There are a series of assumptions that have been used to justify continuous CTG monitoring in labour. One of the assumptions 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 on to “too late, the damage is now irreversible”. The goal of CTG monitoring is to prevent irreversible damage to the fetal brain by recognising when the fetus passes beyond “I’m fine” and into “not okay any more – please get me out” but well before “too late!” happens. If we can precisely pick this transition, we could also avoid needlessly intervening in the progress of labour to birth babies who were fine all along.
There has been much emphasis in guideline development and fetal monitoring education on recognising individual features of the CTG (things like the baseline, and types of decelerations), and in combining these individual features together to categorise the CTG. Category terms like Type II, non-reassuring, and abnormal are used depending on the guideline in question. These categories are then linked to recommendations such as continue to monitor, or expedite birth now! It is important that we base our guidelines, and therefore our education, on research that demonstrates that pattern A is highly predictive for “I’m fine!” while pattern B is highly predictive for “Get me out of here!”. The problem is we haven’t actually done much of that sort of research. Hence, our guidelines are based on people’s best guesses, and this in large part explains why there is variation among guidelines.
Fortunately there are now people working on finding out what happens to fetal heart rate patterns when the oxygen levels run low, and whether you can build a predictive model based on fetal heart rate patterns to predict which fetuses will benefit from expedited birth and those who won’t. Let’s look at three recently published papers.
Fetal sheep research
Ghesquire and colleagues (2022) intermittently blocked the umbilical cord of fetal sheep to see what happens to variability in the fetal heart rate. Heart rate variability (the amount of wiggle up and down around the baseline) that is either reduced or increased is said to indicate signs of fetal hypoxia, so this research was designed to test whether this is the case or not. Note that the researchers didn’t report on decelerations as that wasn’t the aim of the study. The researchers used the types of measures used in computerised analysis of the fetal heart rate to describe changes in fetal heart rate variability, including 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. After repeated occlusions 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. The first finding of note related to where the brain damage occurred: in fetuses with damage to the brain stem, there were changes in fetal heart rate variability, but this didn’t occur with damage to other parts of the brain. 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. The other finding of note: the baseline heart rate and short-term variability after each period of occlusion did not change over time despite the progressively more frequent periods of cord occlusion. This is at odds with what we currently teach about fetal heart rate patterns. The researchers did find that the fetal stress index increased over time.
It is difficult to know how these findings translate into clinical practice. The researchers 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 in that they developed demonstrable 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 basic physiology research has been done to help clinicians understand what they are seeing on CTG traces, and how doing this research opens up new cans of worms.
The next paper looks 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 (brain damage) thought to be due to events happening during labour and another group of 112 babies who were born without signs of damage, then retrospectively reassessed the CTG traces from all babies in detail to see if they could develop a model (a set of CTG characteristics) that could accurately separate the 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 features that were seen more often in the CTGs of babies with encephalopathy: baseline heart rate over 160 bpm, reduced variability, absence of accelerations, and the presence of late decelerations. These are not surprising and have long been recognised as associated with poorer outcome. The longer an abnormal pattern persisted, the stronger the association with poor outcome. The categories of “suspicious” and “pathological” were seen more often when the baby had encephalopathy. However, 50% of babies who were born in good condition had at least one period of “suspicious” CTG and 25% had at least one period of “pathological” CTG.
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.
The same team also looked at whether contraction patterns provide useful predictive information (Reynolds, et al., 2022b). More frequent contractions and slower labour progress occurred more often in babies with brain damage. 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.
It is no wonder then that intrapartum CTG monitoring 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 continue to be done on the basis of abnormal CTG traces yet are unnecessary as there was no possible way they were going to improve outcomes for that particular baby.
Solving this puzzle requires us as a community of researchers and clinicians to develop a deeper 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 such research will demonstrate that there is no such discriminatory pattern. If that is the case, then no matter how many knots we tie ourselves in, trying to develop the best guideline, teach interpretation to clinicians, and ensure that people act appropriately when that pattern occurs, we will never make things better.
The other option to solving the problem is to accept that CTG experiment of the past sixty years as fundamentally flawed and begin the earnest work of finding other ways to reduce poor perinatal outcome while not harming birthing women. How long will we wait before we grasp this opportunity?
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, in press. 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 and 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 and Reproductive Biology, 274, 73-79. https://doi.org/10.1016/j.ejogrb.2022.05.011