When the fetal heart rate pattern seen on CTG monitoring during labour is considered abnormal, clinicians typically use measures that aim at restoring the pattern to normal. This is often called intrauterine resuscitation. Some of the commonly used approaches are to change the birthing woman’s position, give intravenous fluids, or to administer oxygen. This post is part three of a five-part series looking at the evidence for intrauterine resuscitation. You can read part one (recent research about how often intrauterine resuscitation is used) here, and part two (about oxygen therapy) here.
It is important to set out some expectations for the kind of evidence I am looking for in this series. I don’t believe that it is enough for intrauterine resuscitation attempts to simply restore the wiggles on the CTG to a pattern considered to be normal. Recalling that the aim of intrapartum fetal monitoring is to prevent fetal damage from hypoxia, we should be looking for evidence that these practices improve perinatal outcomes. Or at the very least, resuscitation efforts should reduce the use of other interventions, such as fetal blood sampling, instrumental birth, and caesarean section.
For each of these posts, I start by setting out the assumptions about how the therapy is proposed to work, and how that lines up with what we know about physiology. I will then share the existing research and summarise key findings. There’s heavy science content in here for those who (like me) delight in such things. You are also welcome to skip to the “too long, didn’t read” (TL;DR) summary at the end of this post (and each of the ones to come) for an answer to the question – does intrauterine resuscitation (in this case giving intravenous fluids) when the CTG is abnormal make things better for the fetus and the birthing woman?
Exploring the physiology
The apparent logic behind this practice is a bit, well, not very logical when you scrutinise it. I have long suspected that giving a bolus of intravenous fluids when the CTG is abnormal is a version of “do something, don’t just stand there!”, when a period of observation while sitting on your hands is appropriate. (If you are really stuck for something to do, can I suggest knitting?)
There are most definitely circumstances when pathophysiological processes contribute to abnormal fetal heart rate patterns and administering intravenous fluids is appropriate. Managing maternal hypotension after a regional anaesthetic and replacing volume in a woman with heavy and ongoing bleeding come to mind. These are clinically obvious situations that reinforce the adage that treating the woman first is inherently in the best interests of the fetus.
If you give 250, 500, or 1000 mL of intravenous fluid to a woman in labour who is not volume depleted, what happens? The volume is quickly distributed through the intravenous space. Haemoglobin concentration falls marginally due to dilution, but the total oxygen carrying capacity of the entire blood volume remains the same. To get the same number of haemoglobin molecules to the placental bed now that there is more liquid between the molecules, the heart needs to work harder. To do this either or both heart rate and stroke volume (the amount of blood pushed out per heartbeat) must increase. But this isn’t what happens.
Bodies are very keen to maintain haemostasis and physiological processes are initiated to remove additional fluid from the circulation. Baroreceptors detect the increased blood volume and inhibit the sympathetic nervous system, lowering blood pressure and heart rate (and therefore reducing blood flow and oxygen delivery to the placenta marginally). Increased fluid volumes in the vascular system inhibit the release of vasopressin (or antidiuretic hormone) from the posterior pituitary. Glomerular filtration (the passage of liquid out of blood into the tubules of the kidney) is high in pregnancy, so much of the additional fluid ends up excreted into the renal system. Lower levels of vasopressin limit the reabsorption of this extra fluid, so it passes into urine. The woman will fill her bladder faster and need to urinate more often. Going to the toilet is often a cause for poor quality CTG tracing. Increasing urine production is not all that helpful when the CTG is being observed closely to signs of improvement or deterioration.
On the other hand, high levels of oxytocin, whether excreted from the pituitary or given intravenously, have a vasopressin like effect. This limits the excretion of excess fluid as urine and makes it more likely that fluid will shift out of the vascular space into the tissues. Here the fluid turns up as oedema. At worst, fluid overload can result in fluid leaking into the space between the alveoli of the lungs and the pulmonary vessels. This makes it harder for oxygen to enter the blood stream, which would be counterproductive for delivery of adequate levels of oxygen to the fetus.
There is no therefore plausible physiological way that additional intravenous fluids in a woman with a normal blood volume will improve fetal oxygenation. At best this is simply a waste of time and resources while enabling clinicians to feel like they are doing something helpful. At worst, it might increase cardiac workload for the woman and reduce the oxygenation of her blood.
Looking at the research evidence
Let’s again start by imaging what well designed research would look like if it were to answer the question: Does giving intravenous fluids to a woman in labour with an abnormal CTG pattern produce benefits for the fetus? This would require the selection of a group of women who do not have clinical reasons to be given additional intravenous fluids. The CTG abnormality would have to be significant enough to warrant attention, but not so abnormal to require immediate moves to achieve birth. A standard dose of intravenous fluids would be given, possibly several different doses might be included in the trial if a sufficiently large study population can be found to see whether more fluids rather than less made a bigger difference. Ideally there would be a way to blind clinicians, so they were unable to know who was getting the fluids and who was not. Outcome measures would include changes in the CTG pattern over time, outcomes for the baby, and for the birthing woman.
Nothing like this has ever been done.
There is some evidence about the effects of giving intravenous fluids on fetal and maternal outcomes, but none of these studies included women with an abnormal CTG. The focus has been on women having their first birth and the impact administering intravenous fluids had on the course of labour. Most of this research has been conducted in contexts where it is standard practice to not permit women in labour to eat or to drink fluids on demand. Deliberate oral intake restriction doesn’t support physiological processes such as thirst which maintain normal fluid volume during labour so dehydration is more likely.
Back in 2005 when fetal oximetry was still clinically accessible, Simpson and James used fetal oximetry to examine the impact of several different intrapartum practices on fetal oxygen saturation. Nulliparous women whose labour was induced with oxytocin and who planned to use epidural analgesia were enrolled. All had normal fetal heart rate patterns on CTG at enrolment. As one of the practices studied, in preparation for the epidural women were given a bolus of either 500 or 1000 mL of Hartmann’s solution (compound sodium lactate) over 20 minutes. There were 21 women in each group. Before and after comparisons in fetal oxygen saturation were taken. Fetal oxygen saturation increased from baseline in both groups but was only statistically significant when 1000 ml was given. Impact on fetal heart rate pattern was not assessed. While increasing oxygen saturation is a good thing, this occurred only within the normal range and it might not extrapolate to clinically significant improvements in hypoxic fetuses.
A 2013 Cochrane review (Dawood, Dowsell & Quenby) examined the impact of intravenous fluids on the duration of labour in women in their first labour. All women were in spontaneous labour and were considered low risk. They identified two trials that compared Hartmann’s with no intravenous fluids in women with unrestricted oral intake. The group who received intravenous fluids had a shorter labour duration (28 mins), and no difference in the caesarean section rate. Three trials compared 125 vs 250 mL/hr of intravenous fluids (women had no oral fluid restriction), finding shorter labours with the larger volume (23 mins). Again, there were no differences in the caesarean section rates. Four trials in women who were fluid restricted compared 125 with 250 mL/hr. Women given the larger volume of fluids had shorter labours (105 mins), a lower caesarean section rate, and no difference in NICU admissions. None of this research looked at fetal heart rate patterns.
A subsequent systematic review in 2017 (Ehsanipoor, et al.) updated these findings, identifying seven trials, of which two were undertaken in women who had unrestricted oral fluid access. Women were randomised to receive either 125 mL/hr or 250 mL/hr of fluid intravenously. In the trials where oral fluids were not restricted, no difference in caesarean section rates between the groups was seen (9.5 vs 10.9%). For women who were oral fluid restricted, the caesarean section rate was lower with the higher rate of intravenous fluids (13.3 vs 19.2%, RR 0.67, 95% CI 0.5-0.9).
One randomised controlled trial has been conducted after this review was completed. Fong and colleagues (2017) looked at both the rate of intravenous fluids and the use of dextrose (a sugar) in the fluid to assess impact on the course of labour in women in spontaneous labour with their first baby. All women were restricted to sips of water and ice chips. There were no differences in labour length, incidence of labour >12 hours, caesarean section rates (including caesarean for CTG abnormalities), or instrumental birth. There was also no difference in neonatal outcomes, but they didn’t examine hypoglycaemia rates (this is more common when dextrose or glucose is given in labour).
The short version of this post is:
- Giving intravenous fluids to normovolaemic women to improve abnormal fetal heart rate patterns is not physiologically plausible and may lead to fluid overload in a proportion of women
- There is no quality evidence to inform practice relating to the use of intravenous fluids when the CTG is abnormal
- What little research we do have implies that oral fluid restriction is not beneficial to women in labour with respect to labour progress and surgical birth rates
- Giving intravenous fluids at a rate of 250 mL/hr to fluid restricted women may reverse the impact of oral fluid restriction on labour duration and surgical birth
Evidence-based clinical practice would therefore include the administration of intravenous fluids to women with clinical evidence of hypovolaemia, but not for women with no evidence of hypovolaemia and an abnormal CTG. While not the original focus of this post, I would also make a plea to abandon the practice of restricting oral fluids for women in labour.
Dawood, F., Dowswell, T., & Quenby, S. (2013). Intravenous fluids for reducing the duration of labour in low risk nulliparous women. Cochrane Database of Systematic Reviews, 6, CD007715.
Ehsanipoor, R., Saccone, G., Seligman, N., Peirce-Williams, R., Ciardulli, A., & Berghella, V. (2017). Intravenous fluid rate for reduction of cesarean delivery rate in nulliparous women: a systematic review and meta-analysis. Acta Obstetrica et Gynecologica Scandinavica, 96, 804-811.
Fong, A., Serra, A., Caballero, D., Garite, T., & Shrivastava, V. (2017). A randomized, double-blinded, controlled trial of the effects of fluid rate and and/or presence of dextrose in intravenous fluids on the labor course of nulliparas. American Journal of Obstetrics and Gynecology, 217, 208.e1-7.
Simpson, K., & James, D. (2005). Efficacy of intrauterine resuscitation techniques in improving fetal oxygen status during labor. Obstetrics and Gynecology, 105(6), 1362-1368.