Continuous cardiotocography (CTG) as a form of electronic fetal monitoring (EFM) for fetal assessment during labour
Abstract
Background
Cardiotocography (known also as electronic fetal monitoring), records changes in the fetal heart rate and their temporal relationship to uterine contractions. The aim is to identify babies who may be short of oxygen (hypoxic), so additional assessments of fetal well‐being may be used, or the baby delivered by caesarean section or instrumental vaginal birth.
Objectives
To evaluate the effectiveness of continuous cardiotocography during labour.
Search methods
We searched the Cochrane Pregnancy and Childbirth Group Trials Register (31 December 2012) and reference lists of retrieved studies.
Selection criteria
Randomised and quasi‐randomised controlled trials involving a comparison of continuous cardiotocography (with and without fetal blood sampling) with (a) no fetal monitoring, (b) intermittent auscultation (c) intermittent cardiotocography.
Data collection and analysis
Two review authors independently assessed study eligibility, quality and extracted data from included studies.
Main results
Thirteen trials were included with over 37,000 women; only two were judged to be of high quality.
Compared with intermittent auscultation, continuous cardiotocography showed no significant improvement in overall perinatal death rate (risk ratio (RR) 0.86, 95% confidence interval (CI) 0.59 to 1.23, n = 33,513, 11 trials), but was associated with a halving of neonatal seizures (RR 0.50, 95% CI 0.31 to 0.80, n = 32,386, nine trials). There was no significant difference in cerebral palsy rates (RR 1.75, 95% CI 0.84 to 3.63, n = 13,252, two trials). There was a significant increase in caesarean sections associated with continuous cardiotocography (RR 1.63, 95% CI 1.29 to 2.07, n = 18,861, 11 trials). Women were also more likely to have an instrumental vaginal birth (RR 1.15, 95% CI 1.01 to 1.33, n = 18,615, 10 trials).
Data for subgroups of low‐risk, high‐risk, preterm pregnancies and high‐quality trials were consistent with overall results. Access to fetal blood sampling did not appear to influence the difference in neonatal seizures nor any other prespecified outcome.
Authors' conclusions
Continuous cardiotocography during labour is associated with a reduction in neonatal seizures, but no significant differences in cerebral palsy, infant mortality or other standard measures of neonatal well‐being. However, continuous cardiotocography was associated with an increase in caesarean sections and instrumental vaginal births. The challenge is how best to convey these results to women to enable them to make an informed choice without compromising the normality of labour.
PICOs
Plain language summary
Comparing continuous electronic fetal monitoring in labour (cardiotocography, CTG) with intermittent listening (intermittent auscultation, IA)
Monitoring the baby's heartbeat is one way of checking babies' well‐being in labour. By listening to, or recording the baby's heartbeat, it is hoped to identify babies who are becoming short of oxygen (hypoxic) and who may benefit from caesarean section or instrumental vaginal birth. A baby's heartbeat can be monitored intermittently by using a fetal Pinard stethoscope (special trumpet shaped device), or by a hand‐held Doppler device. The heartbeat can also be checked continuously by using a CTG machine. This continuous CTG method is also called electronic fetal monitoring (EFM). It produces a paper recording of the baby's heart rate and mother's labour contractions. Whilst a continuous CTG gives a written record, it prevents women from moving during labour. This means that women may be unable to change positions freely or use a bath to help with comfort and control during labour. It also means that some resources tend to be focused on the needs to constantly interpret the CTG and not on the needs of a woman in labour.
This review included 13 trials involving over 37,000 women that compared continuous CTG monitoring with intermittent auscultation (listening). Most studies were not of high quality and the review is dominated by one large, well‐conducted trial of almost 13,000 women who received one‐to‐one care throughout labour. In this trial, the membranes were ruptured artificially (amniotomy) as early as possible and oxytocin stimulation of contractions was used in about a quarter of the women.
Overall, there was no difference in the number of babies who died during or shortly after labour (about one in 300). Fits (neonatal seizures) in babies were rare (about one in 500 births), but they occurred significantly less often when continuous CTG was used to monitor the fetal heart rate. There was no difference in the incidence of cerebral palsy, however, other possible long‐term effects have not been fully assessed and need further study. Continuous monitoring was associated with a significant increase in caesarean section and instrumental vaginal births. Both procedures are known to carry the risks for mothers although the specific adverse outcomes were not assessed in the included studies.
Authors' conclusions
Summary of findings
| Continuous CTG versus intermittent auscultation for fetal assessment during labour | ||||||
| Patient or population: Women undergoing fetal assessment during labour | ||||||
| Outcomes | Illustrative comparative risks* (95% CI) | Relative effect | No of Participants | Quality of the evidence | Comments | |
| Assumed risk | Corresponding risk | |||||
| Control | Continuous CTG versus intermittent auscultation | |||||
| Perinatal mortality (primary outcome) | Study population | RR 0.86 | 33513 | ⊕⊕⊝⊝ | ||
| 3 per 1000 | 3 per 1000 | |||||
| Moderate | ||||||
| 4 per 1000 | 3 per 1000 | |||||
| Neonatal seizures (primary outcome) | Study population | RR 0.5 | 32386 | ⊕⊕⊕⊝ | ||
| 3 per 1000 | 1 per 1000 | |||||
| Moderate | ||||||
| 4 per 1000 | 2 per 1000 | |||||
| Cerebral palsy (primary outcome) | Study population | RR 1.75 | 13252 | ⊕⊕⊝⊝ | ||
| 3 per 1000 | 4 per 1000 | |||||
| Moderate | ||||||
| 39 per 1000 | 68 per 1000 | |||||
| Caesarean section (primary outcome) | Study population | RR 1.63 | 18861 | ⊕⊕⊝⊝ | ||
| 36 per 1000 | 59 per 1000 | |||||
| Moderate | ||||||
| 66 per 1000 | 108 per 1000 | |||||
| Instrumental vaginal birth (primary outcome) | Study population | RR 1.15 | 18615 | ⊕⊕⊝⊝ | ||
| 102 per 1000 | 118 per 1000 | |||||
| Moderate | ||||||
| 222 per 1000 | 255 per 1000 | |||||
| Cord blood acidosis (primary outcome) | Study population | RR 0.92 | 2494 | ⊕⊝⊝⊝ | ||
| 24 per 1000 | 22 per 1000 | |||||
| Moderate | ||||||
| 24 per 1000 | 22 per 1000 | |||||
| Any pharmacological analgesia (primary outcome) | Study population | RR 0.98 | 1677 | ⊕⊕⊝⊝ | ||
| 754 per 1000 | 739 per 1000 | |||||
| Moderate | ||||||
| 805 per 1000 | 789 per 1000 | |||||
| *The basis for the assumed risk (e.g. the median control group risk across studies) is provided in footnotes. The corresponding risk (and its 95% confidence interval) is based on the assumed risk in the comparison group and the relative effect of the intervention (and its 95% CI). | ||||||
| GRADE Working Group grades of evidence | ||||||
| 1 Limitations in design: Most of the pooled effect provided by studies “B” or “C” without a substantial proportion (i.e. < 40% (actual 33% weight) from studies “C”. | ||||||
Background
The baby's heart beat was first thought to be heard in utero in the middle of the seventeenth or eighteenth century (Grant 1989a; Gibb 1992), but it was not until the early nineteenth century that de Kergeradee suggested that listening to the baby's heartbeat might be clinically useful (Grant 1989a). He proposed that it could be used to diagnose fetal life and multiple pregnancies, and wondered whether it would be possible to assess fetal compromise from variations in the fetal heart rate (FHR). Since then, various methods of listening to the fetal heart have been developed and introduced into maternity care (see Table 1), each with the aim of improving outcomes for babies and reducing the heartache for mothers and families when a baby dies or suffers long‐term disability. Today, monitoring the fetal heart during labour, by one method or another, appears to have become a routine part of care during labour, although access to such care varies across the world.
| Method | Description |
| Fetal stethoscope (Pinard) ‐ for intermittent monitoring (IA) | This is a trumpet‐shaped device, which is placed on the mother's abdomen and the caregiver listens for the heart beat at the other end. This is a simple instrument of relatively low cost. |
| Hand‐held Doppler ultrasound monitor ‐ for intermittent monitoring (IA) | The device is placed on the mother's abdomen with gel smeared on the underside of the ultrasound transducer. This allows the ultrasound beam to travel from the fetal heart to the transducer without interruption. |
| External cardiotocography ‐ for continuous or intermittent monitoring | The fetal heart rate and the activity of the uterine muscle are detected by two transducers placed on the mother's abdomen (one above the fetal heart and the other at the fundus). Doppler ultrasound provides the information which is recorded on a paper strip known as a cardiotocograph (CTG). |
| Internal cardiotocography ‐ for continuous monitoring | An electrode is placed directly on the baby's presenting part to detect the fetal ECG signal. Again the signals are recorded on a paper strip (CTG). This method can only be used if membranes (fore‐waters) have ruptured either spontaneously or artificially. |
Description of the condition
The incidence of neonatal morbidity and mortality varies around the world, although direct comparisons may be difficult because of varying definitions and classifications. Nevertheless, large differences are reported between high‐income countries with average neonatal mortality rates (NMR) of four per 1000 live births) and low/middle‐income countries with average NMRs of 33 per 1000 births) (Lawn 2005). Although the majority of perinatal morbidity and mortality may not be prevented by improved fetal monitoring in labour (Nelson 1996), failure in identifying abnormal FHR patterns and lack of appropriate actions are considered to be significant contributing factors (MCHRC 1997; MCHRC 1998; MCHRC 1999).
Description of the intervention
The baby's heart rate can be monitored either intermittently (at regular intervals during labour) or continuously (recording the baby's heart rate throughout labour, stopping only briefly, e.g. for visits to the toilet) as follows.
(1) Fetal stethoscope (Pinard) and hand‐held Doppler
Intermittent monitoring can be undertaken either by listening to the baby's heart rate using a fetal stethoscope (Pinard), or with a hand‐held Doppler ultrasound device, and by palpating the mother's uterine contractions by hand. This is known as 'intermittent auscultation'.
(2) Cardiotocograph (CTG)
The baby's heart rate and the mother's uterine contractions can be recorded electronically on a paper trace known as a cardiotocograph. This is done by using a Doppler ultrasound transducer to monitor the baby's heart rate and a pressure transducer to monitor uterine contractions, both of which are linked to a recording machine. This is known as external cardiotocography (external CTG). This is usually undertaken continuously in labour, although occasionally it is used intermittently (intermittent CTG). In most units, external CTG requires the mother to wear a belt across her abdomen while monitoring is being conducted, which restricts her mobility. An alternative means of monitoring the baby's heart rate with the CTG machine is to attach an electrode directly to the baby's presenting part, usually its head. This form of continuous monitoring is known as 'internal CTG' and requires a ruptured amniotic sac (either spontaneously or artificially) and a scalp electrode (clip) attached to the baby's head. This also restricts the woman's mobility.
The term 'electronic fetal monitoring' (EFM) is sometimes used synonymously with CTG monitoring, but is considered to be a less precise term because (1) CTG monitoring also includes monitoring the mother's contractions, and (2) other forms of fetal monitoring might also be classed as 'electronic', e.g. fetal ECG, fetal pulse oximetry.
Intermittent auscultation was the predominant method of monitoring during labour until CTGs became widely used in the latter part of the twentieth century (Enkin 2000). Although there is a lack of empirical evidence on the optimal frequency of intermittent auscultation, there is a consensus in the guidelines from professional bodies that the fetal heart should be auscultated at least every 15 minutes in the first stage of labour and at least every five minutes in the second stage of labour (ACOG 1995; Liston 2002; NCCWCH 2008; RANZCOG 2002) with each auscultation lasting at least 60 seconds (Liston 2002; NCCWCH 2008). It appears that these auscultation protocols were developed initially in the context of clinical trials and were based on 'common sense' rather than research evidence. Compliance with these guidelines, whilst maintaining contemporaneous records, poses a significant challenge for caregivers during labour who usually have multiple tasks to fulfil simultaneously.
Information and interpretation
Both intermittent auscultation and CTG provide information on the baseline heart rate (usually between 110 and 160 beats per minute in the term fetus), accelerations (transient increases in the FHR) and decelerations (transient decreases in the FHR). It is known that some aspects of labour will cause natural alterations in FHR patterns. For example, the baby's sleep FHR pattern is different from the FHR pattern when the baby is awake. External stimuli, like uterine contractions and the mother moving, can cause FHR changes, as can the administration of opiates to the mother. Some of these changes are subtle and can only be detected by continuous CTG, e.g. baseline variability, temporal shape of decelerations. Consideration needs to be given to whether such information improves detection and outcome of those babies who are truly compromised and if there are disadvantages with the technology for those who are not compromised.
Sensitivity and specificity
While specific abnormalities of the FHR pattern on CTG are proposed as being associated with an increased risk of cerebral palsy (Nelson 1996), the specificity of CTG for prediction of cerebral palsy is low with a reported false positive rate as high as 99.8%, even in the presence of multiple late decelerations or decreased variability (Nelson 1996).
FHR pattern recognition, including the relationship between the uterine contractions and FHR decelerations, are fundamental to the use of continuous CTG monitoring. Algorithms have been developed to assess and record what is normal, what requires more careful attention and what is considered abnormal requiring immediate delivery of the baby (NCCWCH 2008). However, CTG traces are often interpreted differently by different caregivers (inter‐observer variation) and even by the same caregiver interpreting the same record at different times (intra‐observer variation) (Devane 2005). Such variation in interpretation of CTG tracings may result in inappropriate interventions, or false reassurance and lack of appropriate intervention. Although we were unable to locate studies that sought to investigate inter‐ and intra‐observer variation in intermittent auscultation, it would seem reasonable to suggest that intermittent auscultation is not immune to similar problems caused by inter‐ and intra‐observer variation. However, given that the FHR parameter of interest in intermittent auscultation is the baseline FHR, it is likely that inter‐ and intra‐observer variation is less in intermittent auscultation than that found in CTG interpretation where other aspects of FHR patterns including variability and assessment and deceleration classification require interpretation.
Additional tests
Fetal blood sampling is a procedure whereby a small amount of blood is taken from the baby, usually from the scalp. Performing fetal blood sampling and then measuring the parameters of acid‐base balance (pH, base excess/deficit, etc) seeks to identify those babies who are truly compromised and need to be born immediately from those who are not truly compromised. It is important to establish the value of this test as an adjunct to CTG. This question is addressed by a subgroup analysis in this review.
Other methods have been considered as additional tests, but there is little evidence to support their use, for example, vibroacoustic stimulation (East 2013). Several other methods of fetal monitoring have been proposed, either as an adjunct or an alternative to CTG, e.g. pulse oximetry (Carbone 1997; East 2007), near‐infrared spectroscopy (Mozurkewich 2000), fetal ECG (Neilson 2012), ST segment analysis of the fetal ECG (Luttkus 2004) and fetal stimulation tests (Skupski 2002).
Possible advantages of CTG
-
More measurable parameters related to FHR patterns (see above).
-
The CTG trace gives a continuous recording of the FHR and uterine activity. This is a physical record, which can be examined at anytime in labour, or subsequently if required. The examples where physical records may be useful include clinical audits, counselling parents if there has been as adverse outcome, and medico‐legal situations.
Possible disadvantages of CTG
-
The complexity of FHR patterns makes standardisation difficult.
-
CTG prevents mobility and restricts the use of massage, different positions and/or immersion in water used to improve comfort, control and coping strategies during labour.
-
Shifting staff focus and resources away from the mother may encourage a belief that all perinatal mortality and neurological injury can be prevented.
Specific situations that may influence the effectiveness or otherwise of CTG
-
Continuous CTG is generally recommended for women who are regarded as being at increased risk of perinatal morbidity and mortality (Liston 2002; NCCWCH 2008; RANZCOG 2002). This review addresses the issue of differential effects of CTG in terms of risk status.
-
Induction of labour is primarily performed where it is anticipated that the outcome for the mother and/or infant would be improved were labour to be induced. Given that induction of labour includes iatrogenic stimulation of uterine activity, which puts the baby at greater risk, we determined to perform a subgroup analysis by induction of labour (RCOG 2001b).
-
Preterm birth is associated with an increased risk of mortality and neurological morbidity and these babies might benefit from being monitored more intensively. Further, there is debate about what is normal for the different parameters of the CTG for preterm infants at varying gestational ages. Therefore, we performed a preterm subgroup analysis.
-
Twin pregnancies carry a higher perinatal mortality rate than singleton pregnancies (RCOG 2001b), thus we conducted a subgroup analysis by twin pregnancy.
Women's and professional views
Some studies looking at women's preferences found that the support that women received from staff and labour companions was more important to them than the type of monitoring used (Garcia 1985; Killien 1989). A more recent study of women's views of routine continuous CTG in labour in the UK identified a lack of discussion about the need for, and appropriateness of CTG. In addition, women felt that CTG limited their mobility and led to an acceptance of the machine's place as the focus of attention for the women and her partner (Munro 2004).
In a synthesis of 11 studies on professionals’ views of monitoring the FHR during labour, Smith 2012 identified that, despite an absence of evidence, maternity care professionals perceive the CTG as offering 'proof' of the compromised baby and that this minimises their exposure to criticism and potential litigation. Nevertheless, professionals also recognised that the CTG offered a false sense of security.
How the intervention might work
Through monitoring FHR changes during labour, it is hoped to identify those babies who may be compromised, or potentially compromised, by a shortage of oxygen (fetal hypoxia). If the shortage of oxygen is both prolonged and severe, babies are at risk of being born with a disability (physical and/or mental), or of dying during labour or shortly thereafter. When alterations in the FHR during labour suggest that the baby is hypoxic, or at risk of hypoxia, additional methods of assessment of fetal well‐being (e.g. fetal blood sampling) may be used. Sometimes FHR alterations trigger delivery by caesarean section or by an instrument such as forceps or vacuum extractor even without recourse to additional diagnostic tests.
Why it is important to do this review
Concerns have been raised about the efficacy and safety of routine use of continuous CTG in labour (Thacker 1995). The apparent contradiction between the widespread use of continuous CTG with claims of its effectiveness in lowering early neonatal mortality and morbidity (Chen 2011) and recommendations to limit its routine use on all women (NCCWCH 2008), indicates that a regular reassessment of this practice is warranted.
Several other Cochrane reviews have addressed other methods for assessing the condition of the fetus during labour including fetal electrocardiogram/ECG (Neilson 2012); fetal pulse oximetry (East 2007); near‐infrared spectroscopy (Mozurkewich 2000) and vibroacoustic stimulation (East 2013). Also, the comparison of cardiotocography versus intermittent auscultation of fetal heart as an admission test on arrival to labour ward is assessed elsewhere (Devane 2012).
Objectives
The objective of this review is to evaluate the effectiveness and safety of continuous cardiotocography (CTG) when used as a method to monitor fetal well‐being during labour.
Methods
Criteria for considering studies for this review
Types of studies
All randomised trials and quasi‐randomised studies comparing continuous CTG during labour, with and without fetal blood sampling, with (a) no fetal monitoring, (b) intermittent auscultation of the fetal heart rate with a Pinard stethoscope or hand‐held Doppler ultrasound device, or (c) intermittent CTG. Sensitivity analysis was undertaken for studies graded as low risk of bias based on sequence generation and allocation concealment. .
Types of participants
Pregnant women in labour and their babies.
Types of interventions
The main intervention of interest is continuous CTG during labour.
For the purpose of this review, the intervention is defined as an attempt to produce a continuous and simultaneous hard‐copy recording of the fetal heart rate and uterine contractions in real‐time throughout the woman's labour. As a guide, continuous CTG should be discontinued only for short periods (for example, visits to the toilet) and the CTG should be used for clinical decision making during labour.
Control groups of interest include: (a) no fetal monitoring, (b) intermittent auscultation of the fetal heart rate with a Pinard stethoscope or hand‐held Doppler ultrasound device, or (c) intermittent CTG.
Types of outcome measures
Primary outcomes
-
Perinatal mortality;
-
seizures in the neonatal period, either apparent clinically or detected by electro‐encephalographic recordings;
-
cerebral palsy;
-
caesarean section;
-
instrumental vaginal birth;
-
cord blood acidosis (low pH/low base excess as defined by trialists; where report included a range of pH values we have used cord pH less than 7.10 as a cut off for acidosis);
-
use of all forms of pharmacological analgesia during labour and birth (including epidural but excluding anaesthesia for caesarean section).
Secondary outcomes
-
Hypoxic ischaemic encephalopathy (as defined by trialists);
-
neurodevelopmental disability assessed at 12 months of age or more. Neurodevelopmental disability, defined as any one or combination of the following: non‐ambulant cerebral palsy, developmental delay, auditory and visual impairment. Development should have been assessed by means of a previously validated tool, such as Bayley Scales of Infant Development (Psychomotor Developmental Index and Mental Developmental Index (Bayley 1993);
-
Apgar less than seven at five minutes;
-
Apgar less than four at five minutes;
-
admission to neonatal special care and/or intensive care unit;
-
fetal blood sampling;
-
damage/infection to baby's head from scalp electrode or fetal blood sampling;
-
caesarean section for abnormal fetal heart rate pattern and/or fetal acidosis;
-
instrumental vaginal birth for abnormal fetal heart rate pattern and/or fetal acidosis;
-
spontaneous vaginal birth not achieved;
-
epidural analgesia;
-
use of non pharmacological methods of coping with labour, e.g. transcutaneous electrical nerve stimulation, hydrotherapy;
-
amniotomy (artificial rupture of membranes);
-
oxytocin during labour;
-
perineal trauma requiring repair (including episiotomy);
-
inability to adopt preferred position during labour;
-
dissatisfaction with labour and/or perceived loss of control during labour;
-
postpartum depression;
-
exclusively breastfeeding at discharge from hospital;
-
length of stay in neonatal special care and/or intensive care unit.
Search methods for identification of studies
Electronic searches
We searched the Cochrane Pregnancy and Childbirth Group’s Trials Register by contacting the Trials Search Co‐ordinator (31 December 2012).
The Cochrane Pregnancy and Childbirth Group’s Trials Register is maintained by the Trials Search Co‐ordinator and contains trials identified from:
-
monthly searches of the Cochrane Central Register of Controlled Trials (CENTRAL);
-
weekly searches of MEDLINE;
-
weekly searches of EMBASE;
-
handsearches of 30 journals and the proceedings of major conferences;
-
weekly current awareness alerts for a further 44 journals plus monthly BioMed Central email alerts.
Details of the search strategies for CENTRAL, MEDLINE and EMBASE, the list of handsearched journals and conference proceedings, and the list of journals reviewed via the current awareness service can be found in the ‘Specialized Register’ section within the editorial information about the Cochrane Pregnancy and Childbirth Group.
Trials identified through the searching activities described above are each assigned to a review topic (or topics). The Trials Search Co‐ordinator searches the register for each review using the topic list rather than keywords.
For details of additional author searches carried out for the 2006 update of this review, please see Appendix 1. We chose not to repeat these additional searches for the update as they yielded no additional studies in the original search.
Searching other resources
We searched the reference lists of retrieved studies.
We did not apply any language restrictions.
Data collection and analysis
For all included studies in this review we have used the methodology described by Higgins 2011. In previous versions of the review, we used the Cochrane methodology current at the time, with Higgins 2008 being used in the 2008 version and Higgins 2005 being used in the 2006 version, see Appendix 2, (Alfirevic 2006).
Selection of studies
Two review authors independently assessed for inclusion all the potential studies we identified as a result of the search strategy. We resolved any disagreement through discussion or, if required, we consulted the third author.
Data extraction and management
We designed a form to extract data. At least two review authors extracted the data using the agreed form. We resolved discrepancies through discussion or, if required, we consulted the third author. Data were entered into Review Manager software (RevMan 2012) and checked for accuracy.
When information regarding any of the above was unclear, we attempted to contact the authors of the original reports to provide further details.
Assessment of risk of bias in included studies
Two review authors independently assessed risk of bias for each included study using the criteria outlined in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011). Any disagreement was resolved by discussion or by involving the third author.
(1) Sequence generation (checking for possible selection bias)
We described, for each included study, the methods used to generate the allocation sequence in sufficient detail to allow an assessment of whether it should produce comparable groups.
We assessed the methods as:
-
low risk of bias (e.g. random number table; computer random number generator);
-
high risk of bias (e.g. odd or even date of birth; hospital or clinic record number);
-
unclear risk of bias.
(2) Allocation concealment (checking for possible selection bias)
We described, for each included study, the method used to conceal the allocation sequence in sufficient detail and determine whether intervention allocation could have been foreseen in advance of, or during recruitment, or changed after assignment.
We assessed the methods as:
-
low risk of bias (e.g. telephone or central randomisation; consecutively numbered sealed opaque envelopes);
-
high risk of bias (e.g. open random allocation; unsealed or non‐opaque envelopes; alternation; date of birth);
-
unclear risk of bias.
(3.1) Blinding (checking for possible performance bias)
We described, for each included study, all the methods used, if any, to blind study participants and personnel from knowledge of which intervention a participant received. We have also provided any information relating to whether the intended blinding was effective. We noted where there has been partial blinding (e.g. where it has not been possible to blind participants but where outcome assessment was carried out without knowledge of group assignment). Where blinding was not possible, we assessed whether the lack of blinding was likely to have introduced bias.
We assessed the methods as:
-
low, high or unclear risk of bias for participants;
-
low, high or unclear risk of bias for personnel;
-
low, high or unclear risk of bias for outcome assessors.
The study was judged to be ‘low risk’ when there was blinding, or where, in our judgement, the outcome or the outcome measurement was not likely to have been influenced by lack of blinding.
(3.2) Blinding of outcome assessment (checking for possible detection bias)
We described for each included study the methods used, if any, to blind outcome assessors from knowledge of which intervention a participant received. We considered that studies were at low risk of bias if they were blinded, or if we judged that the lack of blinding could not have affected the results.
We assessed the methods as:·
-
low risk (no blinding of outcome assessment but the authors judged that the outcome was not likely to be influenced by this);
-
high risk (no blinding of outcome assessment and the outcome measurement was likely to have been influenced by this);
-
unclear risk (insufficient information to permit judgment; the study did not address this).
(4) Incomplete outcome data (checking for possible attrition bias through withdrawals, dropouts, protocol deviations)
We described for each included study the completeness of outcome data for each main outcome, including attrition and exclusions from the analysis. We stated whether attrition and exclusions were reported, the numbers included in the analysis at each stage (compared with the total randomised participants), reasons for attrition or exclusion where reported, and any re‐inclusions in analyses which we undertook.
We assessed the methods as:
-
low risk (e.g. where there were no missing data or where reasons for missing data are balanced across groups);
-
high risk (e.g. where missing data are likely to be related to outcomes or are not balanced across groups, or where high levels of missing data are likely to introduce serious bias or make the interpretation of results difficult);
-
unclear risk of bias (e.g. where there is insufficient reporting of attrition or exclusions to permit a judgement to be made).
(5) Selective reporting bias
We described for each included study how the possibility of selective outcome reporting bias was examined by us and what we found.
We assessed the methods as:
-
low risk of bias (where it is clear that all of the study’s pre‐specified outcomes and all expected outcomes of interest to the review have been reported);
-
high risk of bias (where not all the study’s pre‐specified outcomes have been reported; one or more reported primary outcomes were not pre‐specified; outcomes of interest are reported incompletely and so cannot be used; study fails to include results of a key outcome that would have been expected to have been reported);
-
unclear risk of bias.
(6) Other sources of bias
We described for each included study any important concerns we have about other possible sources of bias. For example, was there a potential source of bias related to the specific study design? Was the trial stopped early due to some data‐dependent process? Was there extreme baseline imbalance? Has the study been claimed to be fraudulent?
We assessed whether each study was free of other problems that could put it at risk of bias:
-
low risk of bias;
-
high risk of bias;
-
unclear risk of bias.
(7) Overall risk of bias
We made explicit judgements about risk of bias for important outcomes both within and across studies. With reference to (1) to (6) above, we assessed the likely magnitude and direction of the bias and whether we considered it was likely to impact on the findings. We explored the impact of the level of bias through undertaking sensitivity analyses ‐ seeSensitivity analysis.
Measures of treatment effect
Dichotomous data
For dichotomous data, we presented the results as risk ratio (RR) with 95% confidence intervals (95% CI).
Continuous data
For continuous data, we presented the results as mean difference (MD) with 95% CI. When pooling data across studies we estimated the MD if the outcomes were measured in the same way between trials. We planned to use standardised mean difference to combine trials that measured the same outcome, but used different methods.
Unit of analysis issues
Cluster‐randomised trials
We have not identified any cluster trials as yet, and do not anticipate any cluster‐randomised trials on this topic. However, should we find any, we will include them using the guidance in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011).
Dealing with missing data
We noted the levels of attrition for included studies. We explored, using sensitivity analysis, the impact of including studies with high levels of missing data in the overall assessment of treatment effect.
Intention‐to‐treat analysis (ITT)
For all outcomes, we analysed the data, as far as possible, on an intention‐to‐treat basis, i.e. we attempted to include all participants randomised to each group in the analyses. The denominator for each outcome in each trial was the number randomised minus any participants whose outcomes are known to be missing ('available case' analysis).
We analysed data on all participants with available data in the group to which they are allocated, regardless of whether or not they received the allocated intervention. If in the original reports participants were not analysed in the group to which they were randomised, and there was sufficient information in the trial report, we attempted to restore them to the correct group.
Assessment of heterogeneity
We assessed statistical heterogeneity in each meta‐analysis using the T², I² and Chi² statistics. We regarded heterogeneity as substantial if I² is greater than 50% and either T² is greater than zero, or there is a low P value (less than 0.10) in the Chi² test for heterogeneity.
Assessment of reporting biases
We investigated reporting biases (such as publication bias) using funnel plots for outcomes with 10 or more studies in the meta‐analysis. We assessed funnel plot asymmetry visually. If asymmetry was suggested by a visual assessment, we planned to perform exploratory analyses to investigate it.
Data synthesis
We only synthesised data where we thought it was appropriate, i.e. where trials were examining similar interventions, with similar populations and methods. We used a fixed‐effect meta‐analysis for combining data. However, where there was clinical or methodological heterogeneity between studies sufficient to suggest that treatment effects might differ between trials, we used random‐effects meta‐analysis.
Subgroup analysis and investigation of heterogeneity
We carried out the following subgroup analyses:
-
high risk for perinatal mortality and morbidity (as defined by trialists) versus low risk (absence of identifiable risk factors associated with increased in perinatal mortality and morbidity as defined by trialists);
-
spontaneous onset of labour versus induction of labour;
-
preterm (less than 37 + 0 weeks) versus term (greater than 37 + 0 weeks);
-
singleton pregnancy versus twin pregnancy;
-
access to fetal blood sampling (FBS) during labour versus no access to FBS during labour;
-
primiparous versus multiparous.
The review’s primary outcomes were used in subgroup analyses.
We assessed subgroup differences by interaction tests available within RevMan (RevMan 2012). We reported the results of subgroup analyses quoting the χ2 statistic and P values, and the interaction test I² value. We assumed a P value of more than 0.05 indicative that subgroup results are no different from the overall effect. If a P value was less than 0.05 we did not automatically assume that the intervention has a different effect, but planned to interpret the findings in the clinical context and in the context of plausibility.
Sensitivity analysis
We carried out sensitivity analyses to explore the effect of trial quality for the primary outcomes in the review. Where there was risk of bias associated with a particular aspect of study quality (e.g. inadequate allocation concealment), this was explored by sensitivity analyses.
Results
Description of studies
Results of the search
Our search strategy identified 383 citations corresponding to 17 studies for potential inclusion. Of those, 13 studies with 37,715 women participating were included (Athens 1993; Copenhagen 1985; Dallas 1986; Denver 1976; Denver 1979; Dublin 1985; Lund 1994; Melbourne 1976; Melbourne 1981; New Delhi 2006; Pakistan 1989; Seattle 1987; Sheffield 1978) and four were excluded (Harare 1994; Ioannina 2001; Manchester 1982; North America 2000).
Included studies
Twelve studies, with 33,681 women participating, compared continuous CTG with intermittent auscultation (Athens 1993; Copenhagen 1985; Dallas 1986; Denver 1976; Denver 1979; Dublin 1985; Melbourne 1976; Melbourne 1981; New Delhi 2006; Pakistan 1989; Seattle 1987; Sheffield 1978). Five studies compared continuous CTG plus fetal blood sampling versus intermittent auscultation (Copenhagen 1985; Dublin 1985; Melbourne 1976; Pakistan 1989; Seattle 1987), six compared continuous CTG without fetal blood sampling versus intermittent auscultation (Athens 1993; Dallas 1986; Denver 1976; Melbourne 1981; New Delhi 2006; Sheffield 1978) and one study had three groups comparing continuous CTG with and without fetal blood sampling versus intermittent auscultation (Denver 1979). One study compared continuous CTG with fetal blood sampling versus intermittent CTG with fetal blood sampling (Lund 1994).
Participants were assessed as being at low risk of complications in three studies (Dallas 1986; Lund 1994; Melbourne 1981) and outcome data for women at low risk were available for one outcome, neonatal seizures, from one other study (Dublin 1985). Participants were assessed as being at high risk of complications in six studies (Denver 1976; Denver 1979; Melbourne 1976; New Delhi 2006; Pakistan 1989; Seattle 1987) including one study that specifically included women in preterm labour (28 to 32 weeks) and assessed outcomes for babies below 1750 g birthweight (Seattle 1987). The data for neonatal seizures in women at high risk of complications were available from one other study (Dublin 1985). Participants were assessed as mixed risk (mixture of women at high risk and low risk of complications) in four studies (Athens 1993; Copenhagen 1985; Dublin 1985; Sheffield 1978).
Five studies had overall caesarean section rates below 10% (Athens 1993; Copenhagen 1985; Dublin 1985; Melbourne 1981; Sheffield 1978). The highest overall caesarean section rates were reported in Pakistan 1989 (23.5%) and New Delhi 2006 (28%).
Excluded studies
Four studies were excluded (see Characteristics of excluded studies).
Risk of bias in included studies
Included studies were assessed for methodological quality on the basis of selection (sequence generation and allocation concealment) and attrition bias (see 'Methods of the review' above) (Figure 1).
Methodological quality summary: review authors' judgements about each methodological quality item for each included study.
Allocation
Allocation concealment was graded as 'low risk of bias' in three trials (Dublin 1985; Lund 1994; Melbourne 1976), as 'unclear risk of bias' in six trials (Copenhagen 1985; Denver 1976; Denver 1979; New Delhi 2006; Seattle 1987; Sheffield 1978), and as 'high risk of bias' in four trials (Athens 1993; Dallas 1986; Melbourne 1981; Pakistan 1989).
Blinding
Blinding of participants and personnel was assessed as 'high risk of bias' in all 13 studies. Blinding of outcome assessment was assessed as 'unclear risk of bias' in all but one study where it was assessed as 'high risk of bias' (Athens 1993).
Incomplete outcome data
Attrition bias was graded as 'low risk of bias' in eight trials (Athens 1993; Copenhagen 1985; Denver 1976; Denver 1979; Dublin 1985; Lund 1994; New Delhi 2006; Pakistan 1989), as unclear risk of bias in three trials (Dallas 1986; Melbourne 1976; ; Sheffield 1978), as high risk of bias in two trials (Melbourne 1981; Seattle 1987).
Selective reporting
This was assessed as 'unclear risk of bias' in all 13 studies as we did not have access to any of the trial protocols.
Other potential sources of bias
All 13 studies were considered at low risk for other potential sources of bias.
Effects of interventions
Continuous cardiotocography (CTG) versus intermittent auscultation (IA) (Comaprisons 1‐8)
A total of 12 randomised trials were included in this comparison with over 33,000 women participating (Athens 1993; Copenhagen 1985; Dallas 1986; Denver 1976; Denver 1979; Dublin 1985; Melbourne 1976; Melbourne 1981; New Delhi 2006; Pakistan 1989; Seattle 1987; Sheffield 1978). Denver 1979 was a three‐arm trial comparing continuous CTG alone, versus continuous CTG plus FBS versus intermittent auscultation.
Primary outcomes
For the infant
There was no significant difference in perinatal mortality between the groups. Risk ratio (RR) was 0.86 with, 95% confidence intervals (CIs) ranging from 0.59 to 1.24, n = 33,513, 11 trials, (Analysis 1.1). The funnel plot analysis indicated no missing studies (Figure 2). The quality of the evidence for this outcome was assessed as moderate (Summary of findings table 1).
Funnel plot of comparison: 1 Continuous CTG versus intermittent auscultation, outcome: 1.1 Perinatal mortality (primary outcome).
The use of continuous CTG monitoring in labour halved the risk of neonatal seizures (RR 0.50, 95% CI 0.31 to 0.80, n = 32,386, nine trials (Analysis 1.2). The funnel plot indicated no missing studies (Figure 3) and the quality of the evidence was assessed as moderate (Summary of findings table 1). This reduction was consistent across the trials and subgroups, although the incidence of neonatal seizures varied considerably between trials. In the two largest trials of 14,618 women (Dallas 1986) and 12,964 women (Dublin 1985), the incidence of neonatal seizures in the intermittent auscultation groups was 0.04% and 0.4% respectively (Analysis 1.2). In the two trials of high quality reporting data for this outcome (Dublin 1985; Melbourne 1976), the risk of neonatal seizures was RR 0.40, 95% CI 0.21 to 0.77 (Analysis 8.2).
Funnel plot of comparison: 1 Continuous CTG versus intermittent auscultation, outcome: 1.2 Neonatal seizures (primary outcome).
There was no difference in the incidence of cerebral palsy (average RR 1.75, 95% CI 0.84 to 3.63, n = 13,252, two trials, random‐effects, (Analysis 1.3). The quality of the evidence was assessed as moderate (Summary of findings table 1). The data on cerebral palsy are heavily influenced by one small trial (Seattle 1987) that randomised only very preterm babies (less than 32 weeks) and assessed outcomes for 173 babies of birthweight less than 1750 g with a cerebral palsy rate of 19.5% in the CTG group compared with 7.7% in the controls (RR 2.54, 95% CI 1.10 to 5.86). The other trial in this comparison (Dublin 1985) showed no significant difference in the incidence of cerebral palsy (RR 1.20, 95% CI 0.52 to 2.79, n = 13,079) with a cerebral palsy rate of 0.18% in the continuously CTG group and 0.15% in the intermittently monitored group.
There was no difference in the incidence of cord blood acidosis between the groups (Analysis 1.6). The quality of the evidence was assessed as very low, mainly due to severe heterogeneity and limitation in design of many of the included studies (Summary of findings table 1).
For the mother
There was a significant increase in the caesarean section rate in the CTG group (average RR 1.63, 95% CI 1.29 to 2.07, 18,861, 11 trials, (Analysis 1.4). However, the quality of this evidence was assessed as low, mainly due to severe heterogeneity and limitation in design of many of the included studies (Summary of findings table 1). Risk difference in the caesarean section rate was 5% (95% CI 2 to 8%), with two‐thirds of the data coming from Dublin 1985, where the overall caesarean section rate was 2.3%. In addition, the funnel plot indicated the possibility of missing studies (Figure 4). It appears that the risk of having a caesarean section was not influenced by the quality of trials (Analysis 8.4, interaction test P = 0.31).
Funnel plot of comparison: 1 Continuous CTG versus intermittent auscultation, outcome: 1.4 Caesarean section (primary outcome).
Although numbers needed to treat to benefit or harm (NNTB/NNTH) analyses remain controversial in the context of meta‐analysis and should be interpreted with caution, we have calculated that there will be one additional caesarean section for every 44 women monitored continuously (95% CI 26 to 96). This calculation is based on the pooled caesarean section rate of 3.6% (337/9313) in the IA group from this meta‐analysis. However, in most settings caesarean section rates are likely to be much higher. Assuming a caesarean section rate with intermittent auscultation of around 15%, there would be an additional CS for every 11 women monitored (95% CI 7 to 23).
Continuous CTG was also associated with an increase in instrumental vaginal birth (Analysis 1.5). The funnel plot indicated that some studies might be missing (Figure 5). The quality of this evidence was assessed as low, mainly due to severe heterogeneity and limitation in design of many of the included studies (Summary of findings table 1). There was no difference identified in the use of any pharmacological analgesia (Analysis 1.7), with the quality of the evidence assessed as low (Summary of findings table 1).
Funnel plot of comparison: 1 Continuous CTG versus intermittent auscultation, outcome: 1.5 Instrumental vaginal birth (primary outcome).
Secondary outcomes
For the infant
There was no evidence of any other benefit or harm for the babies in terms of hypoxic Ischaemic encephalopathy (Analysis 1.8), Apgar scores (Analysis 1.10), or admission to neonatal intensive care unit (Analysis 1.12).
For the mother
Women in the continuous CTG group were more likely to have a caesarean section for abnormal fetal heart rate and/or acidosis (Analysis 1.15) and less likely to have a spontaneous vaginal birth, Analysis 1.17).There was no difference in the use of epidural analgesia (Analysis 1.18). The use of fetal blood sampling was reported in two trials (Copenhagen 1985; Dublin 1985) with significantly more sampling tests performed in the continuous CTG group (Analysis 1.13). There were no reported data suitable for analysis for the use of non‐pharmacological methods for coping with labour, amniotomy, perineal trauma, inability to adopt preferred position in labour, dissatisfaction in labour and postpartum depression.
Overall findings
Notwithstanding the caution regarding NNTB/NNTH calculations, when the risk of neonatal seizures is around 3 per 1,000, 667 women have to be continuously monitored during labour to prevent one such seizure (95% CI 484 to 1667). There is an opposite effect on caesarean section. Assuming a 3.6% caesarean section rate with IA, there would be 15 more caesarean sections in this cohort associated with preventing one neonatal seizure. However, if caesarean section with IA is higher (15%), 61 extra caesarean sections would be associated with preventing one neonatal seizure.
Continuous CTG versus IA (Subgroup: pregnancy risk status ‐ high/low/unclear or both ‐ Comparison 2)
Of the 12 studies that compared continuous CTG with intermittent auscultation, six included women at increased risk of complications (Denver 1976; Denver 1979; Melbourne 1976; New Delhi 2006; Pakistan 1989; Seattle 1987), three included women at low risk of complications (Dallas 1986; Melbourne 1981; Sheffield 1978) and three studies included both groups of women or did not specify (Athens 1993; Copenhagen 1985; Dublin 1985). There was a significant difference in the impact of CTG monitoring on caesarean section rate depending on the risk status of women (P = 0.004; I2 = 81.6%), although the heterogeneity can be attributed to the group with combined risk rather than to the subgroups where the risk was clearly defined. There were no other statistically significant differences between the subgroups for any other primary outcomes.
Subgroups analysis by onset of labour (spontaneous/induced/unclear or both ‐ Comparison 3)
None of the included trials provided separate data for spontaneous and induced labours. Hence, there is no information to determine if there might be a difference in the impact of CTG for women in spontaneous labour compared with those with induction of labour.
Subgroup analysis by gestational age (preterm/term/unclear or both ‐ Comparison 4)
Of the 12 studies that compared continuous CTG with intermittent auscultation, one included only preterm labours (Seattle 1987). Three studies included only term labours (Copenhagen 1985; Melbourne 1981; Sheffield 1978) and eight studies included both or did not specify (Athens 1993; Dallas 1986; Denver 1979; Denver 1979; Dublin 1985; Melbourne 1976; New Delhi 2006; Pakistan 1989). We found no evidence of a difference between the subgroups.
Subgroup analysis by number of babies being monitored (singleton/twin pregnancy/unclear or both ‐ Comparison 5)
Eight studies included only singleton pregnancies (Athens 1993; Dallas 1986; Denver 1976; Melbourne 1981; New Delhi 2006; Pakistan 1989; Seattle 1987; Sheffield 1978) and four included both singleton and twin pregnancies or did not specify (Copenhagen 1985; Denver 1979; Dublin 1985; Melbourne 1976). There was a significant subgroup effect for the rate of neonatal acidosis (P = 0.04; I2 = 77%) with more acidosis in CTG monitored singletons and less in CTG monitored twins. There was also a subgroup difference in the use of pharmacological analgesia (P = 0.02; I2 = 83%), but the data were only available for singletons and mixed group with no data for twins only. There were no subgroup difference for the other primary outcome.
Subgroup analysis by access to fetal blood sampling (FBS) during labour (Comparison 6)
Six studies offered FBS alongside the CTG (Copenhagen 1985; Dublin 1985; Melbourne 1976; Melbourne 1981; Pakistan 1989; Seattle 1987), five studies did not use FBS (Athens 1993; Dallas 1986; Denver 1976; New Delhi 2006; Sheffield 1978) and one study randomised to three groups, CTG with FBS, CTG alone and IA (Denver 1979).
There was a significant subgroup effect on instrumental vaginal birth with apparently more instrumental deliveries (P = 0.04; I2 = 77%), but less neonatal acidosis (P = 0.04; I2 = 76.5%), in the FBS subgroup. However, there were no subgroup differences for the other primary outcomes.
Subgroups by parity (primiparous/multiparous women/unclear or both ‐ Comparison 7)
None of the studies included only primiparous women, one study included only multiparous women (New Delhi 2006) and 11 studies included both primiparous and multiparous women (Athens 1993; Copenhagen 1985; Dallas 1986; Denver 1976; Denver 1979; Dublin 1985; Melbourne 1976; Melbourne 1981; Pakistan 1989; Seattle 1987; Sheffield 1978). As only one of these studies reported results based on the parity of the women involved, so it was no possible to perform a meaningful subgroup analysis.
Continuous CTG versus IA (Subgroup: high/low/unclear quality of studies ‐ Comparison 8)
Of the 12 studies that compared continuous CTG with intermittent auscultation, two were considered to be of high methodological quality (Dublin 1985; Melbourne 1976), four studies where considered to be of low methodological quality (Athens 1993; Dallas 1986; Melbourne 1981; Pakistan 1989) and for six studies the methodological quality was unclear (Copenhagen 1985; Denver 1976; Denver 1979; New Delhi 2006; Seattle 1987; Sheffield 1978). It appears that in a high‐quality trial, there was less neonatal acidosis compared with low‐quality trials (P = 0.04; I2 = 76.5%). There was a significant subgroup heterogeneity for instrumental vaginal birth (P = 0.007; I2 = 79.9%), but no clear difference between high‐ and low‐risk subgroups. We found no other subgroups differences for the other primary outcomes.
Continuous CTG versus intermittent CTG (Comparison 9)
Lund 1994 involved 4044 high‐risk pregnant women and found no significant differences in any of the eight outcomes specified in this meta‐analysis.
Discussion
Summary of main results
The main reason for the introduction of continuous intrapartum cardiotocography (CTG) monitoring in clinical practice was a belief that it would reduce rare but devastating outcomes ‐ perinatal death and neonatal hypoxic brain injury in otherwise healthy babies. However, this review found no statistically significant difference in perinatal deaths between pregnancies monitored during labour with continuous CTG compared to those monitored those intermittent auscultation. The overall quality of evidence that underpins this conclusion has been judged as 'moderate' (Summary of findings table 1). It does, however, seem unrealistic to expect that any intrapartum intervention in modern maternity care will result in a statistically significant improvement in perinatal deaths. In order for a trial to test a realistic hypothesis that continuous CTG can prevent one death in one thousand births (0.1%), more than 50,000 women would have to be randomised. It is, therefore, more logical to concentrate on short‐ and long‐term childhood morbidity. Unfortunately, very few clinically relevant neonatal outcomes have been reported consistently in all trials.
For decades, low Apgar scores have been used as a surrogate measure for birth asphyxia and subsequent adverse neurodevelopmental outcomes. Recent evidence has confirmed a strong association between low Apgar score and cerebral palsy in both low and normal birthweight infants (Lie 2010). This review found no evidence that use of continuous intrapartum CTG monitoring has an impact on Apgar score. However, there were very few babies with clinically significant low Apgar scores in studies that assessed this outcome. Therefore, potentially important differences between the two groups cannot be ruled out.
Hypoxic ischaemic encephalopathy, a more robust measure of hypoxic brain injury, was only reported in one study (Athens 1993). In the absence of any meaningful long‐term follow‐up data, the impact of continuous CTG monitoring on a neonate can only be evaluated based on the data from two clinically important outcomes, i.e. neonatal seizures and cerebral palsy.
For both neonatal seizures and cerebral palsy, the majority of data are provided by Dublin 1985. At first glance, the data appear contradictory. There is a significant reduction in neonatal seizures in the continuous CTG group, but no impact on cerebral palsy. If anything, the rates of cerebral palsy appear to be higher in the continuous CTG group, although the pooled result did not reach statistical significance. This apparent increase in cerebral palsy in children monitored by CTG comes from Seattle 1987. However, the results from this study, the only study of CTG monitoring during preterm labour, are not statistically significant using 99% confidence intervals. In addition, this study excluded infants with a birthweight of more than 1750 grams (34% of randomised cohort) which may be a source of bias. Given that all other outcomes in this trial, including caesarean section rates, neonatal seizures and deaths were almost identical this may have been a chance finding and should be interpreted with caution.
It is now generally accepted that cerebral palsy is more often caused by antepartum, rather than intrapartum, events (Palmer 1995). It may, therefore, be unrealistic to expect that intrapartum interventions will have the capacity to achieve a significant reduction in cerebral palsy. There are, clearly, some cases of cerebral palsy that are a direct consequence of intrapartum hypoxic injury. These cases are very rare, and even systematic reviews of randomised trials are unlikely to have sufficient power to test intrapartum CTG as a method to reduce cerebral palsy caused by acute and avoidable intrapartum events.
The reduction in seizures associated with continuous CTG monitoring is important, but has to be interpreted cautiously in the absence of good quality long‐term follow‐up data. It has been suggested that seizures may be a "sentinel event" of a peripartum adversity that does not necessarily always manifest itself as hypoxic encephalopathy (Dennis 1978; Derham 1985, Keegan 1985; Lien 1995; Spellacy 1985). When asphyxia, infection, brain malformations and metabolic causes are excluded, some neonatal seizures are associated with cerebral infarction or neonatal stroke (Estan 1997; Lien 1995). Although the underlying causes are not well understood, neonatal seizures may have long‐term consequences other than cerebral palsy. One longitudinal study found that some babies who had neonatal seizures were classified as normal at five years and had normal overall intelligence in adolescence as assessed by IQ tests, but had some abnormal results on detailed neuropsychological testing (Temple 1995). Clearly, there is a need for comprehensive long‐term follow‐up of the randomised cohorts that is not limited to extreme adverse outcomes such as cerebral palsy, but also includes more subtle neuropsychological assessment.
The results of this review demonstrate that continuous CTG monitoring leads to an increase in caesarean sections. Such an effect of continuous CTG is clinically plausible as CTG monitoring leads to more interventions (e.g. fetal blood sampling, amniotomy) and more diagnoses of presumed fetal compromise for which emergency caesarean section is seen as the only safe management option. However, the overall quality of evidence for this outcome was judged as 'low' (Summary of findings table 1) and, therefore, the observed increase has to be interpreted cautiously. It is noteworthy that size and direction of the effect on caesarean section was consistent for pre‐specified subgroups, including high quality trials and trials where clinicians had access to intrapartum fetal blood sampling. Subgroup interaction test was only significant (I2 = 81.6%) for studies in low‐risk, high‐risk and mixed‐risk status, but the heterogeneity comes from a mixed group. The impact of CTG monitoring on caesarean section in low‐risk and high‐risk populations appears to be virtually identical, which is contrary to recommendations from many professional bodies providing guidance on intrapartum fetal monitoring.
There was some evidence that labour was more painful in the continuous CTG group, but the statistically significant increase in the 'need for any analgesia' included general anaesthesia. It is, therefore, likely that this difference was caused by an increase in the number of caesarean sections, rather than necessarily more painful labour. Women do report more pain when lying on their backs during labour. At the times when the studies in this review were undertaken (between 1976 and 1994), women in the intermittent auscultation group may well also have been on their backs and not using mobility and positions to help them with their labours. There were no data from the trials included in the review to allow any analysis of this potential confounder.
We have prespecified several subgroups that could have been expected to influence the direction and size of the differences compared with results when all trials are considered together. We were conscious that any differences between subgroups and overall results would have to be interpreted with extreme caution (Rothwell 2005). With this proviso, we found no subgroup differences of clinical importance, but the number of trials and women in subgroups was relatively small.
Overall completeness and applicability of evidence
Clearly, the lack of long‐term follow‐up data and inadequate reporting of the data according to the clinically important subgroups is regrettable and limits the applicability of the evidence.
Quality of the evidence
The overall quality of the evidence can be best described as low to moderate and has been summarised in the Summary of findings table 1.
Potential biases in the review process
Our selection of outcomes in general and primary outcomes in particular might have been influenced by our knowledge of the published literature and the first Cochrane review on this topic (Thacker 2001).
Agreements and disagreements with other studies or reviews
Some large cohort studies suggest much more profound benefit on neonatal morbidity and mortality (Chen 2011). Some observational data also suggest the benefit of fetal blood sampling during labour in cases of suboptimal CTG, (Stein 2006) but we found no evidence that the increase in caesarean section rate was greater if fetal blood sampling was unavailable; nor did access to fetal blood sampling influence the difference in neonatal seizures or any other prespecified outcome.
Methodological quality summary: review authors' judgements about each methodological quality item for each included study.
Funnel plot of comparison: 1 Continuous CTG versus intermittent auscultation, outcome: 1.1 Perinatal mortality (primary outcome).
Funnel plot of comparison: 1 Continuous CTG versus intermittent auscultation, outcome: 1.2 Neonatal seizures (primary outcome).
Funnel plot of comparison: 1 Continuous CTG versus intermittent auscultation, outcome: 1.4 Caesarean section (primary outcome).
Funnel plot of comparison: 1 Continuous CTG versus intermittent auscultation, outcome: 1.5 Instrumental vaginal birth (primary outcome).
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 1 Perinatal mortality (primary outcome).
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 2 Neonatal seizures (primary outcome).
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 3 Cerebral palsy (primary outcome).
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 4 Caesarean section (primary outcome).
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 5 Instrumental vaginal birth (primary outcome).
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 6 Cord blood acidosis (primary outcome).
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 7 Any pharmacological analgesia (primary outcome).
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 8 Hypoxic ischaemic encephalopathy.
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 9 Neurodevelopmental disability at at least 12 months of age.
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 10 Apgar score < 7 at 5 minutes.
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 11 Apgar score < 4 at 5 minutes.
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 12 Neonatal ICU admissions.
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 13 Fetal blood sampling.
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 14 Damage/infection from scalp electrode or scalp sampling.
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 15 Caesarean section for abnormal FHR pattern and/or acidosis.
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 16 Instrumental vaginal birth for abnormal CTG or fetal acidosis.
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 17 Spontaneous vaginal birth.
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 18 Epidural analgesia.
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 21 Oxytocin during 1st and/or 2nd stage of labour.
Comparison 1 Continuous CTG versus intermittent auscultation, Outcome 27 Length of stay on NICU.
Comparison 2 Continuous CTG versus IA (pregnancy risk status ‐ high/low), Outcome 1 Perinatal mortality.
Comparison 2 Continuous CTG versus IA (pregnancy risk status ‐ high/low), Outcome 2 Neonatal seizures.
Comparison 2 Continuous CTG versus IA (pregnancy risk status ‐ high/low), Outcome 3 Cerebral palsy.
Comparison 2 Continuous CTG versus IA (pregnancy risk status ‐ high/low), Outcome 4 Caesarean section.
Comparison 2 Continuous CTG versus IA (pregnancy risk status ‐ high/low), Outcome 5 Instrumental vaginal birth.
Comparison 2 Continuous CTG versus IA (pregnancy risk status ‐ high/low), Outcome 6 Cord blood acidosis.
Comparison 2 Continuous CTG versus IA (pregnancy risk status ‐ high/low), Outcome 7 Any pharmacological analgesia.
Comparison 3 Continuous CTG versus IA (onset of labour ‐ spontaneous/induced), Outcome 1 Perinatal mortality.
Comparison 3 Continuous CTG versus IA (onset of labour ‐ spontaneous/induced), Outcome 2 Neonatal seizures.
Comparison 3 Continuous CTG versus IA (onset of labour ‐ spontaneous/induced), Outcome 3 Cerebral palsy.
Comparison 3 Continuous CTG versus IA (onset of labour ‐ spontaneous/induced), Outcome 4 Caesarean section.
Comparison 3 Continuous CTG versus IA (onset of labour ‐ spontaneous/induced), Outcome 5 Instrumental vaginal birth.
Comparison 3 Continuous CTG versus IA (onset of labour ‐ spontaneous/induced), Outcome 6 Cord blood acidosis.
Comparison 3 Continuous CTG versus IA (onset of labour ‐ spontaneous/induced), Outcome 7 Any pharmacological analgesia.
Comparison 4 Continuous CTG versus IA (preterm/term labour), Outcome 1 Perinatal mortality.
Comparison 4 Continuous CTG versus IA (preterm/term labour), Outcome 2 Neonatal seizures.
Comparison 4 Continuous CTG versus IA (preterm/term labour), Outcome 3 Cerebral palsy.
Comparison 4 Continuous CTG versus IA (preterm/term labour), Outcome 4 Caesarean section.
Comparison 4 Continuous CTG versus IA (preterm/term labour), Outcome 5 Instrumental vaginal birth.
Comparison 4 Continuous CTG versus IA (preterm/term labour), Outcome 6 Cord blood acidosis.
Comparison 4 Continuous CTG versus IA (preterm/term labour), Outcome 7 Any pharmacological analgesia.
Comparison 5 Continuous CTG versus IA (singleton/twin pregnancy), Outcome 1 Perinatal mortality.
Comparison 5 Continuous CTG versus IA (singleton/twin pregnancy), Outcome 2 Neonatal seizures.
Comparison 5 Continuous CTG versus IA (singleton/twin pregnancy), Outcome 3 Cerebral palsy.
Comparison 5 Continuous CTG versus IA (singleton/twin pregnancy), Outcome 4 Caesarean section.
Comparison 5 Continuous CTG versus IA (singleton/twin pregnancy), Outcome 5 Instrumental vaginal birth.
Comparison 5 Continuous CTG versus IA (singleton/twin pregnancy), Outcome 6 Cord blood acidosis.
Comparison 5 Continuous CTG versus IA (singleton/twin pregnancy), Outcome 7 Any pharmacological analgesia.
Comparison 6 Continuous CTG versus IA (access to FBS during labour ‐ yes/no), Outcome 1 Perinatal mortality.
Comparison 6 Continuous CTG versus IA (access to FBS during labour ‐ yes/no), Outcome 2 Neonatal seizures.
Comparison 6 Continuous CTG versus IA (access to FBS during labour ‐ yes/no), Outcome 3 Cerebral palsy.
Comparison 6 Continuous CTG versus IA (access to FBS during labour ‐ yes/no), Outcome 4 Caesarean section.
Comparison 6 Continuous CTG versus IA (access to FBS during labour ‐ yes/no), Outcome 5 Instrumental vaginal birth.
Comparison 6 Continuous CTG versus IA (access to FBS during labour ‐ yes/no), Outcome 6 Cord blood acidosis.
Comparison 6 Continuous CTG versus IA (access to FBS during labour ‐ yes/no), Outcome 7 Any pharmacological analgesia.
Comparison 7 Continuous CTG versus IA (primiparous/multiparous women), Outcome 1 Perinatal mortality.
Comparison 7 Continuous CTG versus IA (primiparous/multiparous women), Outcome 2 Neonatal seizures.
Comparison 7 Continuous CTG versus IA (primiparous/multiparous women), Outcome 3 Cerebral palsy.
Comparison 7 Continuous CTG versus IA (primiparous/multiparous women), Outcome 4 Caesarean section.
Comparison 7 Continuous CTG versus IA (primiparous/multiparous women), Outcome 5 Instrumental vaginal birth.
Comparison 7 Continuous CTG versus IA (primiparous/multiparous women), Outcome 6 Cord blood acidosis.
Comparison 7 Continuous CTG versus IA (primiparous/multiparous women), Outcome 7 Any pharmacological analgesia.
Comparison 8 Continuous CTG versus IA (high‐quality studies vs lower‐quality studies), Outcome 1 Perinatal mortality.
Comparison 8 Continuous CTG versus IA (high‐quality studies vs lower‐quality studies), Outcome 2 Neonatal seizures.
Comparison 8 Continuous CTG versus IA (high‐quality studies vs lower‐quality studies), Outcome 3 Cerebral palsy.
Comparison 8 Continuous CTG versus IA (high‐quality studies vs lower‐quality studies), Outcome 4 Caesarean section.
Comparison 8 Continuous CTG versus IA (high‐quality studies vs lower‐quality studies), Outcome 5 Instrumental vaginal birth.
Comparison 8 Continuous CTG versus IA (high‐quality studies vs lower‐quality studies), Outcome 6 Cord blood acidosis.
Comparison 8 Continuous CTG versus IA (high‐quality studies vs lower‐quality studies), Outcome 7 Any pharmacological analgesia.
Comparison 9 Continuous CTG versus intermittent CTG, Outcome 4 Caesarean section (primary outcome).
Comparison 9 Continuous CTG versus intermittent CTG, Outcome 5 Instrumental vaginal birth (primary outcome).
Comparison 9 Continuous CTG versus intermittent CTG, Outcome 6 Cord blood acidosis (primary outcome).
Comparison 9 Continuous CTG versus intermittent CTG, Outcome 10 Apgar score < 7 at 5 minutes.
Comparison 9 Continuous CTG versus intermittent CTG, Outcome 12 Neonatal ICU admissions.
Comparison 9 Continuous CTG versus intermittent CTG, Outcome 15 Caesarean section for abnormal FHR pattern and/or acidosis.
Comparison 9 Continuous CTG versus intermittent CTG, Outcome 17 Spontaneous vaginal birth.
Comparison 9 Continuous CTG versus intermittent CTG, Outcome 18 Epidural analgesia.
| Continuous CTG versus intermittent auscultation for fetal assessment during labour | ||||||
| Patient or population: Women undergoing fetal assessment during labour | ||||||
| Outcomes | Illustrative comparative risks* (95% CI) | Relative effect | No of Participants | Quality of the evidence | Comments | |
| Assumed risk | Corresponding risk | |||||
| Control | Continuous CTG versus intermittent auscultation | |||||
| Perinatal mortality (primary outcome) | Study population | RR 0.86 | 33513 | ⊕⊕⊝⊝ | ||
| 3 per 1000 | 3 per 1000 | |||||
| Moderate | ||||||
| 4 per 1000 | 3 per 1000 | |||||
| Neonatal seizures (primary outcome) | Study population | RR 0.5 | 32386 | ⊕⊕⊕⊝ | ||
| 3 per 1000 | 1 per 1000 | |||||
| Moderate | ||||||
| 4 per 1000 | 2 per 1000 | |||||
| Cerebral palsy (primary outcome) | Study population | RR 1.75 | 13252 | ⊕⊕⊝⊝ | ||
| 3 per 1000 | 4 per 1000 | |||||
| Moderate | ||||||
| 39 per 1000 | 68 per 1000 | |||||
| Caesarean section (primary outcome) | Study population | RR 1.63 | 18861 | ⊕⊕⊝⊝ | ||
| 36 per 1000 | 59 per 1000 | |||||
| Moderate | ||||||
| 66 per 1000 | 108 per 1000 | |||||
| Instrumental vaginal birth (primary outcome) | Study population | RR 1.15 | 18615 | ⊕⊕⊝⊝ | ||
| 102 per 1000 | 118 per 1000 | |||||
| Moderate | ||||||
| 222 per 1000 | 255 per 1000 | |||||
| Cord blood acidosis (primary outcome) | Study population | RR 0.92 | 2494 | ⊕⊝⊝⊝ | ||
| 24 per 1000 | 22 per 1000 | |||||
| Moderate | ||||||
| 24 per 1000 | 22 per 1000 | |||||
| Any pharmacological analgesia (primary outcome) | Study population | RR 0.98 | 1677 | ⊕⊕⊝⊝ | ||
| 754 per 1000 | 739 per 1000 | |||||
| Moderate | ||||||
| 805 per 1000 | 789 per 1000 | |||||
| *The basis for the assumed risk (e.g. the median control group risk across studies) is provided in footnotes. The corresponding risk (and its 95% confidence interval) is based on the assumed risk in the comparison group and the relative effect of the intervention (and its 95% CI). | ||||||
| GRADE Working Group grades of evidence | ||||||
| 1 Limitations in design: Most of the pooled effect provided by studies “B” or “C” without a substantial proportion (i.e. < 40% (actual 33% weight) from studies “C”. | ||||||
| Method | Description |
| Fetal stethoscope (Pinard) ‐ for intermittent monitoring (IA) | This is a trumpet‐shaped device, which is placed on the mother's abdomen and the caregiver listens for the heart beat at the other end. This is a simple instrument of relatively low cost. |
| Hand‐held Doppler ultrasound monitor ‐ for intermittent monitoring (IA) | The device is placed on the mother's abdomen with gel smeared on the underside of the ultrasound transducer. This allows the ultrasound beam to travel from the fetal heart to the transducer without interruption. |
| External cardiotocography ‐ for continuous or intermittent monitoring | The fetal heart rate and the activity of the uterine muscle are detected by two transducers placed on the mother's abdomen (one above the fetal heart and the other at the fundus). Doppler ultrasound provides the information which is recorded on a paper strip known as a cardiotocograph (CTG). |
| Internal cardiotocography ‐ for continuous monitoring | An electrode is placed directly on the baby's presenting part to detect the fetal ECG signal. Again the signals are recorded on a paper strip (CTG). This method can only be used if membranes (fore‐waters) have ruptured either spontaneously or artificially. |
| Study | 1 carer to 1 woman | Induction | ARM | Oxytocin | Mobility | Birth positions | Women's views | Social context | Experience of staff |
| Yes | Induction ‐ 11% overall | No information | Augmentation ‐ 46% overall | No mobility ‐ all women with IV line inserted | Semi‐Fowler or lateral | No information | No information | IA standard practice, EFM intensive training provided | |
| No information | No information | No information | No information | EFM only applied when women no longer wished to walk around. | No information | No information | No information | No information | |
| 2 women : 1 nurse | Excluded women whose labours were induced | No information | Excluded women | No information | No information | No information | No information | No information | |
| IA: yes CTG: no information | Included women whose labours were induced | No information | Included women given oxytocin for augmentation | No information | No information | No information | No information | No information | |
| Yes | No specific information | No information | 29% of women given oxytocin for augmentation | No information | No information | No information | No information | No information | |
| Yes | Included women whose labours were induced | ARM within an hour of admission to check liquor | 23% of women given oxytocin for augmentation | IA, probably more mobile | No information | Women's views sought and published separately. | No information | No information | |
| No information | Included women whose labours were induced | No information | 48% of women were given ocytocin for induction or acceleration | Women in CTG group offered telemetry if wished mobility | No information | No information | No information | No information | |
| No information | Induction ‐ 42% overall | No information | 63% of women given oxytocin in labour | No information | No information | No information | No information | Exp staff. | |
| No information | No information | ARM when in established labour or for obstetric reasons | No information | No information | No information | No information | No information | No information | |
| No information | No information | No information | No information | No information | No information | No information | No information | No information | |
| No information | No information | No information | No information | No information | No information | No information | No information | No information | |
| Yes | No information | ARM at 7 cm unless clinically indicated prior to 7 cm | Included women given oxytocin | No information | No information | Women's views sought and published separately. | No information | No information | |
| No information | Included women whose labours were induced | Augmentation with ARM alone or in combination with oxytocin if progress fell below nomogram. | Oxytocin was administered to all women as indicated | No information | No information | No information | No information | No information | |
| ARM: artificial rupture of membranes | |||||||||
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Perinatal mortality (primary outcome) Show forest plot | 11 | 33513 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.86 [0.59, 1.24] |
| 2 Neonatal seizures (primary outcome) Show forest plot | 9 | 32386 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.50 [0.31, 0.80] |
| 3 Cerebral palsy (primary outcome) Show forest plot | 2 | 13252 | Risk Ratio (M‐H, Random, 95% CI) | 1.75 [0.84, 3.63] |
| 4 Caesarean section (primary outcome) Show forest plot | 11 | 18861 | Risk Ratio (M‐H, Random, 95% CI) | 1.63 [1.29, 2.07] |
| 5 Instrumental vaginal birth (primary outcome) Show forest plot | 10 | 18615 | Risk Ratio (M‐H, Random, 95% CI) | 1.15 [1.01, 1.33] |
| 6 Cord blood acidosis (primary outcome) Show forest plot | 2 | 2494 | Risk Ratio (M‐H, Random, 95% CI) | 0.92 [0.27, 3.11] |
| 7 Any pharmacological analgesia (primary outcome) Show forest plot | 3 | 1677 | Risk Ratio (M‐H, Random, 95% CI) | 0.98 [0.88, 1.09] |
| 8 Hypoxic ischaemic encephalopathy Show forest plot | 1 | 1428 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.46 [0.04, 5.03] |
| 9 Neurodevelopmental disability at at least 12 months of age Show forest plot | 1 | 173 | Risk Ratio (M‐H, Fixed, 95% CI) | 3.88 [0.83, 18.17] |
| 10 Apgar score < 7 at 5 minutes Show forest plot | 6 | 4137 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.95 [0.71, 1.27] |
| 11 Apgar score < 4 at 5 minutes Show forest plot | 3 | 1919 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.80 [0.71, 4.59] |
| 12 Neonatal ICU admissions Show forest plot | 10 | 33167 | Risk Ratio (M‐H, Random, 95% CI) | 1.01 [0.86, 1.18] |
| 13 Fetal blood sampling Show forest plot | 2 | 13929 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.24 [1.05, 1.47] |
| 14 Damage/infection from scalp electrode or scalp sampling Show forest plot | 1 | 200 | Risk Ratio (M‐H, Fixed, 95% CI) | 3.0 [0.12, 72.77] |
| 15 Caesarean section for abnormal FHR pattern and/or acidosis Show forest plot | 11 | 33379 | Risk Ratio (M‐H, Fixed, 95% CI) | 2.38 [1.89, 3.01] |
| 16 Instrumental vaginal birth for abnormal CTG or fetal acidosis Show forest plot | 1 | 12964 | Risk Ratio (M‐H, Fixed, 95% CI) | 2.54 [1.95, 3.31] |
| 17 Spontaneous vaginal birth Show forest plot | 11 | 18861 | Risk Ratio (M‐H, Random, 95% CI) | 0.91 [0.86, 0.96] |
| 18 Epidural analgesia Show forest plot | 8 | 17630 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.00 [0.90, 1.12] |
| 19 Use of non pharmacological methods of coping with labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 20 Amniotomy | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 21 Oxytocin during 1st and/or 2nd stage of labour Show forest plot | 5 | 3683 | Risk Ratio (M‐H, Random, 95% CI) | 1.08 [0.86, 1.37] |
| 22 Perineal trauma needing repair | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 23 Inability to adopt preferred position in labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 24 Dissatisifaction with labour and/or perceived loss of control | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 25 Postpartum depression | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 26 Exclusive breastfeeding at discharge | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 27 Length of stay on NICU Show forest plot | 1 | 206 | Mean Difference (IV, Fixed, 95% CI) | 0.20 [‐1.17, 1.57] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Perinatal mortality Show forest plot | 11 | 33513 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.86 [0.59, 1.24] |
| 1.1 High risk | 5 | 1974 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.04 [0.62, 1.74] |
| 1.2 Low risk | 3 | 16049 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.87 [0.29, 2.58] |
| 1.3 Risk status ‐ mixed or not specified | 3 | 15490 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.68 [0.38, 1.24] |
| 2 Neonatal seizures Show forest plot | 9 | 32386 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.50 [0.31, 0.80] |
| 2.1 High risk | 5 | 4805 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.67 [0.36, 1.24] |
| 2.2 Low risk | 3 | 25175 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.36 [0.16, 0.79] |
| 2.3 Risk status ‐ mixed or not specified | 2 | 2406 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.18 [0.01, 3.80] |
| 3 Cerebral palsy Show forest plot | 2 | 13252 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.74 [0.97, 3.11] |
| 3.1 High risk | 1 | 173 | Risk Ratio (M‐H, Fixed, 95% CI) | 2.54 [1.10, 5.86] |
| 3.2 Low risk | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 3.3 Risk status ‐ mixed or not specified | 1 | 13079 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.20 [0.52, 2.79] |
| 4 Caesarean section Show forest plot | 11 | 18861 | Risk Ratio (M‐H, Random, 95% CI) | 1.63 [1.29, 2.07] |
| 4.1 High risk | 6 | 2069 | Risk Ratio (M‐H, Random, 95% CI) | 1.91 [1.39, 2.61] |
| 4.2 Low risk | 2 | 1431 | Risk Ratio (M‐H, Random, 95% CI) | 2.06 [1.24, 3.45] |
| 4.3 Risk status ‐ mixed or not specified | 3 | 15361 | Risk Ratio (M‐H, Random, 95% CI) | 1.14 [0.95, 1.36] |
| 5 Instrumental vaginal birth Show forest plot | 10 | 18615 | Risk Ratio (M‐H, Random, 95% CI) | 1.15 [1.01, 1.33] |
| 5.1 High risk | 5 | 1823 | Risk Ratio (M‐H, Random, 95% CI) | 1.02 [0.82, 1.27] |
| 5.2 Low risk | 2 | 1431 | Risk Ratio (M‐H, Random, 95% CI) | 1.09 [0.77, 1.54] |
| 5.3 Risk status ‐ mixed or not specified | 3 | 15361 | Risk Ratio (M‐H, Random, 95% CI) | 1.33 [1.20, 1.49] |
| 6 Cord blood acidosis Show forest plot | 2 | 2494 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.16 [0.72, 1.89] |
| 6.1 High risk | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 6.2 Low risk | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 6.3 Risk status ‐ mixed or not specified | 2 | 2494 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.16 [0.72, 1.89] |
| 7 Any pharmacological analgesia Show forest plot | 3 | 1677 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.93, 1.04] |
| 7.1 High risk | 2 | 1173 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.01 [0.96, 1.06] |
| 7.2 Low risk | 1 | 504 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.92 [0.79, 1.07] |
| 7.3 Risk status ‐ mixed or not specified | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Perinatal mortality Show forest plot | 11 | 33513 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.86 [0.59, 1.24] |
| 1.1 Spontaneous labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 1.2 Induction of labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 1.3 Onset of labour ‐ not specified | 11 | 33513 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.86 [0.59, 1.24] |
| 2 Neonatal seizures Show forest plot | 9 | 32386 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.50 [0.31, 0.80] |
| 2.1 Spontaneous labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 2.2 Induction of labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 2.3 Onset of labour ‐ not specified | 9 | 32386 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.50 [0.31, 0.80] |
| 3 Cerebral palsy Show forest plot | 2 | 13252 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.74 [0.97, 3.11] |
| 3.1 Spontaneous labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 3.2 Induction of labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 3.3 Onset of labour ‐ not specified | 2 | 13252 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.74 [0.97, 3.11] |
| 4 Caesarean section Show forest plot | 11 | 18861 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.43 [1.25, 1.64] |
| 4.1 Spontaneous labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 4.2 Induction of labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 4.3 Onset of labour ‐ not specified | 11 | 18861 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.43 [1.25, 1.64] |
| 5 Instrumental vaginal birth Show forest plot | 10 | 18615 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.21 [1.12, 1.31] |
| 5.1 Spontaneous labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 5.2 Induction of labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 5.3 Onset of labour ‐ not specified | 10 | 18615 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.21 [1.12, 1.31] |
| 6 Cord blood acidosis Show forest plot | 2 | 2494 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.16 [0.72, 1.89] |
| 6.1 Spontaneous labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 6.2 Induction of labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 6.3 Onset of labour ‐ not specified | 2 | 2494 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.16 [0.72, 1.89] |
| 7 Any pharmacological analgesia Show forest plot | 3 | 1677 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.93, 1.04] |
| 7.1 Spontaneous labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 7.2 Induction of labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 7.3 Onset of labour ‐ not specified | 3 | 1677 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.93, 1.04] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Perinatal mortality Show forest plot | 11 | 33513 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.86 [0.59, 1.24] |
| 1.1 Preterm labour | 1 | 246 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.96 [0.52, 1.77] |
| 1.2 Term labour | 3 | 2409 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.82 [0.22, 3.03] |
| 1.3 Both or gestation not specified | 7 | 30858 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.81 [0.50, 1.32] |
| 2 Neonatal seizures Show forest plot | 9 | 32386 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.50 [0.31, 0.80] |
| 2.1 Preterm labour | 1 | 246 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.02 [0.37, 2.81] |
| 2.2 Term labour | 2 | 1482 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.33 [0.01, 8.08] |
| 2.3 Both or gestation not specified | 6 | 30658 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.42 [0.24, 0.72] |
| 3 Cerebral palsy Show forest plot | 2 | 13252 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.74 [0.97, 3.11] |
| 3.1 Preterm labour | 1 | 173 | Risk Ratio (M‐H, Fixed, 95% CI) | 2.54 [1.10, 5.86] |
| 3.2 Term labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 3.3 Both or gestation not specified | 1 | 13079 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.20 [0.52, 2.79] |
| 4 Caesarean section Show forest plot | 11 | 18861 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.43 [1.25, 1.64] |
| 4.1 Preterm labour | 1 | 246 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.02 [0.57, 1.82] |
| 4.2 Term labour | 3 | 2400 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.84 [1.25, 2.69] |
| 4.3 Both or gestation not specified | 7 | 16215 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.41 [1.21, 1.63] |
| 5 Instrumental vaginal birth Show forest plot | 10 | 18615 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.21 [1.12, 1.31] |
| 5.1 Preterm labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 5.2 Term labour | 3 | 2400 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.18 [1.01, 1.37] |
| 5.3 Both or gestation not specified | 7 | 16215 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.22 [1.11, 1.34] |
| 6 Cord blood acidosis Show forest plot | 2 | 2494 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.16 [0.72, 1.89] |
| 6.1 Preterm labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 6.2 Term labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 6.3 Both or gestation not specified | 2 | 2494 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.16 [0.72, 1.89] |
| 7 Any pharmacological analgesia Show forest plot | 3 | 1677 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.93, 1.04] |
| 7.1 Preterm labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 7.2 Term labour | 1 | 504 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.92 [0.79, 1.07] |
| 7.3 Both or gestation not specified | 2 | 1173 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.01 [0.96, 1.06] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Perinatal mortality Show forest plot | 11 | 33513 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.86 [0.59, 1.24] |
| 1.1 Singleton | 7 | 18406 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.77 [0.49, 1.21] |
| 1.2 Twins | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 1.3 Both or singleton/twins not specified | 4 | 15107 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.04 [0.55, 1.97] |
| 2 Neonatal seizures Show forest plot | 9 | 32386 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.50 [0.31, 0.80] |
| 2.1 Singleton | 5 | 17279 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.69 [0.32, 1.46] |
| 2.2 Twins | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 2.3 Both or singleton/twins not specified | 4 | 15107 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.41 [0.22, 0.76] |
| 3 Cerebral palsy Show forest plot | 2 | 13252 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.74 [0.97, 3.11] |
| 3.1 Singleton | 1 | 173 | Risk Ratio (M‐H, Fixed, 95% CI) | 2.54 [1.10, 5.86] |
| 3.2 Twins | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 3.3 Both or singleton/twins not specified | 1 | 13079 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.20 [0.52, 2.79] |
| 4 Caesarean section Show forest plot | 11 | 18861 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.43 [1.25, 1.64] |
| 4.1 Singleton | 7 | 3888 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.58 [1.30, 1.93] |
| 4.2 Twins | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 4.3 Both or singleton/twins not specified | 4 | 14973 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.33 [1.11, 1.59] |
| 5 Instrumental vaginal birth Show forest plot | 10 | 18615 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.21 [1.12, 1.31] |
| 5.1 Singleton | 6 | 3642 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.13 [1.00, 1.28] |
| 5.2 Twins | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 5.3 Both or singleton/twins not specified | 4 | 14973 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.25 [1.13, 1.38] |
| 6 Cord blood acidosis Show forest plot | 2 | 2494 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.16 [0.72, 1.89] |
| 6.1 Singleton | 1 | 1419 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.58 [0.89, 2.81] |
| 6.2 Twins | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 6.3 Both or singleton/twins not specified | 1 | 1075 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.45 [0.16, 1.29] |
| 7 Any pharmacological analgesia Show forest plot | 3 | 1677 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.93, 1.04] |
| 7.1 Singleton | 2 | 987 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.93 [0.86, 1.01] |
| 7.2 Twins | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 7.3 Both or singleton/twins not specified | 1 | 690 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.06 [1.00, 1.12] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Perinatal mortality Show forest plot | 11 | 33513 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.85 [0.59, 1.23] |
| 1.1 Continuous CTG plus FBS | 7 | 16131 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.97 [0.64, 1.47] |
| 1.2 Continuous CTG alone ‐ no FBS | 5 | 17382 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.57 [0.26, 1.24] |
| 2 Neonatal seizures Show forest plot | 9 | 32386 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.50 [0.31, 0.80] |
| 2.1 Continuous CTG plus FBS | 5 | 15004 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.49 [0.29, 0.84] |
| 2.2 Continuous CTG alone ‐ no FBS | 5 | 17382 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.51 [0.18, 1.44] |
| 3 Cerebral palsy Show forest plot | 2 | 13252 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.74 [0.97, 3.11] |
| 3.1 Continuous CTG plus FBS | 2 | 13252 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.74 [0.97, 3.11] |
| 3.2 Continuous CTG alone ‐ no FBS | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 4 Caesarean section Show forest plot | 11 | 18861 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.43 [1.25, 1.64] |
| 4.1 Continuous CTG plus FBS | 7 | 16001 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.34 [1.14, 1.58] |
| 4.2 Continuous CTG alone ‐ no FBS | 5 | 2860 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.63 [1.30, 2.06] |
| 5 Instrumental vaginal birth Show forest plot | 10 | 18615 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.21 [1.12, 1.31] |
| 5.1 Continuous CTG plus FBS | 6 | 15755 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.27 [1.16, 1.39] |
| 5.2 Continuous CTG alone ‐ no FBS | 5 | 2860 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.05 [0.90, 1.22] |
| 6 Cord blood acidosis Show forest plot | 2 | 2494 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.16 [0.72, 1.89] |
| 6.1 Continuous CTG plus FBS | 1 | 1075 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.45 [0.16, 1.29] |
| 6.2 Continuous CTG alone ‐ no FBS | 1 | 1419 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.58 [0.89, 2.81] |
| 7 Any pharmacological analgesia Show forest plot | 3 | 1677 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.93, 1.04] |
| 7.1 Continuous CTG plus FBS | 2 | 849 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.98 [0.90, 1.07] |
| 7.2 Continuous CTG alone ‐ no FBS | 2 | 828 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.92, 1.05] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Perinatal mortality Show forest plot | 11 | 33513 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.86 [0.59, 1.24] |
| 1.1 Primaparous women | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 1.2 Multiparous women | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 1.3 Both or parity not specified | 11 | 33513 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.86 [0.59, 1.24] |
| 2 Neonatal seizures Show forest plot | 9 | 32386 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.50 [0.31, 0.80] |
| 2.1 Primaparous women | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 2.2 Multiparous women | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 2.3 Both or parity not specified | 9 | 32386 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.50 [0.31, 0.80] |
| 3 Cerebral palsy Show forest plot | 2 | 13252 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.74 [0.97, 3.11] |
| 3.1 Primaparous women | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 3.2 Multiparous women | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 3.3 Both or parity not specified | 2 | 13252 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.74 [0.97, 3.11] |
| 4 Caesarean section Show forest plot | 11 | 18961 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.44 [1.26, 1.64] |
| 4.1 Primaparous women | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 4.2 Multiparous women | 1 | 100 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.55 [0.81, 2.96] |
| 4.3 Both or parity not specified | 11 | 18861 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.43 [1.25, 1.64] |
| 5 Instrumental vaginal birth Show forest plot | 10 | 18715 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.21 [1.12, 1.30] |
| 5.1 Primaparous women | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 5.2 Multiparous women | 1 | 100 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.33 [0.04, 3.10] |
| 5.3 Both or parity not specified | 10 | 18615 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.21 [1.12, 1.31] |
| 6 Cord blood acidosis Show forest plot | 2 | 2494 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.16 [0.72, 1.89] |
| 6.1 Primaparous women | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 6.2 Multiparous women | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 6.3 Both or parity not specified | 2 | 2494 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.16 [0.72, 1.89] |
| 7 Any pharmacological analgesia Show forest plot | 3 | 1677 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.93, 1.04] |
| 7.1 Primaparous women | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 7.2 Multiparous women | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 7.3 Both or parity not specified | 3 | 1677 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.93, 1.04] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Perinatal mortality Show forest plot | 11 | 33513 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.86 [0.59, 1.24] |
| 1.1 High‐quality trials | 2 | 13434 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.00 [0.49, 2.05] |
| 1.2 Low‐quality trials | 4 | 17173 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.58 [0.28, 1.18] |
| 1.3 Quality of trials unclear | 5 | 2906 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.00 [0.58, 1.71] |
| 2 Neonatal seizures Show forest plot | 9 | 32386 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.50 [0.31, 0.80] |
| 2.1 High‐quality trials | 2 | 13434 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.40 [0.21, 0.77] |
| 2.2 Low‐quality trials | 2 | 16046 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.26 [0.04, 1.60] |
| 2.3 Quality of trials unclear | 5 | 2906 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.83 [0.38, 1.81] |
| 3 Cerebral palsy Show forest plot | 2 | 13252 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.74 [0.97, 3.11] |
| 3.1 High‐quality trials | 1 | 13079 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.20 [0.52, 2.79] |
| 3.2 Low‐quality trials | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 3.3 Quality of trials unclear | 1 | 173 | Risk Ratio (M‐H, Fixed, 95% CI) | 2.54 [1.10, 5.86] |
| 4 Caesarean section Show forest plot | 11 | 18861 | Risk Ratio (M‐H, Random, 95% CI) | 1.63 [1.29, 2.07] |
| 4.1 High‐quality trials | 2 | 13314 | Risk Ratio (M‐H, Random, 95% CI) | 1.27 [0.88, 1.83] |
| 4.2 Low‐quality trials | 3 | 2555 | Risk Ratio (M‐H, Random, 95% CI) | 1.77 [0.92, 3.41] |
| 4.3 Quality of trials unclear | 6 | 2992 | Risk Ratio (M‐H, Random, 95% CI) | 1.81 [1.34, 2.44] |
| 5 Instrumental vaginal birth Show forest plot | 10 | 18615 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.21 [1.12, 1.31] |
| 5.1 High‐quality trials | 2 | 13314 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.26 [1.13, 1.42] |
| 5.2 Low‐quality trials | 3 | 2555 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.39 [1.17, 1.64] |
| 5.3 Quality of trials unclear | 5 | 2746 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.00 [0.87, 1.16] |
| 6 Cord blood acidosis Show forest plot | 2 | 2494 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.16 [0.72, 1.89] |
| 6.1 High‐quality trials | 1 | 1075 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.45 [0.16, 1.29] |
| 6.2 Low‐quality trials | 1 | 1419 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.58 [0.89, 2.81] |
| 6.3 Quality of trials unclear | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 7 Any pharmacological analgesia Show forest plot | 3 | 1677 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.93, 1.04] |
| 7.1 High‐quality trials | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 7.2 Low‐quality trials | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 7.3 Quality of trials unclear | 3 | 1677 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.93, 1.04] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Perinatal mortality (primary outcome) | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 2 Neonatal seizures (primary outcome) | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 3 Cerebral palsy (primary outcome) | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 4 Caesarean section (primary outcome) Show forest plot | 1 | 4044 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.29 [0.84, 1.97] |
| 5 Instrumental vaginal birth (primary outcome) Show forest plot | 1 | 4044 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.16 [0.92, 1.46] |
| 6 Cord blood acidosis (primary outcome) Show forest plot | 1 | 4044 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.43 [0.95, 2.14] |
| 7 Any pharmacological analgesia (primary outcome) | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 8 Hypoxic ischaemic encephalopathy | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 9 Neurodevelopmental disability at at least 12 months of age | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 10 Apgar score < 7 at 5 minutes Show forest plot | 1 | 4044 | Risk Ratio (M‐H, Fixed, 95% CI) | 2.65 [0.70, 9.97] |
| 11 Apgar score < 4 at 5 minutes | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 12 Neonatal ICU admissions Show forest plot | 1 | 4044 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.34 [0.91, 1.98] |
| 13 Fetal blood sampling | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 14 Damage/infection from scalp electrode or scalp sampling | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 15 Caesarean section for abnormal FHR pattern and/or acidosis Show forest plot | 1 | 4044 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.19 [0.66, 2.15] |
| 16 Instrumental vaginal birth for abnormal CTG or fetal acidosis | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 17 Spontaneous vaginal birth Show forest plot | 1 | 4044 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.98 [0.96, 1.00] |
| 18 Epidural analgesia Show forest plot | 1 | 4044 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.06 [0.92, 1.21] |
| 19 Use of non pharmacological methods of coping with labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 20 Amniotomy | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 21 Oxytocin during 1st and/or 2nd stage of labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 22 Perineal trauma needing repair | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 23 Inability to adopt preferred position in labour | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 24 Dissatisifaction with labour and/or perceived loss of control | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 25 Postpartum depression | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 26 Exclusive breastfeeding at discharge | 0 | 0 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 27 Length of stay on NICU | 0 | 0 | Mean Difference (IV, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
