Fetal monitoring in labour: summary and update of NICE guidance
BMJ 2022; 379 doi: https://doi.org/10.1136/bmj.o2854 (Published 16 December 2022) Cite this as: BMJ 2022;379:o2854
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Dear Editor
Whilst revision and updates to guidelines are welcome, I suspect something more than that is required for improving intrapartum outcomes.
To understand why improving intrapartum outcomes need urgent attention, consider this. The second largest contingency fund held by HM Treasury is for babies sustaining avoidable brain damage during delivery.
Staff looking after labouring women are invariably very good at recognising warning signs from fetal monitoring.The problem lies in a the human response to this. When an emergency call goes out for a cardiac arrest, an immediate response happens. This is not necessarily the case when fetal distress is identified. For example some may wait to see if the situation might improve with time. Others may feel it’s worth delaying any immediate action to allow the woman time to be fully dilated - and allowing the opportunity for the mother to have the opportunity of a normal delivery without intervention.
For that reason, I believe there is less need to tighten up on how to provide good intrapartum monitoring. And a lot of need to improvement in taking appropriate action when fetal monitoring points to compromised fetal wellbeing
Competing interests: No competing interests
Re: Fetal monitoring in labour: summary and update of NICE guidance - Gaps in knowledge, practice, and guidance.
Dear Editor
The updated NICE guidelines on intrapartum fetal heart rate (FHR) monitoring [1] make welcome shifts towards a more physiological approach to FHR interpretation and assessment of the risk of intrapartum fetal hypoxia. However, there was no recommendation for the practitioner to adhere to key principles underpinning physiological approach to intrapartum FHR monitoring including, but not limited to, the presence of normal or near-normal FHR pattern (including gestation-appropriate baseline FHR), and normal fetal behavioural state, prior to the emergence of FHR abnormalities. Normal fetal behaviour characterised by alternating sequences of increased versus reduced FHR variability every 15 – 40 minutes, so-called fetal cycling activity, [2,3] is the hallmark behaviour of the neurologically intact term and near-term fetus without significant acidosis or acidaemia at the time of observation. Failure to satisfy these criteria may expose the compromised fetus to labour with the risk of exacerbating a pre-existing insult or injury. Significant numbers of adverse perinatal outcomes reported in national audits and quality improvement programmes [4,5] are attributable to this scenario than to de novo hypoxia arising during labour.
The updated guidelines remain silent on the timing of, and the triggers for, operative delivery in labours complicated by pyrexia, chorioamnionitis, fetal host inflammatory response/ synergistic interaction with hypoxia, meconium, diabetes in pregnancy, varying combinations of these factors, or what constitutes best practice. Individually, or in combination, these noxious factors are overrepresented in adverse perinatal outcomes in national audits.[4,5] Whilst the normal fetus deploys robust cardiovascular and metabolic mechanisms to adapt to intrapartum hypoxia, these mechanisms may break down in fetuses exposed to intrauterine infection and activation of their inflammatory pathways.[6] Fetal inflammatory response sensitises the fetal brain to hypoxic damage and the affected fetus may incur damage by minimal levels of hypoxia. A large case–control study of intrapartum factors associated with neonatal encephalopathy showed that early Caesarean section (CS) was associated with a highly significant reduction in neonatal encephalopathy (OR 0.17, 95% CI 0.05–0.56) in labours complicated by chorioamnionitis, in contrast to two-fold increase in encephalopathy (OR 2.17, 95% CI 1.01–4.64) with in-labour CS, [7] suggesting that early CS may be protective for some babies, but no RCTs have studied this. In addition, the recent focus on ‘Sepsis 6’ has inadvertently shifting the minds of many clinicians that chorioamnionitis is primarily a fetal, not a maternal disease with devastating consequences. A further emerging area with significant implications for intrapartum FHR monitoring is fetal hyperinsulinaemia from diabetes,[8] which induces high metabolic rate, growth of the fetus and placenta, and maldevelopment of the vasculo-syncitial membranes (gas exchange units), by maintaining the large diffusion distance between the intervillous space and the villous capillaries as gestation advances, termed delayed villous maturation. Obstetricians have no reliable evidence-based tools for identifying the fetus at increased risk from these scenarios and rely on their clinical judgement. Exercising that judgement should include avoiding practices, which may amplify the risks of hypoxia such as prolonged labour, uterine hyperstimulation, repetitive or prolonged decelerations, reliance on fetal blood sampling (FBS), and traumatic delivery.
Further important strides in the updated guidelines include the revision of optimum labour contraction frequency from 4 – 5 in 10 minutes to 3 – 4, abolishing the distinction between significant and insignificant amniotic fluid meconium, use of FBS, and the focus on the success or failure of fetal compensation by asking the question, ‘how is the baby?'. However, the recommendation of Pinard’s stethoscope, portable scan, and pulse oximeter for distinguishing the FHR from maternal during the second stage, ahead of fetal scalp electrode (FSE), may be counterproductive. Few midwives train on/practice with Pinards, and scan machines take valuable time locate, wheel in, connect to the mains, & boot up. In the author’s opinion FSE should be first choice.
References
1. O’Heney J, McAllister S, Maresh M, Blott M. Fetal monitoring in labour: summary and update of NICE guidance BMJ 2022;379:o2854
2. Ugwumadu A. Understanding cardiotocographic patterns associated with intrapartum fetal hypoxia and neurologic injury Best Pract Res Clin Obstet Gynaecol 2013;27(4):509-536.
3. Ugwumadu A. Are we (mis)guided by current guidelines on intrapartum fetal heart rate monitoring? Case for a more physiological approach to interpretation.
BJOG. 2014;121(9):1063-1070.
4. The Royal College of Obstetricians and Gynaecologists, Each Baby Counts: 2019 progress report. London; RCOG; 2020 [www.rcog.org.uk/en/guidelines-research-services/audit-quality-improvemen...
5. Ockenden Report - Final March 30, 2022, Findings, Conclusions, and Essential Actions from the Independent Review of Maternity Services at The Shrewsbury and Telford Hospital NHS Trust. [https://www.ockendenmaternityreview.org.uk]
6. Eklind S, Mallard C, Arvidsson P, Hagberg H. Lipopolysaccharide induces both a primary and a secondary phase of sensitization in the developing rat brain. Pediatr Res 2005; 58:112–116.
7. Badawi N, Kurinczuk JJ, Keogh JM, et al. Intrapartum risk factors for newborn encephalopathy: the Western Australian case–control study. Br Med J 1998; 317:1554–1558.
8. Tarvonen M, Hovi P, Sainio S, Vuorela P, Andersson S, Teramo K. Intrapartal cardiotocographic patterns and hypoxia-related perinatal outcomes in pregnancies complicated by gestational diabetes mellitus. Acta Diabetol. 2021;58(11):1563-1573.
Competing interests: Pioneer, practitioner, and instructor, physiological approach to intrapartum fetal heart rate monitoring