17 Use of CTG with Induction and Augmentation of Labour. Handbook CTG

 17

Use of CTG with Induction and

Augmentation of Labour

◈

Ana Piñas Carrillo and Edwin Chandraharan

Handbook of CTG Interpretation: From Patterns to Physiology, ed. Edwin Chandraharan.

Published by Cambridge University Press. © Cambridge University Press 2017.

Key Facts

The rates of both induction (IOL) and augmentation of labour are progressively

increasing due to a better understanding of the course of obstetric and

nonobstetric pathologies in pregnancy such as essential hypertension,

preeclampsia, diabetes and obstetric cholestasis and improved and more

widespread use of diagnostic techniques such as obstetric ultrasound to detect

intrauterine growth restriction (IUGR) or fetal malformations that require an

earlier delivery.

The rate of IOL in the United Kingdom is around 20 per cent, similar to other

developed countries, with 15 per cent of inductions requiring an instrumental

delivery and 22 per cent an emergency caesarean section.

Indications for IOL include maternal reasons such as preeclampsia, diabetes,

obstetric cholestasis and other maternal diseases; fetal reasons include IUGR,

multiple pregnancy and conditions inherent to the pregnancy such as prolonged

rupture of membranes, meconium-stained liquor and postterm pregnancy.Key Features on the CTG Trace

The most common method of IOL is the use of prostaglandin E2 in the form of

pessary, tablet or gel. Other methods include the use of balloon catheter,

oxytocin, prostaglandin E1 and antiprogesterons, the last two only licensed in

cases of intrauterine death.

Oxytocin and prostaglandins have no direct reported effects on the fetus, and

their detrimental effects are mediated through excessive uterine activity and

resultant compression of umbilical cord and/or reduction in oxygenation of

placental venous sinuses.

The most frequent complications occurring during the process of IOL are

tachysystole, hypertonus or uterine hyperstimulation. Other complications

include failed induction, rupture of membranes and occasionally umbilical cord

prolapse, and uterine rupture especially in the presence of a previous uterine

scar.

Scientific evidence suggests that if the intercontraction interval is <2.3 minutes

when oxytocin is used, there may be a rapid drop in oxygenated haemoglobin in

the fetal brain.

‘Tachysystole’ refers to the presence of five or more contractions in 10 minutes

in the absence of changes in the FHR. Tachysystole requires careful observation

until changes on the cardiograph are observed.

‘Uterine hyperstimulation’ refers to the presence of five or more contractions in

10 minutes (and/or increased tone and duration of uterine contractions), but, as

opposed to tachysystole, it produces changes in the FHR. In early stages, typical

variable decelerations appear; if excessive uterine activity (frequency, duration

or strength) continues, the CTG may show atypical and late decelerations

(secondary to reduction in utero-placental oxygenation), rise in baseline heart

rate and loss of variability (‘gradually evolving hypoxia’).Figure 17.1 Note the occurrence of uterine hypertonus with no uterine relaxation.

Key Pathophysiology behind Patterns Seen on

the CTG Trace

‘Hypertonia’ or ‘uterine hypertonus’ refers to a sustained uterine contraction

lasting >60 seconds and has the potential to cause a prolonged deceleration

(Figure 17.1). In cases of previous caesarean section, this can reflect a uterine

rupture (see Chapter 15.)

An evolving uterine hyperstimulation usually produces features suggestive of a

‘gradually evolving hypoxia’ on the CTG trace (decelerations followed by an

absence of accelerations, rise in baseline FHR initially followed by a loss of

baseline variability and a ‘stepladder’ pattern to death due to the onset of

decompensation).

A rapidly evolving or sustained uterine contraction may cause an acute umbilical

cord compression leading to a prolonged deceleration caused by an acute

interruption of fetal oxygenation. This prolonged deceleration is usually

characterized by the presence of good variability within the first 3 minutes of

deceleration (in the absence of three major accidents: abruption, uterine rupture

and cord prolapse). However, if it is not rapidly treated, variability may

subsequently disappear suggestive of hypoxia to the centres in the brain that

control FHR.Recommended Management

Key Tips to Optimize Outcome

In the presence of uterine hyperstimulation, prostaglandins should be removed or

oxytocin should be stopped immediately if labour is being augmented. If CTG

changes persist with no signs of normalization, tocolytics (terbutaline 250 mcg

subcutaneously) should be administered to relax uterine myometrium and to

relieve umbilical cord compression and replenish oxygenation of placental

venous sinuses so as to ensure adequate fetal oxygenation. As soon as the uterine

activity is reduced, the CTG trace should show signs of recovery, with

decelerations becoming narrower and shallower and a progressive reduction of

fetal heart baseline to the initial rate due to a reduction in catecholamine surge

and improvement of baseline variability (if it was reduced in response to

hyperstimulation).

If there is a tachysystole, there is no need to intervene, but if there are any other

risk factors such as a previous uterine scar, IUGR or meconium-stained liquor

among others, the same management as with uterine hyperstimulation should be

considered to avoid further complications (i.e. uterine rupture, meconium

aspiration syndrome or rapid fetal compromise in IUGR due to a reduced

physiological reserve).

If there is a prolonged deceleration secondary to a sustained contraction,

removal of prostaglandins or stoppage of oxytocin infusion are immediate

interventions. If there are no attempts at recovery of FHR to its original baseline,

administration of tocolytics should be considered. In the absence of three major

accidents (abruption, cord prolapse and uterine rupture), the ‘3, 6, 9, 12, 15’

rule can be applied. In this clinical scenario, 90 per cent of prolonged

decelerations recover to normal baseline in 6 minutes and up to 95 per cent in 9

minutes, once the offending agent (prostaglandin or oxytocin) is removed and

tocolytics were administered (if indicated).Individualize every case and appropriately select the method and suitability of

IOL/augmentation. A severely compromised IUGR fetus with redistribution is

unlikely to have sufficient physiological reserves to cope with the process of

IOL.

During augmentation of labour, in the presence of early signs of gradually

evolving hypoxia (variable decelerations, absence of accelerations), anticipate

further changes and review the need to continue increasing oxytocin if regular

contractions have been achieved. One may need to re-examine a woman in 2

hours instead of 4 hours to assess the progress of labour, because if there is

evidence of progress, further increments of oxytocin dosage are not necessary.

Remember that as labour progresses, the number of oxytocin receptors increases

in the fundus, making the myometrium more sensitive to circulating oxytocin, and

therefore, less oxytocin may be needed as labour advances.

Current scientific evidence suggests that the use of oxytocin to augment

spontaneous labour reduces the mean duration of labour by approximately 2

hours without influencing the mode of birth. Therefore, in the light of this

evidence, caution should be exercised in the use of oxytocin in high-risk labour

(previous caesarean section, IUGR, meconium, clinical chorioamnionitis) as the

benefit of 2-hour reduction in the duration of labour may not outweigh the risks

of uterine rupture, fetal hypoxic-ischaemic injury, synergistic hypoxic

neurological damage in chorioamnionitis or meconium aspiration syndrome.

If oxytocin is restarted, the lowest possible dose to ensure optimum uterine

contractions should be used. For practical purposes, half the dose that resulted in

uterine hyperstimulation should be tried, if appropriate.

During second stage of labour, oxytocin should be used with great caution as

uterine myometrium is maximally sensitive to oxytocin during this time and

injudicious use of oxytocin may result in rapidly evolving hypoxia and fetal

neurological injury.Pitfalls

Consequences of Mismanagement

Exercise

Failure to incorporate the clinical picture into the management. The presence of

meconium-stained liquor, chorioamnionitis or IUGR should be taken into account

when considering augmentation of labour. In the presence of any of these risk

factors, increasing the hypoxic stress can have dramatic consequences on the

fetus.

Interrupting the process of IOL in the presence of a tachysystole. In the absence

of fetal compromise, there is no need to remove prostaglandins or administer

tocolytics.

Injudicious use of oxytocin especially only concentrating on the frequency of

uterine contractions without considering uterine activity (frequency, duration and

strength).

Failure to ensure adequate intercontraction interval to facilitate optimal

oxygenation of placental venous sinuses when oxytocin is used to induce or

augment labour.

Meconium aspiration syndrome with increased perinatal morbidity and mortality

Intrapartum stillbirth

Neonatal death

Hypoxic-ischaemic encephalopathy

Uterine rupture

Unnecessary operative interventions1. A 30-year-old, G2 P1, previous caesarean section is being induced for postdates (41

+ 4 weeks of gestation). She had prostaglandin pessary inserted for 24 hours, following

which she had an artificial rupture of membranes (ARMs) that showed meconium grade

1. Two hours later, she was started on oxytocin infusion. Oxytocin has been augmented

every 30 minutes as per protocol. CTG trace before the ARM was normal with a

baseline FHR of 130 bpm, variability of 10–15 bpm, presence of accelerations with no

decelerations and she had two contractions in 10 minutes.

CTG after 8 hours of oxytocin augmentation shows the following features:

Figure 17.2

a. What is your diagnosis?

b. What is your management?

c. What other complications do you expect?

Further Reading

1. McCarthy FP, Kenny LC. Induction of labour. Obstet, Gynaecol, Reprod Med. 2013;

24(1): 9–15.

2. National Institute for Health and Clinical Excellence. Induction of labour. Clinical

guideline 70. Available at www.nice.org.uk/CG070; July 2008.

3. WHO recommendations for augmentation of labour. 2014

4. McDonnell S, Chandraharan E. The pathophysiology of CTGs and types of intrapartum

hypoxia. Curr Women’s Health Rev. 2013; 9: 158–168.5. Chandraharan E, Arulkumaran S. Acute tocolysis. Curr Opin Obstet Gynecol. 2005; 17:

151–156.