High Dose Versus Low Dose Oxytocin For Augmentation of Delayed Labour. PDF

High-dose versus low-dose oxytocin for augmentation of
delayed labour (Review)

Kenyon S, Tokumasu H, Dowswell T, Pledge D, Mori R
This is a reprint of a Cochrane review, prepared and maintained by The Cochrane Collaboration and published in The Cochrane Library
2013, Issue 7
http://www.thecochranelibrary.com
High-dose versus low-dose oxytocin for augmentation of delayed labour (Review)
Copyright 2013 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.
T A B L E O F C O N T E N T S
1 HEADER . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1 ABSTRACT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2 PLAIN LANGUAGE SUMMARY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3 BACKGROUND . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3 OBJECTIVES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3 METHODS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
7 RESULTS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
9 DISCUSSION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
9 AUTHORS CONCLUSIONS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
9 ACKNOWLEDGEMENTS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
10 REFERENCES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
12 CHARACTERISTICS OF STUDIES . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
19 DATA AND ANALYSES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Analysis 1.1. Comparison 1 High versus low dose of oxytocin (all women), Outcome 1 Neonatal mortality. . . . . 20
Analysis 1.2. Comparison 1 High versus low dose of oxytocin (all women), Outcome 2 Caesarean section. . . . . 21
Analysis 1.3. Comparison 1 High versus low dose of oxytocin (all women), Outcome 3 Length of labour (hour; oxytocin to
delivery). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21
Analysis 1.4. Comparison 1 High versus low dose of oxytocin (all women), Outcome 4 Length of labour (minute; onset of
rst stage to delivery). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22
Analysis 1.5. Comparison 1 High versus low dose of oxytocin (all women), Outcome 5 Support received by staff. . . 23
Analysis 1.6. Comparison 1 High versus low dose of oxytocin (all women), Outcome 6 Womens internal control during
labour and birth. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23
Analysis 1.7. Comparison 1 High versus low dose of oxytocin (all women), Outcome 7 Womens external control during
labour and birth. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24
Analysis 1.8. Comparison 1 High versus low dose of oxytocin (all women), Outcome 8 Spontaneous vaginal birth. . 24
Analysis 1.9. Comparison 1 High versus low dose of oxytocin (all women), Outcome 9 Diagnosis of chorioamnionitis. 25
Analysis 1.10. Comparison 1 High versus low dose of oxytocin (all women), Outcome 10 Incidence of hyperstimulation. 26
Analysis 1.11. Comparison 1 High versus low dose of oxytocin (all women), Outcome 11 Instrumental vaginal birth. 27
Analysis 1.12. Comparison 1 High versus low dose of oxytocin (all women), Outcome 12 Incidence of postpartum
haemorrhage. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
Analysis 1.13. Comparison 1 High versus low dose of oxytocin (all women), Outcome 13 Epidural analgesia. . . . 28
Analysis 1.14. Comparison 1 High versus low dose of oxytocin (all women), Outcome 14 Pathological cardiotocography
(CTG) leading to immediate birth without fetal blood sampling. . . . . . . . . . . . . . . . . 29
Analysis 1.15. Comparison 1 High versus low dose of oxytocin (all women), Outcome 15 Neonatal admission to special
care baby units. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29
Analysis 1.16. Comparison 1 High versus low dose of oxytocin (all women), Outcome 16 Apgar score less than 7 at 5
minutes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
Analysis 1.17. Comparison 1 High versus low dose of oxytocin (all women), Outcome 17 Umbilical cord (artery) pH. 31
Analysis 1.18. Comparison 1 High versus low dose of oxytocin (all women), Outcome 18 Subgroup analysis: Caesarean
section by parity. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32
32 WHATS NEW . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
33 CONTRIBUTIONS OF AUTHORS . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
33 DECLARATIONS OF INTEREST . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
33 SOURCES OF SUPPORT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
33 DIFFERENCES BETWEEN PROTOCOL AND REVIEW . . . . . . . . . . . . . . . . . . . . .
34 INDEX TERMS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
i High-dose versus low-dose oxytocin for augmentation of delayed labour (Review)
[Intervention Review]
High-dose versus low-dose oxytocin for augmentation of
delayed labour
Sara Kenyon
1
, Hironobu Tokumasu
2
, Therese Dowswell
3
, Debbie Pledge
4
, Rintaro Mori
5
1
School of Health and Population Sciences, University of Birmingham, Edgbaston, UK.
2
Neonatology, Kagoshima City Hospital,
Kagoshima, Japan.
3
Cochrane Pregnancy and Childbirth Group, Department of Womens and Childrens Health, The University of
Liverpool, Liverpool, UK.
4
National Collaborating Centre for Womens and Childrens Health, London, UK.
5
Department of Health
Policy, National Center for Child Health and Development, Tokyo, Japan
Contact address: Rintaro Mori, Department of Health Policy, National Center for Child Health and Development, 2-10-1 Okura,
Setagaya-ku, Tokyo, Tokyo, 166-0014, Japan. rintaromori@gmail.com.
Editorial group: Cochrane Pregnancy and Childbirth Group.
Publication status and date: New search for studies and content updated (no change to conclusions), published in Issue 7, 2013.
Review content assessed as up-to-date: 4 July 2013.
Citation: Kenyon S, Tokumasu H, Dowswell T, Pledge D, Mori R. High-dose versus low-dose oxytocin for augmentation of delayed
labour. Cochrane Database of Systematic Reviews 2013, Issue 7. Art. No.: CD007201. DOI: 10.1002/14651858.CD007201.pub3.
A B S T R A C T
Background
A major cause of failure to achieve spontaneous vaginal birth is delay in labour due to presumed inefcient uterine action. Oxytocin
is given to increase contractions and high-dose regimens may potentially increase the number of spontaneous vaginal births, but as
oxytocin can cause hyperstimulation of the uterus, there is a possibility of increased adverse events.
Objectives
To compare starting dose and increment dose of oxytocin for augmentation for women delayed in labour to determine whether
augmentation by high-dose regimens of oxytocin improves labour outcomes and to examine the effect on both maternal/neonatal
outcomes and womens birth experiences.
Search methods
We searched the Cochrane Pregnancy and Childbirth Groups Trials Register (31 May 2013) and reference lists of retrieved studies.
Selection criteria
We included all randomised and quasi-randomised controlled trials for women in delayed labour requiring augmentation by oxytocin
comparing high-dose regimens (dened as starting dose and increment of equal to or more than 4 mU per minute) with low-dose
regimens (dened as starting dose and an increment of less than 4 mU per minute). Increase interval: between 15 and 40 minutes. The
separation of low- and high-dose regimens is based on an arbitrary decision.
Data collection and analysis
Four review authors undertook assessment of trial eligibility, risk of bias, and data extraction independently.
1 High-dose versus low-dose oxytocin for augmentation of delayed labour (Review)
Main results
We included four studies involving 644 pregnant women. Three studies were randomised controlled trials and one trial was a quasi-
randomised study. A higher dose of oxytocin was associated with a signicant reduction in length of labour reported from one trial
(mean difference (MD) -3.50 hours; 95% condence interval (CI) -6.38 to -0.62; one trial, 40 women). There was a decrease in the
rate of caesarean section (risk ratio (RR) 0.62; 95% CI 0.44 to 0.86 four trials, 644 women) and an increase in the rate of spontaneous
vaginal birth in the high-dose group (RR 1.35; 95% CI 1.13 to 1.62, three trials, 444 women), although for both of these outcomes
there were inconsistencies between studies in the size of effect. When we carried out sensitivity analysis (temporarily removing a study
at high risk of bias) the differences between groups were no longer statistically signicant
There were no signicant differences between high- and low-dose regimens for instrumental vaginal birth, epidural analgesia, hyper-
stimulation, postpartum haemorrhage, chorioamnionitis or womens perceptions of experiences. For neonatal outcomes, there was no
signicant difference between groups for Apgar scores, umbilical cord pH, admission to special care baby unit, or neonatal mortality.
The following outcomes were not evaluated in the included studies: perinatal mortality, uterine rupture, abnormal cardiotocography,
womens pyrexia, dystocia and neonatal neurological morbidity.
Authors conclusions
Higher-dose regimens of oxytocin (4 mU per minute or more) were associated with a reduction in the length of labour and in caesarean
section, and an increase in spontaneous vaginal birth. However, there is insufcient evidence to recommend that high-dose regimens
are advised routinely for women with delay in the rst stage of labour. Further research should evaluate the effect of high-dose regimens
of oxytocin for women delayed in labour and should include maternal and neonatal outcomes as well as the effects on women.
P L A I N L A N G U A G E S U M M A R Y
Oxytocin in high versus low doses for augmentation of delayed labour
Women have different lengths of labour, with rst labours lasting on average eight hours (and unlikely to last more than 18 hours)
and second and subsequent labours lasting an average of ve hours and unlikely to last more than 12 hours. Assessment of progress
in labour takes into account not just cervical dilatation, but also descent and rotation of the fetal head and the strength, duration and
frequency of contractions. Some evidence suggests that up to one-third of women in their rst labour experience delay. They are often
given a synthetic version of the hormone oxytocin to increase uterine contractions and shorten labour. Surprisingly for such a routine
treatment, the ideal dose at which it should be given is not known, although some comparisons suggest that higher-dose regimens
of oxytocin could shorten labour and reduce the chance of caesarean section with an increase in the numbers of women having a
spontaneous vaginal birth compared with lower-dose regimens. However, there are potentially harmful side effects as oxytocin may
cause the uterus to contract too quickly, and the baby to become distressed. Clinicians attempt to mitigate these side effects by adjusting
the dose of oxytocin with the contractions to reduce the chances of the baby being distressed in labour.
From the four randomised controlled trials involving 644 pregnant women that we included in this review, results indicate that a higher
dose of oxytocin (4-7 mU per minute, compared with 1-2 mU per minute) reduced the length of labour and the rate of caesarean
sections with increased spontaneous vaginal births, but the studies did not provide enough evidence on possible differences between
the high- and low-dose regimens on adverse events including hyperstimulation of the uterus, and outcomes for the newborn infant.
Only one trial reported on the possible effect on women. The overall quality of the included trials was mixed, but this might reect
how clinical trials were reported in the past.
While the current evidence is promising and suggests that the high-dose regimens reduce the length of labour and the rate of caesarean
sections, this evidence is not strong enough to recommend that high-dose regimens are used routinely for women delayed in labour.
We recommend that further research is carried out.
B A C K G R O U N D
Description of the condition
Length of labour varies between women, with rst labours lasting
on average eight hours (and unlikely to last more than 18) and
second and subsequent labours lasting on average ve hours (and
unlikely to last more than 12 hours). Progress in labour should
take into account not just cervical dilatation, but also descent and
rotation of the fetal head and strength, duration and frequency of
contractions. The denition of delay varies, but cervical dilatation
of 2 cm in four hours is widely accepted as being normal (NICE
2007). The incidence of delay in labour is not accurately known.
Some evidence suggests that up to one-third of women in their
rst labours experience delay (Williams 1998). Other evidence
suggests the incidence of prolonged labour is more than 10% of
women (DOH 2004), and about 40% to 60% of these women
have their labour augmented with oxytocin due to slow progress
or other reasons in rst stage of labour (Gottschall 1997; Impey
2000). Many women would have already had their membranes
ruptured spontaneously, and amniotomy is not recommended as
routine practice (Smyth 2007).
Description of the intervention
Oxytocin has been widely used in obstetric practice and increases
both the frequency and strength of uterine contractions in labour.
In doses under 4 mU/min, it has been shown to shorten labour
but not alter mode of birth (Wei 2007).
How the intervention might work
It is plausible that increasing both the dose and speed of the oxy-
tocin will increase the number of women having a spontaneous
vaginal birth. It is currently routine treatment for women delayed
in labour, and while it does carry potentially harmful side effects,
clinicians routinely effectively titrate the dose against uterine con-
tractions.
Why it is important to do this review
Evidence suggests that high doses of oxytocin may increase spon-
taneous vaginal birth but not enough is known about neonatal
outcomes or how this might affect womens birth experience. One
non-Cochrane systematic review included trials that compared
high versus lowdoses of oxytocin for augmentation of labour (Wei
2010) but some of the trials were undertaken in the context of
active management of labour.
This review intends to assess the risks and benets of high- and
low-dose regimens of oxytocin for augmentation of labour due to
delayed rst stage of labour. We have excluded trials undertaken
in the context of active management of labour (one-to-one con-
tinuous support, strict denition of established labour, early am-
niotomy, routine two-hourly vaginal examinations and oxytocin
if labour becomes slow), or as part of induction of labour.
O B J E C T I V E S
To compare starting dose as well as increment dose of oxytocin for
augmentation in delayed labour to determine whether augmen-
tation by high dose of oxytocin improves labour outcomes and
womens satisfaction.
M E T H O D S
Criteria for considering studies for this review
Types of studies
All randomised and quasi-randomised controlled trials. We in-
tended to include both published or unpublished trials.
Types of participants
Women in labour assessed as requiring augmentation by oxytocin
for delay or slow progress in labour. We only included women
with live fetuses.
Types of interventions
High starting and increment dose (4 micro unit (mU) per minute
or more) of oxytocinfor augmentationindelayedlabour compared
with low dose (less than 4 mU per minute). We dened amount
of oxytocin as below:
high-dose regimens: dened as starting dose and increment
of equal to or more than 4 mU per minute;
low-dose regimens: dened as starting dose and an
increment of less than 4 mU per minute;
increase interval: between 15 and 40 minutes.
The separation of low and high doses is based on an arbitrary
decision.
Types of outcome measures
Primary outcomes
1. Perinatal mortality rate (as dened by trial authors)
2. Neonatal mortality rate
3. Caesarean section rate
4. Womens satisfaction (measured quantitatively using
validated questionnaires)
5. Length of labour
Secondary outcomes
1. Spontaneous vaginal birth
2. Instrumental vaginal birth
3. Incidence of hyperstimulation (contracting greater than ve
in 10 minutes for at least 20 minutes with fetal heart rate
changes)
4. Incidence of ruptured uterus
5. Diagnosis of chorioamnionitis
6. Incidence of postpartum haemorrhage (blood loss more
than 500/1000 mL)
7. Use of epidural analgesia
8. Incidence of abnormal cardiotocography (considered only if
blindly assessed)
9. Incidence of womens pyrexia
10. Incidence of dystocia
11. Neonatal outcomes of Apgar scores, umbilical cord pH,
neurological morbidity, admission to special care baby units
Search methods for identication of studies
Electronic searches
We contacted the Trials Search Co-ordinator to search the
Cochrane Pregnancy and Childbirth Groups Trials Register (31
May 2013).
The Cochrane Pregnancy and Childbirth Groups Trials Register
is maintained by the Trials Search Co-ordinator and contains trials
identied from:
1. monthly searches of the Cochrane Central Register of
Controlled Trials (CENTRAL);
2. weekly searches of MEDLINE;
3. weekly searches of Embase;
4. handsearches of 30 journals and the proceedings of major
conferences;
5. 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 pro-
ceedings, and the list of journals reviewed via the current aware-
ness service can be found in the Specialized Register section
within the editorial information about the Cochrane Pregnancy
and Childbirth Group.
Trials identied 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.
Searching other resources
We searched the reference lists of retrieved studies.
We did not apply any language restrictions.
Data collection and analysis
We used the following methods when assessing the reports iden-
tied by the search.
Selection of studies
Review authors Rintaro Mori (RM), Hironobu Tokumasu (HT),
Therese Dowswell (TD) and Sara Kenyon (SK) independently
assessed for inclusion all the potential studies identied as a result
of the search strategy. We intended to resolve any disagreement
through discussion or, if required, consult Debbie Pledge (DP);
there was no disagreement found.
Data extraction and management
We designed a formto extract data prior to the review. For eligible
studies, RM, HTand TDextracted the data using the agreed form,
which was checked by SK. We resolved discrepancies through dis-
cussion or, if required, we planned to consult DP (though we were
able to resolve all discrepancies by discussion). We entered data
into Review Manager software (RevMan 2012) and checked for
accuracy.
Assessment of risk of bias in included studies
RM, HT, TD and SK independently assessed risk of bias for each
study using the criteria outlined in the Cochrane Handbook for
Systematic Reviews of Interventions (Higgins 2011). We resolved all
disagreement by discussion.
(1) Random sequence generation (checking for possible
selection bias)
We describe for each included study the method used to generate
the allocation sequence in sufcient detail to allow an assessment
of whether it should produce comparable groups.
We assessed the method as:
low risk of bias (any truly random process, e.g. random
number table; computer random number generator);
high risk of bias (any non-random process, 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 describe for each included study the method used to conceal
allocation to interventions prior to assignment and assess 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 (open random allocation; unsealed or non-
opaque envelopes, alternation; date of birth);
(3) Blinding of participants, personnel and outcome
assessment (checking for possible performance bias)
We describe for each included study the methods used, if any, to
blind study participants and personnel from knowledge of which
intervention a participant received. We considered studies to be
at low risk of bias if they were blinded, or if we judged that the
lack of blinding would be unlikely to affect results. We assessed
blinding separately for different outcomes or classes of outcomes.
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 assessment.
(4) Incomplete outcome data (checking for possible attrition
bias due to the amount, nature and handling of incomplete
outcome data)
We describe for each included study, and for each outcome or class
of outcomes, the completeness of data including attrition and ex-
clusions from the analysis. We state whether attrition and exclu-
sions were reported and the numbers included in the analysis at
each stage (compared with the total randomised participants), rea-
sons for attrition or exclusion where reported, and whether miss-
ing data were balanced across groups or were related to outcomes.
Where sufcient information is reported, or was supplied by the
trial authors, we re-included missing data in the analyses which
we have undertaken.
We assessed methods as:
low risk of bias (e.g. no missing outcome data; missing
outcome data balanced across groups);
high risk of bias (e.g. numbers or reasons for missing data
imbalanced across groups; as treated analysis done with
substantial departure of intervention received from that assigned
at randomisation);
(5) Selective reporting (checking for reporting bias)
We describe for each included study how we investigated the pos-
sibility of selective outcome reporting bias and what we found.
low risk of bias (where it is clear that all of the studys pre-
specied outcomes and all expected outcomes of interest to the
review have been reported);
high risk of bias (where not all the studys pre-specied
outcomes have been reported; one or more reported primary
outcomes were not pre-specied; 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);
(6) Other bias (checking for bias due to problems not
covered by 1 to 5 above)
We describe for each included study any important concerns we
had about other possible sources of bias.
We assessed whether each study was free of other problems that
could put it at risk of bias:
low risk of other bias;
high risk of other bias;
unclear whether there is risk of other bias.
(7) Overall risk of bias
We made explicit judgements about whether studies are at highrisk
of bias, according to the criteria given in the Handbook (Higgins
2011). With reference to (1) to (6) above, we assessed the likely
magnitude and direction of the bias and whether we considered
it is likely to impact on the ndings. We planned to explore the
impact of the level of bias through undertaking sensitivity analyses
- see Sensitivity analysis.
Measures of treatment effect
We carried out statistical analysis using the Review Manager soft-
ware (RevMan 2012). We used xed-effect meta-analysis for com-
bining data where trials examined the same intervention, and the
trials populations and methods were judged to be sufciently sim-
ilar. Where we suspected clinical or statistical heterogeneity be-
tween studies, sufcient to suggest that treatment effects might
differ between trials, we carried out random-effects meta-analysis.
Dichotomous data
For dichotomous data, we presented results as summary risk ratio
with 95% condence intervals.
Continuous data
For continuous data, we used the meandifference if outcomes were
measured inthe same way betweentrials. We used the standardised
mean difference to combine trials that measure the same outcome,
but used different methods.
Unit of analysis issues
Cluster-randomised trials
We did not identify any cluster-randomised trials for inclusion in
this review. However, if we identify cluster-randomised trials for
inclusion in future updates, we will include them in the analy-
ses along with individually-randomised trials. We will adjust their
sample sizes using the methods described in the Handbook using
an estimate of the intracluster correlation co-efcient (ICC) de-
rived fromthe trial (if possible), froma similar trial or froma study
of a similar population. If we use ICCs fromother sources, we will
report this and conduct sensitivity analyses to investigate the effect
of variation in the ICC. If we identify both cluster-randomised
trials and individually-randomised trials, we plan to synthesise the
relevant information. We will consider it reasonable to combine
the results from both if there is little heterogeneity between the
study designs, and the interaction between the effect of interven-
tion and the choice of randomisation unit is considered to be un-
likely.
Cross-over trials
We did not include cross-over trials.
Dealing with missing data
For included studies, we noted levels of attrition. We planned to
explore the impact of including studies with high levels of missing
data (over 10% for outcomes where data were collected in labour)
in the overall assessment of treatment effect by using Sensitivity
analysis. In this version of the review we did not carry out planned
sensitivity analysis because labour outcomes studies were rated as
being at low risk of bias with little loss of follow-up or missing
data reported.
For all outcomes, we carried out analyses, as far as possible, on an
intention-to-treat basis, i.e. we attempted to include all partici-
pants randomised to each group in the analyses, and analysed all
participants in the group to which they were allocated, regardless
of whether or not they received the allocated intervention. The
denominator for each outcome in each trial was the number ran-
domised minus any participants whose outcomes were known to
be missing.
Assessment of heterogeneity
We assessed statistical heterogeneity in each meta-analysis using
the T, I and Chi statistics. We regarded heterogeneity as sub-
stantial if a T was greater than zero and either an I was greater
than 30% or there was a low P value (less than 0.10) in the Chi
test for heterogeneity.
Assessment of reporting biases
Where we suspected reporting biases (such as publication bias),
we attempted to contact study authors asking them to provide
missing outcome data.
In future updates of this review, if more data become available
and there are 10 or more studies in the meta-analysis, we will
investigate reporting biases (such as publication bias) using funnel
plots. We will assess funnel plot asymmetry visually, and use formal
tests for funnel plot asymmetry. For continuous outcomes, we
will use the test proposed by Egger 1997, and for dichotomous
outcomes, we will use the test proposed by Harbord 2006. If we
detect asymmetry in any of these tests or by a visual assessment,
we will perform exploratory analyses to investigate it.
Data synthesis
We carried out statistical analysis using the Review Manager soft-
ware (RevMan 2012). We used xed-effect meta-analysis for com-
bining data where it was reasonable to assume that studies were
estimating the same underlying treatment effect: i.e. where trials
were examining the same intervention, and the trials populations
and methods were judged sufciently similar. If there was clinical
heterogeneity sufcient to expect that the underlying treatment
effects differ between trials, or if high statistical heterogeneity was
identied, we planned to use random-effects meta-analysis to pro-
duce an overall summary if an average treatment effect across trials
was considered clinically meaningful. For random-effects analysis
the effect estimate represents the average treatment effect and we
will discuss the clinical implications of treatment effects differ-
ing between trials. If the average treatment effect is not clinically
meaningful, we will not combine trials.
If we use random-effects analyses, we will present the results as the
average treatment effect with its 95% condence interval, and the
estimates of T and I.
Subgroup analysis and investigation of heterogeneity
We intended to conduct planned subgroup analysis using the
methods described by Deeks 2001 and set out in the Cochrane
Handbook for Systematic Reviews of Interventions (Higgins 2011).
1. By parity (nulliparous versus multiparous women).
2. By previous experience of caesarean section (women who
had a caesarean before this delivery versus those who had not).
We planned to use the following outcomes in subgroup analysis.
Perinatal mortality rate.
Neonatal mortality rate.
Womens satisfaction.
Mode of birth.
We were only able to carry out limited subgroup analysis due
to insufcient data. We assessed differences between subgroups
using the subgroup interaction tests available in Revman (RevMan
2012).
Sensitivity analysis
The quality of included studies varied in terms of risk of bias; one
of the studies used a method at high risk of bias for allocation con-
cealment and, where data were available, we carried out sensitivity
analysis by temporarily removing this study from the analyses to
examine the impact on results.
R E S U L T S
Description of studies
Results of the search
The search of the Pregnancy and Childbirth Groups Trials Reg-
ister found 18 studies. We also identied, and subsequently ex-
cluded, two additional reports from the reference lists of retrieved
studies (Cummiskey 1989; Satin 1994). In total, we initially con-
sidered 20 studies published in 24 articles/reports. From these, we
included four studies and excluded 15 studies, and one trial is still
ongoing. One trial that was included in the previous version of the
review was excluded fromthis update; careful consideration of the
inclusion criteria for this study froma translation of the published
report led us to conclude that women recruited to the trial were
not necessarily experiencing delay in labour (Supajitkulchi 2003).
We did not identify any unpublished trials. For further informa-
tion on trial characteristics, please refer to the Characteristics of
included studies and Characteristics of excluded studies tables.
Included studies
We included four studies, involving 644 women. Please refer to
Characteristics of included studies for the further details.
Among the included trials, three trials (Bidgood 1987; Jamal
2004; Kenyon 2013) were randomised controlled trials and one
trial (Xenakis 1995) employed a quasi-randomised design, where
allocation of intervention was made on the basis of the day of the
week.
With the exception of one, three-armed trial (Bidgood 1987), all
of the included studies were two-armed trials. Data from one arm
of the three-arm trial were not used as the data did not meet our
inclusion criteria.
Two trials included only nulliparous women (Bidgood 1987;
Kenyon 2013), while the other two trials included both nulli-
parous and parous women (Jamal 2004; Xenakis 1995). In the
Xenakis 1995 trial, separate data on mode of birth were pro-
vided for nulliparous and parous women. Three trials excluded
women with previous caesarean section (Jamal 2004; Kenyon
2013; Xenakis 1995).
Possible maximum dose for oxytocin was reported by one trial
(Bidgood 1987) as 40 mU/min, and by (Kenyon 2013) as 64 mU/
min for the high-dose group and 32 mU/min for the low-dose
group.
Excluded studies
We excluded 15 studies. Please see Characteristics of excluded
studies for the further details.
One report (Alderman 1974) was a letter with no primary data.
Six trials (Arulkumaran 1989; Lazor 1993; Lowensohn 1990;
Majoko 2001; Satin 1994; Seitchik 1982) examined different rates
of oxytocinadministrationfor augmentationof labour; their stated
doses are outside of the preset criteria of low and high doses.
One trial (Cummiskey 1989) compared pulsatile administration
of oxytocin for augmentation with continuous administration.
One trial (Parpas 1995) compared high and low doses of oxytocin
for augmentation and induction of labour but the two populations
were not reported separately.
One trial (Vorherr 1963) compared effectiveness of oxytocin for
augmentation with placebo.
One trial (Merrill 1999) included women with planned routine
augmentation of labour by oxytocin; hence these women did not
necessarily have delayed labour.
One trial (Akoury 1993) was excluded because it was carried out
in the context of active management of labour.
Two trials (Hayakungchat 2011; Supajitkulchi 2003) enrolled
women with inadequate contractions rather than women with de-
layed labour.
One trial (Doppa 2011) enrolled women requiring induction of
labour rather than augmentation.
Risk of bias in included studies
Allocation
We rated random sequence generation as high risk of bias in
one trial where allocation was according to day of the week (
Xenakis 1995). The other trials all used a method to generate
the randomisation sequence that we assessed as low risk of bias:
in Bidgood 1987 envelopes containing allocations were shufed
at the beginning of the study; in Jamal 2004 a table of random
numbers was used; and Kenyon 2013 used an external telephone
randomisation service.
Allocation to groups at the point of randomisation was concealed
in two trials (Bidgood 1987; Kenyon 2013). Bidgood 1987 used
sealed envelopes opened by an investigator not involved in carry-
ing out initial assessments on women recruited to the trial, and in
the trial by Kenyon 2013, allocation was by a telephone service.
In the Jamal 2004 trial, it was not clear how allocation was con-
cealed at the point of randomisation. There was no concealment
of allocation in the (Xenakis 1995) trial where women requiring
augmentation were allocated to groups according to days of the
week. It was not clear whether all other aspects of care were the
same on different days of the week.
Blinding
Blinding was not attempted in two trials (Bidgood 1987; Xenakis
1995), but the other two trials were double blinded with both
caregivers and pregnant women blinded to allocation (Jamal 2004;
Kenyon 2013).
Incomplete outcome data
All of these trials were rated as being at low risk of bias for labour
and delivery outcomes with little loss to follow-up or missing data
reported. Only one of the studies reported data relating to womens
experiences of childbirth; in this trial the response rate to postal
questionnaire was 63% (59/94) (Kenyon 2013).
Selective reporting
We had sufcient information to assess outcome reporting bias
for only one study (Kenyon 2013) where a published protocol was
available.
Other potential sources of bias
Assessment of risk of bias was hampered by lack of information
on methods in three of the included trials (Bidgood 1987; Jamal
2004; Xenakis 1995). Baseline characteristics were reported as be-
ing similar in all four of the trials, although in Xenakis 1995, there
were fewer nulliparous womeninthe high-dose group (47%) com-
pared with the low-dose group (60%). Other bias was not appar-
ent, although Bidgood 1987 reported that due to lack of time only
30 rather than 50 women were recruited to each arm.
Effects of interventions
Primary outcomes
There was a signicant reduction in length of labour with higher
dose of oxytocin reported from one trial (mean difference (MD) -
3.50 hours; 95% condence interval (CI) -6.38 to -0.62; one trial,
40 women (Analysis 1.3)).
There was evidence of a reduction in caesarean section in the
high-dose group (risk ratio (RR) 0.62; 95% CI 0.44 to 0.86,
four trials, 644 women (Analysis 1.2)). However, for this outcome
there was inconsistency in ndings from the trials and substantial
statistical heterogeneity (I
2
= 58%). More than half of the weight
in this analysis was from one trial which was at high risk of bias
due to lack of allocation concealment. We therefore carried out
a sensitivity analysis, temporarily removing this study from the
analysis to examine the impact on results. Removing the Xenakis
1995 trial led to a reduction in heterogeneity (I
2
= 0%) and the
difference between groups for caesarean section was no longer
statistically signicant (RR 0.89, 95% CI 0.57 to 1.38; data not
shown).
There was no estimable data for neonatal mortality (reported in
three trials). No signicant differences were seen in womens per-
ceptions of the birth experience (namely support received by staff,
womens internal control during labour and birth, and womens
external control during labour and birth measured by the SCIB
(Support and Control in Birth) questionnaire (Ford 2009) (MD
2.20, 95% CI -2.19 to 6.59, (Analysis 1.5); MD -0.30, 95% CI -
4.99 to 4.39, (Analysis 1.6); and MD2.60, 95%CI -2.25 to 7.45,
(Analysis 1.7), respectively). None of the included trials reported
effects on perinatal mortality.
Secondary outcomes
There was signicant evidence of increases in spontaneous vaginal
birth (RR 1.35; 95% CI 1.13 to 1.62, three trials, 444 women
(Analysis 1.8)). We carried out sensitivity analysis for this outcome
by temporarily removing one study at high risk of bias from the
analysis (Xenakis 1995); without data from this study the differ-
ence between groups for spontaneous vaginal birth was no longer
statistically signicant (RR 1.24, 95% CI 0.68 to 2.25; data not
shown).
No signicant difference was seen in the incidence of instrumental
vaginal birth (RR 0.83, 95% CI 0.61 to 1.13 (Analysis 1.11));
hyperstimulation (RR1.47, 95%CI 0.73 to 2.94 (Analysis 1.10));
chorioamnionitis (RR 0.70, 95% CI 0.44 to 1.12 (Analysis 1.9));
postpartumhaemorrhage (RR0.95, 95%CI 0.61to1.48(Analysis
1.12)); epidural analgesia (RR0.98, 95%CI 0.86 to 1.12 (Analysis
1.13)); admissionto neonatal units (RR0.50, 95%CI 0.22 to 1.15
(Analysis 1.15)); pathological cardiotocography (CTG) (RR 0.60,
95% CI 0.29 to 1.23 (Analysis 1.14)); Apgar score less than seven
at ve minutes (RR 0.37, 95% CI 0.02 to 8.50 (Analysis 1.16));
or umbilical cord pH (MD 0.00, 95% CI -0.03 to 0.03 (Analysis
1.17)). No trials reported incidences of ruptured uterus, womens
pyrexia and dystocia, and infant neurological morbidities.
Subgroup analyses
By parity
One trial set out data for mode of birth separately for nulliparous
and parous women (Xenakis 1995) and two trials recruited only
nulliparous women. We therefore carried out subgroup analysis by
parity for caesarean section. The subgroup interaction test showed
noclear differences ininterventioneffect betweennulli- andmulti-
parous women (Analysis 1.18) although as in the main analysis,
there was evidence of variations in the size and direction of treat-
ment effect between trials and substantial statistical heterogeneity.
Previous caesarean section
No trial considered women with previous caesarean section sep-
arately, and therefore we did not conduct subgroup analysis by
previous caesarean section.
D I S C U S S I O N
Summary of main results
Available evidence showed that a higher-dose regimen of oxytocin
for augmentation of delayed labour reduced the length of labour
and may reduce the number of caesarean sections and increase the
number of spontaneous vaginal births. One trial reported effects
on womens birth experience, though due to unbalance and in-
completeness of the follow-up, it was difcult to reach a conclu-
sion based upon the data. There was no evidence of difference in
incidence of adverse events, though this could be due to the small
number of included trials and women. Since this reviewcompared
only higher- versus lower- dose regimens with the same intervals,
we can draw no conclusion on the optimal intervals or doses out-
side the ranges that this review assessed. There is little informa-
tion on the effect in subgroups of women with previous caesarean
section and with different parities.
Quality of the evidence
The overall quality of the included trials was mixed although as-
sessing bias was partly hampered by insufcient information on
methods inthree of the includedtrials (Bidgood 1987; Jamal 2004;
Xenakis 1995); the most recent trial was mainly rated as being at
low risk of bias (Kenyon 2013) and this may reect changes in
reporting of trials. One of the trials was at high risk of bias for allo-
cation concealment (Xenakis 1995) and removing data from this
trial fromthe analyses had an impact on results for outcomes relat-
ing to mode of birth with other trials showing a less pronounced
effect for high-dose regimens.
Potential biases in the review process
We were aware of the possibility of introducing bias at every stage
of the review process. We attempted to reduce bias in a number
of ways: two review authors independently assessed eligibility for
inclusion, carried out data extraction and assessed risk of bias.
Nevertheless, assessment of risk of bias, for example, is not an exact
science and involves subjective judgements. Further, the process
of reviewing research studies is known to be affected by attitudes
and beliefs and it is not easy to control for this type of bias in the
reviewing process. One of the review authors (S Kenyon) was an
investigator inone of the included trials, and for this trial two other
review authors (R Mori and T Dowswell) carried out independent
data extraction and assessment of risk of bias.
Agreements and disagreements with other
studies or reviews
While other reviews have not focused onwomendelayed inlabour,
but have also included women having active management of
labour, which is a package of care, this review also highlights the
uncertainty in the evidence regarding the use of high-dose oxy-
tocin regimens to reduce caesarean section and increase sponta-
neous vaginal birth for women with delayed labour and empha-
sises the need for further research to be undertaken.
A U T H O R S C O N C L U S I O N S
Implications for practice
The available evidence shows that high-dose oxytocin regimens
for women delayed in labour may reduce the number of caesarean
sections and increase spontaneous vaginal birth, as well as accel-
erate the progress of labour. However, there is not enough evi-
dence to recommend routine use of high-dose oxytocin regimens
for women delayed in the rst stage of labour.
Implications for research
Further research should be conducted to evaluate high-dose oxy-
tocin regimens for delay in labour and such research should in-
clude robust assessment of both labour effects (hyperstimulation)
as well as neonatal outcomes and any effect on womens birth ex-
perience.
A C K N O W L E D G E M E N T S
The 2013 updated systematic review was nancially supported by
the UNDP-UNFPA-UNICEF-WHO-World Bank Special Pro-
gramme of Research, Development and Research Training in
Human Reproduction (HRP), the Department of Reproductive
Health and Research (RHR), World Health Organization. The
named authors alone are responsible for the views expressed in this
publication.
The protocol of this reviewwas developed with contributions from
Dr Roz Ullman and Mr Steven Walkinshaw.
As part of the pre-publication editorial process, the rst version
of this review was commented on by three peers (an editor and
two referees who are external to the editorial team), a member
of the Pregnancy and Childbirth Groups international panel of
consumers and the Groups Statistical Adviser (Mori 2011).
We are grateful to Maria Kalousi for translating Parpas 1995, Tip-
pawan Liabsuetrakul for translating Supajitkulchi 2003 and Kate
Kaminski for translating Vorherr 1963.
The National Institute for Health Research (NIHR) is the largest
single funder of the Cochrane Pregnancy and Childbirth Group.
The views and opinions expressed therein are those of the authors
and do not necessarily reect those of the NIHR, NHS or the
Department of Health.
R E F E R E N C E S
References to studies included in this review
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oxytocin augmentation of labour. 1. Obstetric outcome.
British Journal of Obstetrics and Gynaecology 1987;94:5127.
Bidgood KA, Steer PJ. A randomized control study of
oxytocin augmentation of labour. 2. Uterine activity.
British Journal of Obstetrics and Gynaecology 1987;94:
51822.
Bidgood KA, Steer PJ. Oxytocin augmentation of labour.
Proceedings of the 24th British Congress of Obstetrics and
Gynaecology;1986 April 15-18; Cardiff, UK. 1986:239.
Jamal 2004 {published data only}
Jamal A, Kalantari R. High and low dose oxytocin in
augmentation of labor. International Journal of Gynecology
& Obstetrics 2004;87:68.
Kenyon 2013 {published data only}
Bird D. High or low dose syntocinon (oxytocin) for delay in
labour. Current Controlled Trials 2010.
Xenakis 1995 {published data only}
Xenakis EM, Langer O, Piper JM, Conway D, Berkus

MD. Low-dose versus high-dose oxytocin augmentation of
labor--a randomized trial. American Journal of Obstetrics and
Gynecology 1995;173:18748.
Xenakis EMJ, Field N, Barshes D, Langer O. Efcacy of
high dose vs low dose oxytocin in labor augmentation.
American Journal of Obstetrics and Gynecology 1994;170:
378.
References to studies excluded from this review
Akoury 1993 {published data only}
Akoury H, Brodie G, Caddick R, Chandbry N, Pugh N,
Rowell Y. Oxytocin augmentation of labour: a comparison
between high and low dose protocol and perinatal outcome
a nulliparous women. Proceedings of 49th Annual Clinical
Meeting of the Society of Obstetricians and Gynaecologists
of Canada; 1993 June 22-26; Ottawa, Ontario, Canada.
1993:14.
Alderman 1974 {published data only}
Alderman B. Letter: Dangers of oxytocin-induced labour to
fetuses. British Medical Journal 1974;4:445.
Arulkumaran 1989 {published data only}
Arulkumaran S, Yang M, Ingemarsson I, Singh P, Ratnam
SS. Augmentation of labour: does oxytocin titration to
achieve preset active contraction area values produce better
obstetric outcome?. Asia-Oceania Journal of Obstetrics and
Gynaecology 1989;15:3337.
Cummiskey 1989 {published data only}
Cummiskey KC, Gall SA, Yusoff DM. Pulsatile
administration of oxytocin for augmentation of labor.
Obstetrics & Gynecology 1989;74(6):86972.
Doppa 2011 {published data only}
Doppa GJ. Low dose vs high dose oxytocin in augmentation
of labour in KVGMC. Clinical Trials Registry - India 2011.
Hayakungchat 2011 {published data only}
Swadpanich US. The effects of high versus low dose
oxytocin on cesarean section rate, fetal and maternal
outcomes for augmentation of labor in pregnant women
gestational age > 37 weeks. Australian New Zealand Clinical
Trials Registry (www.anzctr.org.au) 2011.
Lazor 1993 {published data only}
Lazor LZ, Philipson EH, Ingardia CJ, Kobetitsch ES,

Curry SL. A randomized comparison of 15- and 40-minute
dosing protocols for labor augmentation and induction.
Obstetrics & Gynecology 1993;82:100912.
Lazor LZ, Philipson EH, Ingardia CJ, Kobetitsch ES, Curry
SL. A randomized prospective comparison of oxytocin
dosing protocols for labor augmentation in nulliparous
women. American Journal of Obstetrics and Gynecology 1993;
168:295.
Lowensohn 1990 {published data only}
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and augmentation of labor. Proceedings of 10th Annual
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23-27; Houston, Texas, USA. 1991:76.
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for augmentation of labour in nulliparous women. Central
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Merrill 1999 {published data only}
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45563.
Parpas 1995 {published data only}
Parpas G, Gondry J, Verhoest P, Martinez C, Boulanger
JCh. Randomised trial of 2 dosages of oxytocin for labour
induction or augmentation [Utilisation de locytocine
(syntocinon) dans le declenchement ou la direction du
travail: faible ou forte posologie, comparaison]. Journal de
Gynecologie, Obstetrique et Biologie de la Reproduction 1995;
24(8):873.
Satin 1994 {published data only}
Satin AJ, Leveno KJ, Sherman L, McIntire D. High-dose
oxytocin: 20- versus 40-minute dosage interval. Obstetrics
& Gynecology 1994;83(2):238.
Seitchik 1982 {published data only}
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dysfunctional labor? I. Clinical data. American Journal of
Obstetrics and Gynecology 1982;144:899905.
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augmentation of delayed labour. ClinicalTrials.gov 2012.
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DOH 2004
Government Statistical Service for the Department of
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in meta-analysis detected by a simple, graphical test. BMJ
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Gottschall DS, Borgida AF, Mihalek JJ, Sauer F, Rodis JF.
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References to other published versions of this review
Mori 2011
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Indicates the major publication for the study

C H A R A C T E R I S T I C S O F S T U D I E S
Characteristics of included studies [ordered by study ID]
Bidgood 1987
Methods A 3-arm randomised controlled trial.
Participants Nulliparous women in spontaneous labour with vertex at term (the high-dose group: 19
women, the low-dose group: 21 women)
Interventions Intervention: oxytocin started at 7 mU/min, increased by 7 mU/min every 15 minutes,
to a maximum of a frequency of 7 contractions in 15 minutes or by abnormality in the
fetal heart rate tracing
Control: oxytocin started at 2 mU/min, increased by 2 mU/min every 15 minutes, to a
maximum of 40 mU/min until a table phase of uterine activity was detected or uterine
activity integral exceeded 1500 kPas/15 minutes
Oxytocin was deferred for 8 hours for the third group. This review only included the
above 2 groups
Outcomes Mode of delivery, incidence of hyperstimulation, length of labour, umbilical cord pH,
Apgar scores at 1 and 5 minutes
Notes
Risk of bias
Bias Authors judgement Support for judgement
Random sequence generation (selection
bias)
Low risk envelopes shufed at the beginning of the
study.
Allocation concealment (selection bias) Low risk drawing consecutive sealed envelopes contain-
ing instruction. It was not clear that the en-
velopes were opaque, but it was stated that the
person opening the envelopes was not aware of
the initial observations on women recruited
Blinding (performance bias and detection
bias)
All outcomes
High risk Study not blinded and no placebo.
Incomplete outcome data (attrition bias)
All outcomes
Low risk There is no loss of follow-up reported.
Womens experience
Unclear risk Not reported.
Selective reporting (reporting bias) Unclear risk There is no information to make an appropriate
judgement on this
Bidgood 1987 (Continued)
Other bias Unclear risk Our original plan was to recruit 50 women in
each group... However, this was not achieved
due to limitation of time. 60 women recruited.
It was stated that characteristics of women in the
intervention and control groups were similar at
baseline
Jamal 2004
Methods A randomised controlled trial.
Participants Pregnant women with cervical dilatation of 3 cmor greater and gestational age 37 weeks
and more
Both parous and nulliparous women were included. Women with previous caesarean
section were excluded
ineffective uterine contraction in the beginning of active labour
Amniotimy was performed in those with intact membrane
(the high-dose group: 100 women, the low-dose group: 100 women)
Interventions Intervention: 4.5 mU/min and increased by 4.5 mU/min every 30 minutes
Control: 1.5 mU/min and increased by 1.5 mU/min every 30 minutes
Outcomes Mode of delivery, length of labour.
Notes
Risk of bias
bias)
Low risk Stated that a table of random numbers was used.
Allocation concealment (selection bias) Unclear risk This was a double blind trial and it was stated that high
and low-dose infusions were prepared by a member of
staff not involved in patient care. It was not clear what
happened at the point of randomisation
bias)
All outcomes
Low risk to reduce the bias of the study randomization and
preparation of the solutions were performed by the
chief resident who did not participate directly in mon-
itoring of patients. Infusion bags were described as
identical. Staff collecting data were reported to be blind
to treatment allocation
All outcomes
Low risk It was reported that 200 women were randomised and
all appeared to be accounted for in the results. Loss to
follow-up not mentioned
Jamal 2004 (Continued)
Womens experience
Selective reporting (reporting bias) Unclear risk Assessed from published study reports.
Other bias Low risk It was reported that baseline characteristics were simi-
lar.
Kenyon 2013
Methods A randomised controlled trial.
Participants Nulliparous women with a singleton pregnancy at term (37-42 weeks) with conrmed
delay in labour and with ruptured membranes
(The high-dose group: 47 women, the low-dose group: 47 women.)
Interventions Intervention: 4mU/min increased every 30 minutes to 64 mU/min
Control: 2mU/min increased every 30 minutes to 32 mU/min.
Outcomes Mode of delivery, incidences of hyperstimulation, pathological CTG, epidural analgesia,
postpartum haemorrhage, chorioamnionitis, length of labour, perineal trauma, status at
birth, Apgar scores, adverse outcomes
Notes Maternal perceptions of support and control in labour and mother-to-infant bonding
were also measured using validated tools with a response rate of 63% (59/94)
Risk of bias
bias)
Low risk Telephone randomisation service with computer-gen-
erated program
Allocation concealment (selection bias) Low risk External randomisation service.
bias)
All outcomes
Low risk Double blind trial (identical vials produced by manu-
facturer)
All outcomes
Low risk The completion rate was 91/94.
Womens experience
High risk Data of only 27 out of 47 women in the high-dose
group and 32 out of 47 women in the low-dose group
were obtained. Characteristics of responders and non
responders to the postal questionnaire were, however,
assessed as similar
Kenyon 2013 (Continued)
Selective reporting (reporting bias) Low risk A protocol was published prior to the study.
Other bias Low risk No other issues indentied.Table sets out baseline
characteristics which appeared similar in the two ran-
domised groups
Xenakis 1995
Methods A quasi-randomised controlled trial.
Participants Pregnant women requiring augmentation at term.
Women with malpresentation, placenta praevia, previous caesarean section or multiple
gestation were excluded
Both nulliparous and parous women were included
(the high-dose group: 154 women, the low-dose group: 156 women)
Interventions Intervention: oxytocin started at 4 mU/min, increased by 4 mU/min every 15 minutes
Control: oxytocin started at 1 mU/min, increased by 1 mU/min every 30 minutes
Outcomes Neonatal mortality, mode of delivery, incidence of hyperstimulation, incidence of
chorioamnionitis, epidural analgesia, incidence of dystocia, neonatal admission to spe-
cial care, Apgar scores at 5 and 10 minutes
Notes
Risk of bias
bias)
High risk The allocation was based upon days of week;
hence a quasi-randomised controlled trial
Allocation concealment (selection bias) High risk No allocation concealment.
bias)
All outcomes
High risk Neither caregivers nor pregnant women were
masked.
All outcomes
Low risk All women appeared to be accounted for in the
analyses. No loss to follow-up reported
Womens experience
Selective reporting (reporting bias) Unclear risk There was not enough information to make a
judgement.
Xenakis 1995 (Continued)
Other bias Unclear risk It was stated that group characteristics were sim-
ilar at baseline but 60% primiparous in low-dose
group vs 47% in high-dose group (some results
reported by parity)
cm: centimetre
CTG: cardiotocography
mU/min: 0.001 unit per minutes
kPas: kilo pascal
vs: versus
Characteristics of excluded studies [ordered by study ID]
Study Reason for exclusion
Akoury 1993 Trial was carried out in the context of active management of labour. Relevant information is not available
Alderman 1974 Letter, not a primary study.
Arulkumaran 1989 Both groups received 2.5 mU/min of oxytocin up to different criteria for an optimal dose
Cummiskey 1989 Pulsatile administration was compared with continuous administration
Doppa 2011 The intervention is induction by oxytocin with different doses
Hayakungchat 2011 Whether labour was delayed or not was unclear in the study population
Lazor 1993 Both intervention and control were classied as low dose.
Lowensohn 1990 Both intervention and control were classied as high dose.
Majoko 2001 Both intervention and control were classied as high dose.
Merrill 1999 The study population was pregnant women with planned routine augmentation. This implies that the study
population were not women with a diagnosis of delayed labour
Parpas 1995 The populations included both those for augmentation and those for induction. These were not separately
reported
Satin 1994 Both intervention and control were classied as high dose.
Seitchik 1982 Two groups were classied as low dose and the third group was by a physicians choice
(Continued)
Supajitkulchi 2003 Whether labour was delayed or not was unclear in the study population
Vorherr 1963 Compared oxytocin with placebo.
mU/min: 0.001 unit per minutes
Characteristics of ongoing studies [ordered by study ID]
Berg 2012
Trial name or title
Methods A randomised controlled trial
Participants Healthy nulliparous women with delay or arrest of active labour with singleton pregnancy, cephalic presen-
tation, spontaneous onset of labour at term (37 to 42 weeks)
Interventions High- versus low-dose of oxytocin infusion, though details not described
Outcomes Mode of delivery, length of labour, incidence of hyperstimulation of contraction, postpartum haemorrhage,
epidural analgesia, childbirth experience, Apgar score, admission to neonatal unit
Starting date
Contact information
Notes This study was scheduled to start in March 2013 and to complete in December 2015
D A T A A N D A N A L Y S E S
Comparison 1. High versus low dose of oxytocin (all women)
Outcome or subgroup title
No. of
studies
No. of
participants
Statistical method Effect size
1 Neonatal mortality 3 604 Risk Ratio (M-H, Fixed, 95% CI) 0.0 [0.0, 0.0]
2 Caesarean section 4 644 Risk Ratio (M-H, Fixed, 95% CI) 0.62 [0.44, 0.86]
3 Length of labour (hour; oxytocin
to delivery)
1 40 Mean Difference (IV, Fixed, 95% CI) -3.50 [-6.38, -0.62]
4 Length of labour (minute; onset
of rst stage to delivery)
1 92 Std. Mean Difference (IV, Fixed, 95% CI) -0.10 [-0.51, 0.31]
5 Support received by staff 1 59 Mean Difference (IV, Fixed, 95% CI) 2.20 [-2.19, 6.59]
6 Womens internal control during
labour and birth
1 59 Mean Difference (IV, Fixed, 95% CI) -0.30 [-4.99, 4.39]
7 Womens external control during
labour and birth
1 59 Mean Difference (IV, Fixed, 95% CI) 2.60 [-2.25, 7.45]
8 Spontaneous vaginal birth 3 444 Risk Ratio (M-H, Fixed, 95% CI) 1.35 [1.13, 1.62]
9 Diagnosis of chorioamnionitis 2 404 Risk Ratio (M-H, Fixed, 95% CI) 0.70 [0.44, 1.12]
10 Incidence of hyperstimulation 4 644 Risk Ratio (M-H, Random, 95% CI) 1.47 [0.73, 2.94]
11 Instrumental vaginal birth 3 444 Risk Ratio (M-H, Fixed, 95% CI) 0.83 [0.61, 1.13]
12 Incidence of postpartum
haemorrhage
1 94 Risk Ratio (M-H, Fixed, 95% CI) 0.95 [0.61, 1.48]
13 Epidural analgesia 2 404 Risk Ratio (M-H, Fixed, 95% CI) 0.98 [0.86, 1.12]
14 Pathological cardiotocography
(CTG) leading to immediate
birth without fetal blood
sampling
15 Neonatal admission to special
care baby units
16 Apgar score less than 7 at 5
minutes
17 Umbilical cord (artery) pH 2 134 Mean Difference (IV, Fixed, 95% CI) 0.0 [-0.03, 0.03]
18 Subgroup analysis: Caesarean
section by parity
18.1 Nulliparous women 3 300 Risk Ratio (M-H, Fixed, 95% CI) 0.71 [0.47, 1.06]
18.2 Multiparous women 1 144 Risk Ratio (M-H, Fixed, 95% CI) 0.43 [0.19, 0.97]
Analysis 1.1. Comparison 1 High versus low dose of oxytocin (all women), Outcome 1 Neonatal mortality.
Review: High-dose versus low-dose oxytocin for augmentation of delayed labour
Comparison: 1 High versus low dose of oxytocin (all women)
Outcome: 1 Neonatal mortality
Study or subgroup High dose Low dose Risk Ratio Weight Risk Ratio
n/N n/N M-H,Fixed,95% CI M-H,Fixed,95% CI
Jamal 2004 0/100 0/100 Not estimable
Kenyon 2013 0/47 0/47 Not estimable
Xenakis 1995 0/154 0/156 Not estimable
Total (95% CI) 301 303 Not estimable
Total events: 0 (High dose), 0 (Low dose)
Heterogeneity: not applicable
Test for overall effect: not applicable
Test for subgroup differences: Not applicable
0.01 0.1 1 10 100
Favours high dose Favours low dose
Analysis 1.2. Comparison 1 High versus low dose of oxytocin (all women), Outcome 2 Caesarean section.
Outcome: 2 Caesarean section
Xenakis 1995 16/154 40/156 56.5 % 0.41 [ 0.24, 0.69 ]
Jamal 2004 5/100 9/100 12.8 % 0.56 [ 0.19, 1.60 ]
Bidgood 1987 5/19 7/21 9.4 % 0.79 [ 0.30, 2.07 ]
Kenyon 2013 17/47 15/47 21.3 % 1.13 [ 0.64, 1.99 ]
Total (95% CI) 320 324 100.0 % 0.62 [ 0.44, 0.86 ]
Heterogeneity: Chi
2
= 7.13, df = 3 (P = 0.07); I
2
=58%
Test for overall effect: Z = 2.82 (P = 0.0049)
0.01 0.1 1 10 100
Analysis 1.3. Comparison 1 High versus low dose of oxytocin (all women), Outcome 3 Length of labour
(hour; oxytocin to delivery).
Outcome: 3 Length of labour (hour; oxytocin to delivery)
Study or subgroup High dose Low dose
Mean
Difference Weight
Mean
Difference
N Mean(SD) N Mean(SD) IV,Fixed,95% CI IV,Fixed,95% CI
Bidgood 1987 19 7.8 (2.7) 21 11.3 (6.1) 100.0 % -3.50 [ -6.38, -0.62 ]
Total (95% CI) 19 21 100.0 % -3.50 [ -6.38, -0.62 ]
-100 -50 0 50 100
Analysis 1.4. Comparison 1 High versus low dose of oxytocin (all women), Outcome 4 Length of labour
(minute; onset of rst stage to delivery).
Outcome: 4 Length of labour (minute; onset of rst stage to delivery)
Std.
Mean
Difference Weight
Std.
Mean
Difference
Kenyon 2013 46 917 (239) 46 943 (260) 100.0 % -0.10 [ -0.51, 0.31 ]
Total (95% CI) 46 46 100.0 % -0.10 [ -0.51, 0.31 ]
-100 -50 0 50 100
Analysis 1.5. Comparison 1 High versus low dose of oxytocin (all women), Outcome 5 Support received by
staff.
Outcome: 5 Support received by staff
Mean
Difference Weight
Mean
Difference
Kenyon 2013 27 51.2 (6.9) 32 49 (10.2) 100.0 % 2.20 [ -2.19, 6.59 ]
Total (95% CI) 27 32 100.0 % 2.20 [ -2.19, 6.59 ]
-100 -50 0 50 100
Favours low dose Favours high dose
Analysis 1.6. Comparison 1 High versus low dose of oxytocin (all women), Outcome 6 Womens internal
control during labour and birth.
Outcome: 6 Womens internal control during labour and birth
Mean
Difference Weight
Mean
Difference
Kenyon 2013 27 34.6 (9.3) 32 34.9 (9) 100.0 % -0.30 [ -4.99, 4.39 ]
Total (95% CI) 27 32 100.0 % -0.30 [ -4.99, 4.39 ]
-100 -50 0 50 100
Analysis 1.7. Comparison 1 High versus low dose of oxytocin (all women), Outcome 7 Womens external
control during labour and birth.
Outcome: 7 Womens external control during labour and birth
Mean
Difference Weight
Mean
Difference
Kenyon 2013 27 38.4 (9.1) 32 35.8 (9.9) 100.0 % 2.60 [ -2.25, 7.45 ]
Total (95% CI) 27 32 100.0 % 2.60 [ -2.25, 7.45 ]
-100 -50 0 50 100
Analysis 1.8. Comparison 1 High versus low dose of oxytocin (all women), Outcome 8 Spontaneous vaginal
birth.
Outcome: 8 Spontaneous vaginal birth
Bidgood 1987 6/19 5/21 5.0 % 1.33 [ 0.48, 3.65 ]
Kenyon 2013 12/47 10/47 10.5 % 1.20 [ 0.58, 2.50 ]
Xenakis 1995 110/154 81/156 84.5 % 1.38 [ 1.15, 1.65 ]
Total (95% CI) 220 224 100.0 % 1.35 [ 1.13, 1.62 ]
Heterogeneity: Chi
2
= 0.13, df = 2 (P = 0.94); I
2
=0.0%
0.01 0.1 1 10 100
Analysis 1.9. Comparison 1 High versus low dose of oxytocin (all women), Outcome 9 Diagnosis of
chorioamnionitis.
Outcome: 9 Diagnosis of chorioamnionitis
Kenyon 2013 1/47 1/47 2.8 % 1.00 [ 0.06, 15.52 ]
Xenakis 1995 24/154 35/156 97.2 % 0.69 [ 0.43, 1.11 ]
Total (95% CI) 201 203 100.0 % 0.70 [ 0.44, 1.12 ]
Heterogeneity: Chi
2
= 0.07, df = 1 (P = 0.80); I
2
=0.0%
0.01 0.1 1 10 100
Analysis 1.10. Comparison 1 High versus low dose of oxytocin (all women), Outcome 10 Incidence of
hyperstimulation.
Outcome: 10 Incidence of hyperstimulation
n/N n/N
M-
H,Random,95%
CI
M-
H,Random,95%
CI
Bidgood 1987 7/19 0/21 5.7 % 16.50 [ 1.01, 270.78 ]
Jamal 2004 14/100 8/100 37.6 % 1.75 [ 0.77, 3.99 ]
Kenyon 2013 6/47 5/47 26.1 % 1.20 [ 0.39, 3.66 ]
Xenakis 1995 7/154 8/156 30.5 % 0.89 [ 0.33, 2.38 ]
Total (95% CI) 320 324 100.0 % 1.47 [ 0.73, 2.94 ]
Heterogeneity: Tau
2
= 0.16; Chi
2
= 4.40, df = 3 (P = 0.22); I
2
=32%
0.01 0.1 1 10 100
Analysis 1.11. Comparison 1 High versus low dose of oxytocin (all women), Outcome 11 Instrumental
vaginal birth.
Outcome: 11 Instrumental vaginal birth
Bidgood 1987 8/19 9/21 13.3 % 0.98 [ 0.48, 2.02 ]
Kenyon 2013 17/47 21/47 32.6 % 0.81 [ 0.49, 1.33 ]
Xenakis 1995 28/154 35/156 54.1 % 0.81 [ 0.52, 1.26 ]
Total (95% CI) 220 224 100.0 % 0.83 [ 0.61, 1.13 ]
Heterogeneity: Chi
2
= 0.23, df = 2 (P = 0.89); I
2
=0.0%
0.01 0.1 1 10 100
Analysis 1.12. Comparison 1 High versus low dose of oxytocin (all women), Outcome 12 Incidence of
postpartum haemorrhage.
Outcome: 12 Incidence of postpartum haemorrhage
Kenyon 2013 21/47 22/47 100.0 % 0.95 [ 0.61, 1.48 ]
Total (95% CI) 47 47 100.0 % 0.95 [ 0.61, 1.48 ]
0.01 0.1 1 10 100
Analysis 1.13. Comparison 1 High versus low dose of oxytocin (all women), Outcome 13 Epidural analgesia.
Outcome: 13 Epidural analgesia
Kenyon 2013 35/47 34/47 24.1 % 1.03 [ 0.81, 1.31 ]
Xenakis 1995 103/154 108/156 75.9 % 0.97 [ 0.83, 1.13 ]
Total (95% CI) 201 203 100.0 % 0.98 [ 0.86, 1.12 ]
Heterogeneity: Chi
2
= 0.19, df = 1 (P = 0.66); I
2
=0.0%
0.01 0.1 1 10 100
Analysis 1.14. Comparison 1 High versus low dose of oxytocin (all women), Outcome 14 Pathological
cardiotocography (CTG) leading to immediate birth without fetal blood sampling.
Outcome: 14 Pathological cardiotocography (CTG) leading to immediate birth without fetal blood sampling
Kenyon 2013 9/47 15/47 100.0 % 0.60 [ 0.29, 1.23 ]
Total (95% CI) 47 47 100.0 % 0.60 [ 0.29, 1.23 ]
0.01 0.1 1 10 100
Analysis 1.15. Comparison 1 High versus low dose of oxytocin (all women), Outcome 15 Neonatal
admission to special care baby units.
Outcome: 15 Neonatal admission to special care baby units
Kenyon 2013 1/47 7/47 43.9 % 0.14 [ 0.02, 1.12 ]
Xenakis 1995 7/154 9/156 56.1 % 0.79 [ 0.30, 2.06 ]
Total (95% CI) 201 203 100.0 % 0.50 [ 0.22, 1.15 ]
Heterogeneity: Chi
2
= 2.27, df = 1 (P = 0.13); I
2
=56%
0.01 0.1 1 10 100
Analysis 1.16. Comparison 1 High versus low dose of oxytocin (all women), Outcome 16 Apgar score less
than 7 at 5 minutes.
Outcome: 16 Apgar score less than 7 at 5 minutes
Bidgood 1987 0/19 1/21 100.0 % 0.37 [ 0.02, 8.50 ]
Kenyon 2013 0/47 0/47 Not estimable
Xenakis 1995 0/154 0/156 Not estimable
Total (95% CI) 220 224 100.0 % 0.37 [ 0.02, 8.50 ]
0.01 0.1 1 10 100
Analysis 1.17. Comparison 1 High versus low dose of oxytocin (all women), Outcome 17 Umbilical cord
(artery) pH.
Outcome: 17 Umbilical cord (artery) pH
Mean
Difference Weight
Mean
Difference
Bidgood 1987 19 7.27 (0.08) 21 7.27 (0.11) 23.0 % 0.0 [ -0.06, 0.06 ]
Kenyon 2013 47 7.24 (0.08) 47 7.24 (0.08) 77.0 % 0.0 [ -0.03, 0.03 ]
Total (95% CI) 66 68 100.0 % 0.0 [ -0.03, 0.03 ]
Heterogeneity: Chi
2
= 0.0, df = 1 (P = 1.00); I
2
=0.0%
-100 -50 0 50 100
Analysis 1.18. Comparison 1 High versus low dose of oxytocin (all women), Outcome 18 Subgroup analysis:
Caesarean section by parity.
Outcome: 18 Subgroup analysis: Caesarean section by parity
1 Nulliparous women
Bidgood 1987 5/19 7/21 11.1 % 0.79 [ 0.30, 2.07 ]
Kenyon 2013 17/47 15/47 24.9 % 1.13 [ 0.64, 1.99 ]
Xenakis 1995 8/72 26/94 37.5 % 0.40 [ 0.19, 0.83 ]
Subtotal (95% CI) 138 162 73.5 % 0.71 [ 0.47, 1.06 ]
Heterogeneity: Chi
2
= 5.03, df = 2 (P = 0.08); I
2
=60%
2 Multiparous women
Xenakis 1995 8/82 14/62 26.5 % 0.43 [ 0.19, 0.97 ]
Subtotal (95% CI) 82 62 26.5 % 0.43 [ 0.19, 0.97 ]
Total (95% CI) 220 224 100.0 % 0.64 [ 0.44, 0.91 ]
Heterogeneity: Chi
2
= 6.63, df = 3 (P = 0.08); I
2
=55%
Test for subgroup differences: Chi
2
= 1.16, df = 1 (P = 0.28), I
2
=14%
0.01 0.1 1 10 100
W H A T S N E W
Last assessed as up-to-date: 4 July 2013.
Date Event Description
18 June 2013 New citation required but conclusions have not changed Review updated.
18 June 2013 New search has been performed The review was updated following a new search in May
2013. Data from one new trial have been included
(Kenyon 2013). One trial that was previously included
(Continued)
has now been excluded following full translation of the
report as it was not clear that trial participants met the
inclusion criteria for the review (Supajitkulchi 2003).
Two further trials have been excluded (Doppa 2011;
Hayakungchat 2011) andone trial is ongoing (Berg 2012)
. A new author helped to update the review.
C O N T R I B U T I O N S O F A U T H O R S
For the 2013 update, Rintaro Mori (RM), Tokumasu Hironobu (TH), Therese Dowswell (TD) and Sara Kenyon (SK) reviewed the
identied studies. RM wrote the rst draft of the review with substantial input from SK and TD. Debbie Pledge (DP) approved the
version for editorial approval.
For the rst version of the review, Rintaro Mori (RM), Tokumasu Hironobu (TH) and Sara Kenyon (SK) reviewed the identied studies.
RM wrote the rst draft of the review which was substantially commented on by SK. RM revised the document. DP commented at
each stage of the development of the review and approved the version for editorial approval.
D E C L A R A T I O N S O F I N T E R E S T
SKis the chief investigator of an included trial, and hence the trial was assessed by TDand RMindependently. None known, otherwise.
S O U R C E S O F S U P P O R T
Internal sources
National Center for Child Health and Development, Japan.
The University of Liverpool, UK.
External sources
Ministry of Health. Labour and Welfare, Japan.
The study was partially funded by Ministry of Health, Labour and Welfare of Japan through a research grant.
UNDP-UNFPA-UNICEF-WHO-World Bank Special Programme of Research, Development and Research Training in Human
Reproduction (HRP), the Department of Reproductive Health and Research (RHR), World Health Organization, Switzerland.
D I F F E R E N C E S B E T W E E N P R O T O C O L A N D R E V I E W
We have updated the methods to reect the latest Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011). We have
claried that this review only includes women whose labours were delayed, rather than routine augmentation in normal labour. We
have removed the secondary outcome Assisted vaginal delivery and added Spontaneous vaginal birth and Instrumental vaginal birth
as secondary outcomes.
I N D E X T E R M S
Medical Subject Headings (MeSH)
Administration, Oral; Cesarean Section [utilization]; Labor Stage, First [drug effects]; Labor Stage, Second [drug effects; physiology];
Obstetric Labor Complications [
drug therapy]; Oxytocics [
administration & dosage; adverse effects]; Oxytocin [
administration &
dosage; adverse effects]; Randomized Controlled Trials as Topic; Time Factors
MeSH check words
Female; Humans; Pregnancy

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High-dose versus low-dose oxytocin for augmentation of

delayed labour (Review)

Bidgood KA, Steer PJ. A randomized control study of

Xenakis EM, Langer O, Piper JM, Conway D, Berkus

Lazor LZ, Philipson EH, Ingardia CJ, Kobetitsch ES,

Indicates the major publication for the study

drug therapy]; Oxytocics [

administration & dosage; adverse effects]; Oxytocin [

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