Originally written in 2022, this post has been revised and republished.
A series of assumptions have been used to justify continuous CTG monitoring in labour. One assumption is that there are specific fetal heart rate patterns that can reliably detect when a fetus moves from:
- “my oxygen levels are a bit low but I’m fine”
- to “my oxygen levels are low and my brain is starting to be damaged”
- and well before reaching the point of “too late, the damage is now irreversible”.
If we can precisely pick the difference between these three situations, maternity professionals can step in a do things that can prevent brain injury and also avoid needlessly intervening in the progress of labour for babies who were fine all along.
You might be forgiven for thinking that researchers long ago did great research that linked certain heart rate patterns to clinical outcomes. And that these patterns are the ones that are described in fetal monitoring guidelines. The problem is that no one has actually done much of that sort of research, and a lot of it was of not great quality. Hence, our guidelines are based on people’s best guesses, and this in large part explains why there is variation among guidelines about what features of a heart rate trace indicate a problem, which ones don’t, and when to recommend intervention.
Fortunately there are now people working on finding out what happens to fetal heart rate patterns when oxygen levels run low. Researchers are looking at whether you can build a predictive model identify which fetuses will benefit from expedited birth and those who won’t. Let’s look at three papers published in 2022 and see what they can teach us. One used fetal sheep for the research, the other two come from one big human study.
Heart rate variability and the fetal stress index
Ghesquire and colleagues (2022) intermittently blocked the umbilical cord of fetal sheep to see what would happen to variability in the fetal heart rate. Heart rate variability (the amount of wiggle up and down around the baseline) is said to indicate signs of fetal hypoxia when it is either reduced or increased. This research was designed to test whether this is the case or not.
The researchers also used a new measure called the “fetal stress index”. The fetal stress index isn’t a heart rate pattern you can see visually on the CTG – it requires computerised interpretation. After repeated blockages of the umbilical cord, nine fetal sheep developed severe hypoxia and seven were subsequently found on post-mortem assessment to have brain injury from this low oxygen level.
A few of their findings stood out for me. First, baseline heart rate and short-term variability after each period of cord blockage did not change, even when the cord was blocked more frequently with less breaks in between. This is at odds with what we currently teach about fetal heart rate patterns. The idea that progressive hypoxia leads to a rising baseline and a reduction in heart rate variability didn’t pan out here.
The researchers did find the fetal stress index increased over time. However, the results of the fetal stress index didn’t predict which sheep ended up with brain injury and which did not.
The other finding of note related to where the brain damage occurred. In fetuses who had signs of damage to the brain stem, there were changes in fetal heart rate variability. This isn’t surprising as the brain stem is the part of the brain that controls heart rate – injure it and the ability to regulate heart rate is affected. But changes in variability didn’t occur with damage to other parts of the brain.
It is difficult to know how to apply what the researchers learned to clinical practice. They were not aiming to find patterns that identified the transition from “I’m ok” to “get me out of here!”. Their findings relate to fetuses that mostly ended up in the “too late” group as they developed significant brain damage. Knowing what that looks like won’t help our efforts to prevent damage from happening.
What this paper does highlight however, is just how little we know about what different heart rate patterns can tell us.
Heart rate patterns in babies with brain injury
The next paper looked at the problem from the other direction. Rather than causing damage, it looks backwards in time, starting with babies who had brain damage. A research team in Dublin (Reynolds, et al., 2022a) identified a group of 52 babies with neonatal encephalopathy (a form of brain damage seen soon after birth) thought to be due to events happening during labour. They selected another group of 112 babies who were born without any signs of brain damage. They reassessed the CTG traces from all these babies in detail to see if it was possible to develop a picture of the types of heart rate patterns that could accurately separate babies who were born with damage from those who were not. They used the NICE guideline definitions for both individual features of the CTG and to assign categories.
They found some individual heart rate features that were seen more often in the CTGs of babies with brain injury. These were:
- baseline heart rate over 160 bpm,
- reduced variability,
- absence of accelerations, and
- late decelerations.
The longer an abnormal pattern persisted, the stronger the association with a poor outcome.
Adding the different features together to group them into categories to see whether they worked to predict outcome was also looked at. The categories of “suspicious” and “pathological” were seen more often when the baby had encephalopathy. So far this sound like promising information that monitoring the heart rate can provide information to help decide when to take action and when not to.
Zooming back out a bit – things are not that straight forward. Half of the babies who were born completely healthy had at least one period of “suspicious” CTG and 25% had at least one period of “pathological” CTG. Being born healthy happens MUCH more often than brain injury – so when abnormal heart rate patterns are present, the most likely outcome is still a healthy baby.
When the researchers tried to build a model based on individual heart rate features, with or without including the overall category, they were unable to come up with combinations that worked well. In their best fit model, when keeping the false positive rate to only 5% (that is, one in twenty CTGs were considered abnormal), only one third of babies of who were born with encephalopathy would have been detected.
Contraction patterns and brain injury
The same research team also looked at whether contraction patterns provide useful predictive information (Reynolds, et al., 2022b). The same babies were studied and the contraction patterns were determined from the same CTGs as their heart rate study.
More frequent contractions were seen with babies with brain damage than those without. The difference between 7.7 every 15 minutes rather than 7.0 every 15 minutes would be impossible to detect in a real world setting though. The gap between contractions was not different between healthy babies and those with encephalopathy. When the researchers combined contraction patterns with the best fetal heart rate model from the previous study, the predictive capability of the model did not improve further.
Now what?
It is no wonder then that CTG monitoring in labour has been and continues to be plagued by two problems. First, babies continue to die in labour and be born with brain injury despite the use of CTG monitoring. And second, many caesarean sections are done on the basis of abnormal CTG traces but didn’t need to be done as the baby was going to be fine if they had been left to continue labour.
Solving this puzzle requires a community of researchers and clinicians to develop a deep understanding of fetal physiology to be able to identify fetal heart rate patterns that do reliably provide the ability to discriminate the time when the fetus moves from “I’m okay” to “get me out of here!”. I suspect that if this research ever does get done, it will show that there is no way to tell the difference based on information from the CTG. If that is the case, then no matter how hard anyone tries to develop the best guideline, teach interpretation to clinicians, and ensure they act appropriately when that pattern occurs, we will never make things better.
The other option is to accept that CTG experiment of the past sixty years was fundamentally flawed all along and abandon it. Then we can begin the earnest work of finding other ways to reduce poor perinatal outcome while not harming birthing women. How much longer will it take before we do this?
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References
Ghesquiere, L., Perbet, R., Lacan, L., Hamoud, Y., Stichelbout, M., Sharma, D., Nguyen, S., Storme, L., Houfflin-Debarge, V., De Jonckheere, J., & Garabedian, C. (2022). Associations between fetal heart rate variability and umbilical cord occlusions-induced neural injury: An experimental study in a fetal sheep model. Acta Obstetricia et Gynecologica Scandinavica, 101(7), 758-770. https://doi.org/10.1111/aogs.14352
Reynolds, A. J., Murray, M. L., Geary, M. P., Ater, S. B., & Hayes, B. C. (2022a). Fetal heart rate patterns in labor and the risk of neonatal encephalopathy: A case control study. European Journal of Obstetrics & Gynecology & Reproductive Biology, 273, 69-74. https://doi.org/10.1016/j.ejogrb.2022.04.021
Reynolds, A. J., Murray, M. L., Geary, M. P., Ater, S. B., & Hayes, B. C. (2022b). Uterine activity in labour and the risk of neonatal encephalopathy: a case control study. European Journal of Obstetrics & Gynecology & Reproductive Biology, 274, 73-79. https://doi.org/10.1016/j.ejogrb.2022.05.011
Categories: CTG, EFM, New research, Perinatal brain injury
Tags: caesarean section, fetal sheep, Fetal stress index, guidelines, heart rate patterns, Neonatal encephalopathy, NICE guidelines, Physiology, variability
Birth Small Talk 
Thanks Kirsten. I was hoping you were going to tackle fetal physiology. Re contraction patterns in Reynolds’ second paper, I was thinking about the links between slow dilatation and more frequent contractions, both might lead to oxytocin administration under hospital care, but this wasn’t mentioned in their paper as far as I could see. Our UK birthplace study (BMJ 2011) found labour shorter under midwifery led care in birth centres, even shorter at home, which would have neither CTG nor exogenous oxytocin (at least until transfer). At the online RSM event you spoke at last year, I remember Philip Steer mentioning that ?up to? a third of damaged babies’ mothers had had their labour augmented by oxytocin, (though I don’t think I’ve seen this officially reported on, but I may have missed it). Have you found a link between hyperstimulation and brain damage anywhere? A quick google search brought up lawyer websites!
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OK, I found the CONDISOX trial in the BMJ and would appreciate your thoughts, thanks.
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Hi Margaret, Thanks for your interest. I haven’t specifically written about the CONDISOX trial, but I recently did a post about whether stopping oxytocin as part of “intra-uterine resuscitation” is a good idea. You might find answers there. https://birthsmalltalk.com/2022/04/06/stopping-the-oxytocin-infusion-when-the-ctg-is-abnormal/
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Thank you, Kirsten for this (as usual ) honest and clear description of the limitations of intrapartum CTG. I look forward to the day when we can find a tool/method of identifying that baby that needs to get out. Meanwhile, we continue to walk that tight rope of minimising unnecessary interventions and yet not losing the baby that did need to come out NOW!
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