn, but it is inconsistent and insufficient to support the conclusion that an association generally exists
The rationale for the proposed link between excessive uterine activity (UA) and fetal hypoxia is based on physiological studies of the haemodynamic changes that occur in the utero-placental and fetal circulations during a contraction
Summary
Increased uterine activity (UA) may not allow adequate recovery time for foetal oxygenation. The rationale for the proposed link between excessive uterine activity (UA) and fetal hypoxia is based on physiological studies of the haemodynamic changes that occur in the utero-placental and fetal circulations during a contraction. Tocolysis for fetal distress may improve umbilical artery (UmA) base excess (BE) values and reduce neonatal intensive care unit admission at the expense of increasing caesarean delivery [5]. Current guidelines are based on the opinion that when there is an abnormal FHR pattern in association with frequent uterine contractions, increased UA may cause fetal hypoxia [7]. The UK National Institute for Health and Care Excellence guidelines on labour management state that where the FHR pattern is suspicious or pathological any uterine hyperstimulation should be corrected [9].
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