15 Labour with a Uterine Scar

 15

Labour with a Uterine Scar

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The Role of CTG

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

Uterine scar dehiscence refers to the disruption of uterine myometrium but with

an intact serosa (peritoneal covering), whereas uterine rupture refers to the total

disruption of the entire uterine wall, including the serosa.

The increasing rate of caesarean sections in modern obstetric practice is

responsible for the rise in the number of women labouring with a previous

uterine scar.

Labour in the presence of a uterine scar has a risk of uterine rupture of 0.5 per

cent in spontaneous labour, 0.8 per cent with the use of oxytocin for

augmentation of labour and 2.4 per cent with the use of prostaglandins for

induction of labour.

The dehiscence/rupture of the uterus compromises the placental circulation, and

this results in fetal heart rate (FHR) changes, frequently one of the first signs of

uterine rupture. Continuous intrapartum fetal monitoring is essential in order toKey Features on the CTG Trace

Key Pathophysiology behind Patterns Seen on

the CTG Trace

diagnose the onset of FHR abnormalities so as to institute timely delivery to

avoid maternal and fetal complications.

The classical signs of uterine rupture such as vaginal bleeding, scar or

abdominal pain, receding presenting part, changes in the shape of the uterus and

palpation of fetal parts are not always present and often unreliable.

The CTG features observed depend on the type of dehiscence/rupture.

Uterine rupture can result in a prolonged deceleration lasting >3 minutes. The

specific features that should elicit a high index of suspicion of uterine rupture

include a total loss of variability within the first 3 minutes of deceleration, FHR

dropping >60 bpm from the initial baseline and/or baseline FHR dropping <80

bpm. This may be associated with a sustained contraction (uterine hypertonus) or

a sudden cessation of uterine activity recorded on the ‘toco’ component of the

CTG.

Repetitive variable or late decelerations and reduced variability may be

observed preceding a final prolonged deceleration.

Uterine rupture is frequently preceded by tachysystole (presence of more than

five contractions in 10 minutes without CTG changes) or hyperstimulation

(increased frequency, duration or tone of uterine contractions associated with

changes on the CTG trace).

Recurrent variable decelerations may occur secondary to prolapsed loop of

umbilical cord through the ruptured uterine scar into the peritoneal cavity, and its

resultant compression and late decelerations occur secondary to progressiveRecommended Management

placental separation leading to progressive fetal hypoxia and acidosis and

resultant ‘chemoreceptor stimulation’.

An acute prolonged deceleration may occur secondary to the expulsion of the

fetus into the peritoneal cavity that results in a total separation of the placenta. If

this persists for >10 minutes, it is termed terminal bradycardia.

In cases of uterine rupture presenting with acute hypoxia shown on the CTG

trace by a prolonged deceleration, immediate laparotomy to avoid fetal hypoxicischaemic injury and delivery within 10–15 minutes (category 1 caesarean

section) is indicated in this situation. If delivery is imminent, one should

consider immediate operative vaginal delivery followed by a laparotomy for

repair to avoid fetal hypoxic ischaemic injury.

The neonatal team should be informed of the suspicion of uterine rupture as it is

likely that the fetus will be born in poor condition and would need intensive

neonatal resuscitation, especially in cases of complete uterine rupture when the

fetus is found extruded in the abdominal cavity.

In women labouring with a previous uterine scar, the presence of repetitive

variable and late decelerations and reduced variability should arouse a high

index of suspicion of uterine dehiscence/rupture, and this needs to be excluded

before continuing with labour.

The use of transabdominal ultrasound scan to detect free fluid within the

abdominal cavity or disruption of the myometrium with bulging membranes may

be useful in cases where there is a strong clinical suspicion but with no classical

symptoms and signs of uterine rupture and when the changes observed on the

CTG are less marked or just ‘suspicious’.

In the presence of uterine tachysystole in a patient with a previous uterine scar,

clinicians should consider tocolysis even in the absence of FHR changes to

avoid the risk of uterine rupture.Key Tips to Optimize Outcome

Pitfalls

Consequences of Mismanagement

Baseline FHR variability will be rapidly reduced within the first 3 minutes of a

prolonged deceleration due to ongoing fetal hypotension and resultant sudden

reduction in fetal cerebral blood flow.

Seek immediate senior obstetric and midwifery input and ensure effective

multidisciplinary communication and team working to accomplish immediate

delivery.

If the CTG trace before the prolonged deceleration was normal, scientific

evidence suggests that if the delivery is accomplished within 18 minutes, fetal

neurological injury is unlikely. However, if there are already ongoing

decelerations prior to the onset of acute prolonged deceleration, fetal

neurological injury may ensue after 10 minutes.

‘3, 6, 9, 12, 15’ rule for a prolonged deceleration is not applicable in this case.

Immediate delivery is indicated.

Relying on vaginal bleeding or abdominal pain to diagnose uterine rupture in the

presence of a suspicious trace should be avoided. These symptoms are

commonly absent; looking at the clinical picture (use of oxytocin and/or

prostaglandins, hyperstimulation, sustained contraction) together with the CTG

features should arouse a suspicion of uterine rupture/dehiscence.

Attempting additional tests of fetal well-being such as fetal ECG (STAN), fetal

scalp pH or lactate when there is clear evidence of hypoxia to the central organs

on the CTG trace should be avoided as it would merely delay delivery and

worsen maternal and fetal complications.Exercise

1. A 36-year-old gravida 2 para 1 with a previous caesarean section for failure to

progress in labour was admitted with spontaneous onset of labour. Cervix was 6 cm

dilated and the presenting part was at 0 station and the CTG trace was classified as

normal. Oxytocin was commenced at 23:00 hours for failure to progress in labour as her

cervix had remained 6 cm 2 hours after artificial rupture of membranes.

a. Classify the CTG trace (using the ‘8C’ format).

b. What are effects of oxytocin on myometrial contractions and what changes would you

observe on the CTG trace?

c. Consider the CTG trace from 02:58 hours.

1. What is the type of hypoxia?

2. What are the differential diagnoses?

3. What immediate actions would you take?

d. What is the likelihood of the observed CTG change to return back to normal in this

case?

e. What would you expect to see in the umbilical cord gases if delivery was

accomplished within 20 minutes of the onset of this acute, prolonged decelerations?

Intrapartum fetal death

Early neonatal death

Severe hypoxic ischaemic encephalopathy

Long-term fetal neurological sequelae secondary to delayed treatment of

hypotension

Maternal collapse, need for multiple blood transfusion and, rarely, maternal

deathFigure 15.1

Figure 15.2

Further Reading

1. Gibb D, Arulkumaran S. Fetal Monitoring in Practice. 3rd edn. Elsevier, 2008.

2. Chandraharan E, Arulkumaran S. Obstetric and Intrapartum Emergencies. A Practical

Guide to Management. Cambridge, 2012.

3. Chandraharan E. Rational approach to electronic fetal monitoring during labour in ‘all’

resource settings. Sri Lanka J Obstet Gynaecol. 2010; 32: 77–84.

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

hypoxia. Curr Women’s Health Revs. 2013; 9: 158–168.