As a medical student in the 80s I was taught that early decelerations in the fetal heart rate are due to head compression, and are a reassuring sign of normal fetal oxygenation. I have been told this many, many times since. As I started doing background work in the lead up to my PhD I began to recognise that this sounded more like received wisdom (eat your crusts, they’ll make you hair curly) than scientific evidence (in this particular population, under these specific circumstances, researchers A & B showed that in 79% of the population….). I wanted to get under the surface of the story that head compression is a cause of decelerations and find out when and where the story started, who started it, and whether it is really backed up by evidence.
How the story begins
Tracking down the early deceleration story proved to be fascinating and it reveals a lot about how obstetric knowledge is constructed. The beginning of the story takes place in 1958, in Connecticut in the USA, with Obstetrician Edward Hon. Hon was later to go on and become a director of a company called Corometrics, who manufactured CTG monitors for clinical use. In 1958 we find him writing a paper (Hon, 1958) which he offered as a preliminary report about the electronic evaluation of fetal heart rate patterns during labour.
Hon made electronic recordings of the fetal heart rate using an external ECG monitor which recorded both maternal and fetal ECG patterns, and then subtracted the maternal ECG so the fetal ECG could be recorded. Contractions were recorded manually, presumably by a labour and delivery nurse. His study included 80 women in “normal” labour (his use of quote marks – not mine) without explaining what this meant. No information was provided in the paper about these women, their pregnancy or labour, or medical interventions that might have been used. It is important to bear in mind that the use of heavy sedation during labour was not uncommon at this point in time.
The drop in fetal heart rate noted with contractions was related to the degree of cervical dilatation present. In normal labour this was not noted before 4 cm or after 8 cm of dilatation. Initially this was puzzling…. The possibility that fetal bradycardia might be related to increased intracranial pressure rather than momentary anoxia following compression of the placenta was then explored. …
In an attempt to determine experimentally the effect of increased intracranial pressure, patients who had exhibited no drop in fetal heart rate with contractions were taken to the delivery room after 8 cm of dilatation. Between contractions pressure was applied to the fetal skull with the examining hand and minimal drops in the fetal heart rate noted. Similar results were obtained when a 3 cm ring pessary was placed on the fetal skull and pressure applied. However, when a 6 cm pessary was applied and pressure exerted a marked bradycardia similar to that noted with uterine contractions in other labours was obtained consistently.p 1219 – 1222
No indication was given about the number of women this which this technique was employed. Two illustrative graphs accompany this text (again no clinical information is provided), so we know that at least two women contributed to generating this data. Whether they were the only two can’t be determined from the description provided.
Let’s stop for a moment and consider this from the women’s perspective. There is no indication in the paper that their consent was sought to participate in this experiment. It is possible that they were deeply sedated and unaware of what was being done. A clinician, possibly Hon, inserted first their hand, then a series of different sized objects into their vagina, and pushed upwards over an extended period of time in order to deliberately place pressure on the fetal skull to see what would happen. This provides another example of how obstetric knowledge has been built on experiments conducted on women without their consent.
On the basis of this experimentation, Hon went on to postulate:
from the available data it seems reasonable attribute the “physiologic” drop in fetal heart rate at the height of a contraction to an increase in intracranial pressure. The final mechanism by which this is accomplished is not known, but it may be relation to variation in blood flow to the brain stem as a result of altered intracranial dynamics.p. 1223
Does the story hold up to scrutiny?
Skipping forward almost sixty years, we encounter Christopher Lear, a physiologist who has been working on understanding the fetal response to hypoxia. His work has been experimental in nature, using pregnant sheep and their fetuses, permitting experiments that are simply not possible for human fetuses. In 2016, Lear and his co-authors reviewed the physiology literature and summarised:
Direct fetal head compression inconsistently causes decelerations and so is very unlikely to be a major contributor to intrapartum decelerations during the majority of labours. … If decelerations due to head compression do occur, for example during obstructed labour when the fetal head is engaged in the birth canal, these data suggest that such decelerations reflect severe cerebral hypoperfusion and hypoxia and in contrast with current proposed interpretation (the NICE and FIGO guidelines), should not be considered benign.p. 4713 – 4714
Lear’s subsequent physiological research has confirmed that all decelerations, regardless of their shape or timing in relation to contractions, are related to lower oxygen levels in the fetus, and represent efforts to actively compensate for the reduction in oxygen in order to prevent tissue damage (Lear et al., 2018).
Do current fetal monitoring guidelines accurately describe the evidence on fetal physiology?
Lear’s findings are a significant departure from the simple mantra of “early decelerations are due to head compression and are a reassuring sign of normal fetal oxygenation”. While the message “all decelerations are a sign of fetal compensation to hypoxia” is more soundly based in physiology, this evidence has not yet been taken up by obstetric professional organisations who write guidelines.
As increasing evidence that intrapartum CTG monitoring doesn’t prevent fetal harm from hypoxia has accumulated, the common response has been to argue that people interpreting CTGs didn’t do it correctly. If (and this is far from being a given) intrapartum CTG monitoring has the potential to actually detect hypoxia during the critical window period between compensation to physiological levels of stress and the onset of tissue damage so that clinicians can intervene, then the best hope of achieving this is to acknowledge that our understanding of fetal physiology is deeply flawed and we need a new evidence base. This evidence base should be built on sound research, rather than guesses derived from unconsented experimentation on a handful of women’s bodies.
Hon, E. H. (1958,). The electronic evaluation of the fetal heart rate. American Journal of Obstetrics and Gynecology, 75(6), 1215-1230.
Lear, C. A., Galinsky, R., Wassink, G., Yamaguchi, K., Davidson, J. O., Westgate, J., Bennet, L., & Gunn, A. J. (2016). The myths and physiology surrounding intrapartum decelerations: the critical role of the peripheral chemoreflex. The Journal of Physiology, 594(17), 4711-4725. https://doi.org/10.1113/JP271205
Lear, C. A., Wassink, G., Westgate, J., Nijhuis, J. G., Ugwumadu, A., Galinsky, R., Bennet, L., & Gunn, A. J. (2018). The peripheral chemoreflex: indefatigable guardian of fetal physiological adaptation to labour. The Journal of Physiology, 596(23), 5611-5623. https://doi.org/10.1113/JP274937