I’m 41 weeks pregnant. What’s the deal with CTG monitoring?

RANZCOG released its fifth edition of the guideline in November 2025. (By the way – I’m planning a workshop on how to get the best from the guideline. Let me know what you would like me to cover.)

The thing that I keep getting messaged about most is the inclusion of prolonged pregnancy (defined in the guideline as being more than 41 weeks pregnant) as a “risk factor for intrapartum fetal compromise” on page seven. Prolonged pregnancy is listed in the table here as having “moderate certainty evidence”. (Note that this blog post is all about CTG use in labour – not about the practice of recommending CTG monitoring during pregnancy to women once they pass 41 weeks. I don’t have a post specifically about prolonged pregnancy and antenatal CTG use –but this one will still give you the answer you are looking for…)

Is this a new recommendation?

The first Intrapartum Fetal Surveillance guideline was produced by RANZCOG in 2002. Prolonged pregnancy was on the list – but it was defined as being more than 42 weeks pregnant. This was also the case for the second edition in 2006. In the third edition, RANZCOG added a section to their list of risk factors saying that when one of these is present CTG use is not indicated, but when there is more than one risk factor, then it is. Being 41 weeks pregnant was included here, with 42 weeks still appearing on the main list. This persisted into the fourth edition in 2019.

So it’s not really a new inclusion, it’s simply that the “you need to have more than one thing going on” section has been removed in the new fifth edition.

Let’s dig in and see how they supported this recommendation with evidence.

What are the right questions to ask?

Before I do that, it is important to decide what we are looking for first. I’ve set this out before with similar posts, like this one about CTG use for women with bigger bodies. The goal of fetal heart rate monitoring (of any type) during labour is to prevent death or injury during labour from low oxygen levels (hypoxia). So, you would want to look for evidence that women who are more than 41 weeks pregnant are more or less likely to experience one of the following:

Long term brain damage due to low oxygen levels in labour
Stillbirth during labour due to low oxygen levels
Neonatal death due to low oxygen levels in labour
Neonatal seizures or other signs of brain injury due to low oxygen levels in labour

Fetal heart rate monitoring in labour can’t change outcomes that happen before labour. And it isn’t intended to change outcomes that are not due to low oxygen levels (like trauma, or genetic disorders). I’m personally not so interested in outcomes like cord pH levels, Apgar scores, or nursery admission. The first two are only weakly linked with poor long term outcomes. Admission to the nursery is heavily determined by what is happening on the day, hospital policy, and that particular neonatologist’s decision-making – and not so much the condition of the baby. Nonetheless, these three are often included in analyses, as is the case here.

So now let’s look at the research they found…

What evidence did RANZCOG use when they made this recommendation?

RANZCOG have taken a new approach to providing evidence for their recommendations in this edition (and I think that’s a good thing). There’s a summary of the evidence for the list of risk factors that runs from page 24 through to page 30. They also provide more detail in Appendix F (p. 99 – 114). The information about prolonged pregnancy spans pages 102 to 103. They used five studies as their evidence base. I have looked at the original papers and cross checked that the summary given in the guideline accurately reflects the original. Here’s a summary of the five papers:

Author, year	Country	No of births	Study design	Outcome(s)	Grade of evidence
Badawi, 1998	Australia	564	Case-control	Compared to 39 weeks Neonatal encephalopathy (moderate to severe) – 41 weeks aOR 3.34 (2.09 – 5.35) – 42 weeks aOR 13.2 (5.03 – 34.38)	Low
Hilder, 1998	UK	171,527	Retrospective cohort	Compared to 40 weeks Stillbirth rate per total births – 41 weeks RR 1.2 (0.8 – 1.7) – 42 weeks RR 1.3 (0.8 – 1.7)	Low
Liljestrom, 2018	Sweden	692,428	Retrospective cohort	Compared to 37-40 weeks Hypoxic ischaemic encephalopathy (moderate to severe) – 41 weeks aOR 1.68 (1.26 – 2.23) – 42+ weeks OR 2.01 (1.38 – 2.93)	Low
Rydahl, 2019	not given	Varies with outcome	Systematic review	IOL at 41 weeks vs IOL at 42 weeks Apgar score < 7 at 5 mins – RR 0.9 (0.52 – 1.56) pH < 7.10 – RR 1.9 (1.48 – 2.43) Nursery admission – RR 1.08 (0.68 – 1.71) Perinatal death – RR 0.22 (0.04 – 1.32)	Low
Alkmark*, 2020	not given	4,561	Systematic review	IOL at 41 weeks vs IOL at 42 weeks Perinatal death – OR 0.21 (0.06 – 0.78) Apgar < 7 at 5 mins – OR 0.9 (0.52 – 1.56) Nursery admission for > 4 days – OR 0.52 (0.32 – 0.85)	Low to moderate

*note there’s a typo in the RANZCOG guideline – they give the first author as Alkman.

I have put the outcomes with a significant difference in italics to make them easier to see at a glance.

The guideline summarises this as (p. 26)

Increased odds of stillbirth (conflicting studies), neonatal encephalopathy, and metabolic acidosis. Induction of labour at 41 weeks associated with reduced odds of perinatal death compared to continued pregnancy to 42 weeks.

Looking at the evidence they use, we see a different picture. The chance of acidosis was actually lower when induction was delayed to 42 weeks – not higher as the guideline says. There were no statistically significant reductions in death rates in the Hilder and Rydahl studies – the 95% confidence intervals cross one. The rate was reduced in the Alkmark study.

It is disappointing to once again see a lack of attention to detail in the “evidence” in a RANZCOG guideline.

What does all that mean?

The RANZCOG guideline writing team found no research that specifically looked specifically at the risk of a poor outcome happening DURING labour, and that also related only to outcomes due to low oxygen levels. Instead, the studies looked at outcomes that include these possibilities, along with others. For example – nursery admissions can be for monitoring blood glucose levels, or jaundice, not only for caring for a baby injured by low oxygen levels. Encephalopathy can be due to a metabolic problem, not low oxygen levels and it might have happened before labour started.

That’s not all that surprising and reflects my experience of attempting to do these types of analysis myself. There just isn’t the right sort of research, so you have to end up using something that gets you vaguely close to the information you want instead. It’s like going to the shops to buy Sugar-free Vanilla Coke but coming home with homebrand regular cola instead…

Two of the sources of information were answering an entirely different question to the one we are focussed on. They looked at whether there were differences in outcomes when labour was induced at 41 weeks or at 42 weeks – not whether women who labour after 41 weeks (either spontaneously or after induction) are more likely to have a baby with poor outcome than women who labour before 41 weeks (either spontaneously or after induction). I would personally exclude these. That leaves us with three.

All three provide low grade evidence (that’s according to RANZCOG – I haven’t repeated the grading myself). They show –

A statistically significant rise in brain injury from any cause, at any time, in babies born after 41 and 42 weeks compared to babies born at 39 weeks (Badawi 1998). Because this was a case control study, the incidence of brain injury at each gestational age can’t be calculated. Overall it was 38 per 10,000 births.
No significant difference in the stillbirth rate (including death before labour started and for any reason) for babies born after 41 and 42 weeks, compared to babies born at 40 weeks (Hilder 1998).
A statistically significant rise in brain injury due to low oxygen levels (happening at any time, not just during labour) for babies born at 41 or 42 weeks compared to babies born between 37 and 40 weeks (Liljestrom 2018). The incidence of brain injury at 37 – 40 weeks was 5.2 per 10,000 births, at 41 weeks 9.2 per 10,000 births, and at 42 weeks it was 13.3 per 10,000 births.

So yes – there is low grade evidence that brain injury might happen more often in babies born after 41 or 42 weeks gestation. The chance of that happening remains low. That chance also includes injuries that happen before labour starts and that are therefore not able to be changed (at least in theory) by using fetal heart rate monitoring.

I simply can’t see how the evidence the guideline writers provide translates to a “strong” recommendation. It isn’t “moderate certainty evidence” – even by their assessment of this. I think gestational age or more than 41 weeks (and the same applies to more than 42 weeks) belongs in the “conditional – low to very low certainty evidence” part of the table.

If you are 41 weeks pregnant – what do you need to know?

The decision about whether to use CTG monitoring or intermittent auscultation, or neither during your labour is YOUR decision to make. It isn’t up to the writers of this, or any other guideline. It isn’t up to your maternity professional or the hospital you give birth in either.

The first “good practice statement” in the guideline sets out the responsibility of maternity professionals to support YOUR decision making (p. 6). And on page 9, “evidence-based recommendation 5” says “it is suggested that continuous CTG should be offered in labour when risk factors for fetal compromise have been identified”. Your maternity professional’s responsibility is to let you know that CTG monitoring is a choice available to you.

And that is it.

It is – and always was – up to you to decide how you want your baby to be monitored in labour.

Are you a maternity professional working in Australia or New Zealand?

Let me show you how to use the RANZCOG guideline and support women to make decisions about fetal monitoring.

I’m working on a plan for a workshop to help you get the best out of the RANZCOG fetal monitoring guideline. Tell me what you need me to cover so I can solve your challenges when working with the guideline. Click the link below and pop some details in the form. I’ll be in touch with details about the workshop once I have the details sorted out…

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References

Alkmark, M., Keulen, J. K. J., Kortekaas, J. C., Bergh, C., van Dillen, J., Duijnhoven, R. G., Hagberg, H., Mol, B. W., Molin, M., van der Post, J. A. M., Saltvedt, S., Wikstrom, A. K., Wennerholm, U. B., & de Miranda, E. (2020). Induction of labour at 41 weeks or expectant management until 42 weeks: A systematic review and an individual participant data meta-analysis of randomised trials. PLoS Med, 17(12), e1003436. https://doi.org/10.1371/journal.pmed.1003436

Badawi, N., Kurinczuk, J. J., Keogh, J. M., Alessandri, L. M., O’Sullivan, F., Burton, P. R., Pemberton, P. J., & Stanley, F. J. (1998). Antepartum risk factors for newborn encephalopathy: The Western Australian case-control study. British Medical Journal, 317(7172), 1549-1553. https://doi.org/10.1136/bmj.317.7172.1549

Hilder, L., Costeloe, K., & Thilaganathan, B. (1998, Feb). Prolonged pregnancy: evaluating gestation-specific risks of fetal and infant mortality. BJOG: An International Journal of Obstetrics and Gynaecology, 105(2), 169-173. https://doi.org/ https://doi.org/10.1111/j.1471-0528.1998.tb10047.x

Liljestrom, L., Wikstrom, A. K., Agren, J., & Jonsson, M. (2018, May). Antepartum risk factors for moderate to severe neonatal hypoxic ischemic encephalopathy: a Swedish national cohort study. Acta Obstetrica et Gynecologica Scandinavica, 97(5), 615-623. https://doi.org/10.1111/aogs.13316

Royal Australian and New Zealand College of Obstetricians and Gynaecologists. (2025). Intrapartum fetal surveillance. Clinical guideline (5th ed.). https://ranzcog.edu.au/wp-content/uploads/Intrapartum-Fetal-Surveillance.pdf

Rydahl, E., Eriksen, L., & Juhl, M. (2019). Effects of induction of labor prior to post-term in low-risk pregnancies: a systematic review. JBI Database Systematic Reviews & Implementation Reports, 17(2), 170-208. https://doi.org/10.11124/JBISRIR-2017-003587