Methods

All included studies were parallel group randomised controlled trials and involved two arms. The randomisation method was not always well described and in one study the allocation process was not truly random, and so was assessed as being 'quasi‐randomised' (Dalfrà 2009). All of the studies were described as being 'open‐label' and therefore not blinded. Two studies were multi‐centre trials: one was based in Canada and involved 31 hospitals in Canada, England, Scotland, Spain, Italy, Ireland and the USA (Feig 2017); and one involved 22 hospitals, university, teaching and non‐teaching hospitals in the Netherlands and one university hospital in Belgium (Voormolen 2018). The remaining trials were single centre (Dalfrà 2009; di Biase 1997; Hanson 1984; Manderson 2003; Murphy 2008; Petrovski 2011; Secher 2013; Stubbs 1980; Varner 1983; Wojcicki 2001).

Trial dates

Trial dates were not reported in the study reports for six trials (Dalfrà 2009; di Biase 1997; Manderson 2003; Petrovski 2011; Stubbs 1980; Wojcicki 2001).

For the remaining studies, trials dates were reported as follows: 25 March 2013 to 22 March 2016 (Feig 2017); 1 October 1979 to 1 October 1982 (Hanson 1984); September 2003 to 2006 (Murphy 2008); 15 February 2009 to 15 February 2011 (Secher 2013); 1 February 1980 to 16 September 1981 (Varner 1983); and July 2011 to September 2015 (Voormolen 2018).

Participants

The trials included in this review involved a total of 944 women; 660 with type 1 diabetes, 113 with type 2 diabetes, and 171 women with either type 1 or type 2 diabetes (data not reported separately).

Hanson 1984, Murphy 2008 and Secher 2013 included women with pre‐existing type 1 and type 2 diabetes (however, only Secher 2013 presented the results separately for type 1 and type 2 diabetes). Only women with pre‐existing type 1 diabetes were eligible to participate in di Biase 1997Feig 2017, Manderson 2003,Petrovski 2011,Stubbs 1980,Varner 1983, and Wojcicki 2001. In one trial (Feig 2017), they ran two trials in parallel for pregnant women and for women planning a pregnancy with type 1 diabetes. However the results for most outcomes were reported separately and so we have included the data for the pregnant women in this review. Women with pre‐existing type 1 diabetes and gestational diabetes participated in Dalfrà 2009, however the results are presented separately so only data for women with type 1 diabetes are included in this review. Women with pre‐existing type 1 and type 2 diabetes and gestational diabetes participated in Voormolen 2018, however the results are presented separately for some of the outcomes, so only data for women with type 1 and type 2 diabetes are included in this review. The ethnicity of the women was not mentioned in all trials. As these trials originated from the European countries and the USA, it is assumed that majority of the women were white or Caucasians.

Interventions and comparisons

Continuous glucose monitoring (CGM) was compared with intermittent glucose monitoring in trials by Feig 2017, Murphy 2008, Secher 2013 and Voormolen 2018. Stubbs 1980 and Varner 1983 compared self‐monitoring of blood glucose (SMBG) at home with standard care. In Stubbs 1980 the SMBG group measured blood glucose with a glucometer seven times a day, twice weekly and the standard care group (non‐meter group) checked urine glucose four times daily, with random blood glucose measured at fortnightly clinic visits. In Varner 1983, the SMBG group carried out daily home glucose monitoring four times daily and the standard care group carried out weekly venipuncture three times daily, measured on one day weekly. Hanson 1984 compared self‐monitoring blood glucose at home from the 32nd week until the 36th week of gestation, with weekly hospital visits, and hospitalisation during the 37th week to delivery with a group who were hospitalised from 32nd week until delivery. Manderson 2003 compared timing of glucose monitoring, i.e. pre‐prandial versus post‐prandial. Pre‐prandial refers to measurement of blood glucose before meals while post‐prandial refers to blood glucose measured two hours after a meal. Automated telemedicine monitoring versus conventional system were compared in studies by Dalfrà 2009, di Biase 1997 and Wojcicki 2001. Automated telemedicine monitoring refers to automated transmission of blood glucose values via telephone or Internet to the physicians, which allows immediate attention from the physicians. Petrovski 2011 compared constant CGM with intermittent CGM. CGM refers to glucose measured in subcutaneous tissues every 10 seconds and an average value is stored every five minutes, providing up to 288 measurements per day.

Outcomes

The primary outcome composite outcome, hypertensive disorders of pregnancy was reported by Feig 2017 (including pre‐eclampsia, pregnancy‐induced hypertension and worsening chronic hypertension), and by Voormolen 2018 (pre‐eclampsia and pregnancy‐induced hypertension); caesarean section was reported by Dalfrà 2009; Feig 2017; Hanson 1984; Manderson 2003; Murphy 2008; Petrovski 2011; Secher 2013; Varner 1983; large‐for‐gestational age was reported by Feig 2017; Manderson 2003; Murphy 2008;Secher 2013, (defined as birthweight 90th centile or above); perinatal mortality was reported by Hanson 1984; Manderson 2003; Murphy 2008;Varner 1983); neonatal mortality or morbidity composite was reported by Dalfrà 2009; Feig 2017; Varner 1983; and neurosensory disability was not reported by any trials.

Secondary maternal outcomes reported by the included studies were pre‐eclampsia (Feig 2017; Hanson 1984; Manderson 2003; Murphy 2008;Secher 2013; Voormolen 2018), pregnancy‐induced hypertension (Feig 2017; Hanson 1984; Voormolen 2018), placental abruption (Hanson 1984), weight gain during pregnancy (Feig 2017; Dalfrà 2009; Manderson 2003;Petrovski 2011), behaviour changes associated with the intervention (Feig 2017 (using hypoglycaemia fear survey (HFS II) behaviour subscale which measures two distinct aspects of behavioural avoidance to prevent hypoglycaemia), sense of well‐being and quality of life (Feig 2017 (using three different questionnaires (blood glucose monitoring system rating questionnaire (BGMSRQ), problem areas in diabetes (PAID), short‐form‐12)), use of additional pharmacotherapy (use of additional insulin therapy: Dalfrà 2009; insulin dose: di Biase 1997; Manderson 2003;Petrovski 2011), glycaemic control during/end of treatment (HbA1c) (Dalfrà 2009; di Biase 1997; Feig 2017; Manderson 2003; Murphy 2008; Petrovski 2011; Varner 1983;Wojcicki 2001), maternal hypoglycaemia (Feig 2017; Petrovski 2011) and miscarriage (Feig 2017; Murphy 2008; Secher 2013;Varner 1983).

Secondary perinatal/neonatal outcomes reported by the included studies were stillbirth (reported by Feig 2017; Manderson 2003), neonatal mortality (Murphy 2008; Varner 1983; Voormolen 2018), gestational age at birth (Dalfrà 2009; di Biase 1997; Manderson 2003; Murphy 2008; Varner 1983; Wojcicki 2001), preterm birth less than 37 weeks' gestation (Feig 2017; Hanson 1984; Manderson 2003; Murphy 2008; Petrovski 2011; Secher 2013), preterm birth less than 34 weeks' gestation (Feig 2017;) macrosomia (Feig 2017; Dalfrà 2009; Feig 2017; Manderson 2003; Petrovski 2011; Voormolen 2018: defined as birthweight greater than 4 kg in four studies and birthweight above 90th centile in two studies), small‐for‐gestational age (Feig 2017; Murphy 2008: defined as birthweight 10th centile or below), birthweight (Feig 2017; Dalfrà 2009; Manderson 2003; Murphy 2008; Stubbs 1980; Varner 1983), head circumference (Feig 2017), length (Feig 2017), adiposity (sum of four skin folds (triceps, subscapular, biceps, flank: Feig 2017 ) and (triceps skinfold thickness and subscapular skinfold thickness: Manderson 2003), shoulder dystocia (Feig 2017), respiratory distress syndrome (Feig 2017, Hanson 1984; Manderson 2003; Varner 1983), hypoglycaemia (Feig 2017; Hanson 1984; Manderson 2003; Murphy 2008; Petrovski 2011; Secher 2013; Varner 1983), hyperbilirubinaemia (Feig 2017; Hanson 1984; Manderson 2003; Varner 1983), neonatal hypocalcaemia (Varner 1983), polycythaemia (Varner 1983), relevant biomarker changes associated with the intervention (neonatal cord vein c‐peptide: Feig 2017; Varner 1983, (cord IGF‐1: Manderson 2003), and major anomalies (Feig 2017; Hanson 1984; Murphy 2008).

The only secondary health service use outcomes reported were antenatal hospital admission (Feig 2017; Hanson 1984), neonatal intensive care (NICU) admissions (Manderson 2003; Murphy 2008) and NICU length of admission > 24 hours (Feig 2017).

Outcomes that were not pre‐specified, but are reported in this review are maternal diabetic ketoacidosis (Feig 2017; Petrovski 2011), birth trauma (shoulder dystocia, bone fracture and nerve palsy, pre‐specified as individual outcomes but reported as a composite: Feig 2017; Manderson 2003), neonatal glucose at age one hour (Manderson 2003), transient tachypnoea (Manderson 2003), and feeding difficulties (Hanson 1984). Instrumental vaginal birth was reported in one trial (Voormolen 2018), but the data were not presented separately for women with pre‐existing diabetes and women with GDM. No other trial reported on instrumental vaginal birth.

Secondary maternal outcomes not reported by any of the included studies were: induction of labour, perineal trauma, postpartum haemorrhage, postpartum infection, adherence to the intervention, relevant biomarker changes associated with the intervention (e.g. adiponectin, free fatty acids, triglycerides, high‐density lipoproteins, low‐density lipoproteins, insulin), views of the intervention, maternal mortality.

Secondary perinatal/neonatal outcomes not reported by any of the included studies were: Apgar score (less than seven at five minutes), head circumference and z‐score, length and z‐score, ponderal index, adiposity measured by body mass index (BMI), and minor anomalies.

Health service use outcomes not reported by any of the included studies were: health service use, number of hospital or health professional visits (e.g. midwife, obstetrician, physician, dietician, diabetic nurse), number of antenatal visits, length of antenatal stay, length of postnatal stay (mother), length of postnatal stay (baby), costs to families associated with the management provided, costs associated with the intervention, cost of maternal care, and cost of offspring care.

No studies reported long‐term maternal outcomes (postnatal depression, postnatal weight retention or return to pre‐pregnancy weight, BMI, impaired glucose tolerance, cardiovascular health (as defined by trialists, including blood pressure, hypertension, cardiovascular disease, metabolic syndrome)), later infant or childhood outcomes (weight and z‐scores, height and z‐scores, head circumference and z‐scores, adiposity (e.g. as measured by BMI, skinfold thickness), blood pressure, type 1 diabetes, type 2 diabetes, impaired glucose tolerance, dyslipidaemia or metabolic syndrome, educational achievement), or child in adulthood outcomes (weight, height, adiposity (e.g. as measured by BMI, skinfold thickness), cardiovascular health (as defined by trialists, including blood pressure, hypertension, cardiovascular disease, metabolic syndrome), type 1 diabetes, type 2 diabetes, impaired glucose tolerance, dyslipidaemia or metabolic syndrome, employment, education and social status/achievement).

Some outcomes were reported in a form that could not be used in this review. Hanson 1984 reported the median antenatal hospital stay and neonatal hospital stay, but did not report the standard deviation of blood glucose values, and only reported HbA1c graphically. Manderson 2003 reported the median and interquartile range for cord insulin and length of stay in neonatal unit, and Secher 2013 reported weight gain in pregnancy, HbA1c, plasma glucose, gestational age at birth, and birthweight as median and range. Where results were reported as medians, we felt it was unlikely that the results were normally distributed, and excluded them from meta‐analyses. Percentage of maternal hypoglycaemic episodes was reported by Wojcicki 2001, however the total of all blood glucose data was not available, therefore the frequency was not estimable. Feig 2017 reported the median and interquartile range for the following outcomes, weight gain during pregnancy, postnatal weight retention or return to pre‐pregnancy weight, gestational age at birth and length of antenatal stay. Voormolen 2018 reported on many of the outcomes of this review (see Characteristics of included studies), but did not report these separately for pre‐gestational and gestational diabetes (we have written to authors requesting separate data for the pre‐gestational diabetes group of women).

Sources of trial funding

Sources of trial funding were not reported in two trials (Dalfrà 2009; di Biase 1997).

In Feig 2017, the trial was funded by the Juvenile Diabetes Research Foundation (JDRF) and grants under the JDRF Canadian Clinical Trial Network, a public‐private partnership. Metronic supplied the CGM sensors and CGM systems at reduced cost. In Hanson 1984, the source of funding was reported as being Expressens Perinatal forskningsfond, AIImanna Barnbordshusets Minnesfond, Svenska Diabetesstiftelsen, Nordisk Insulinfond, Swedish Medical Research Council (Project No. 3787), and Tielman's Fund for Pediatric Research. The Department of Health and Social Sevices, Northern lreland, the Northern Ireland Mother and Baby Appeal, the Metabolic Unit Research Fund, Royal Victoria Hospital Belfast, the Royal Maternity Hospital, and the Irish Perinatal Society funded the trial by Manderson 2003. Murphy 2008 was an investigator‐initiated study funded by the Ipswich Diabetes Centre Charity Research Fund. The study equipment (six CGMS Gold monitors and 300 sensors) was donated free of charge by Medtronic UK. The research was sponsored by Ipswich Hospital NHS Trust and was independent of all the study funders (Murphy 2008). The Macedonion Ministry of Health and the Health Care Fund of Macedonia funded Petrovski 2011. In Secher 2013, one of the authors received financial support from the European Foundation of the Study of Diabetes and LifeScan, Rigshopitalet's Research Foundation, the Capital Region of Denmark, the Medical Facuty Foundation of Copenhagen University, Aase and Ejnar Danielsen Foundation, and Master Joiner Sophus Jacobsen and his wife Astrid Jacobsens' Foundation. Stubbs 1980 was funded by the Medical Research Council Project Grant and the British Diabetic Association. Varner 1983 was funded by a Research Fellowship from the Iowa Affiliate of the American Diabetes Association. Voormolen 2018 was funded by ZonMw, The Dutch Organization for Health Research and Development .Continuous glucose monitors were purchased at a discounted price from Medtronic® and were reported as having no role in the study design, data collection, data analysis, data interpretation, or writing of the report. Wojcicki 2001 was supported by grants from the Polish State Committee for Scientific Research, the Bayer Diagnostic Division Warsaw, and the Polish Cellular Telephony Centertel.

Trial authors' declarations of interest

Trial authors' declarations of interest were not reported in Dalfrà 2009; di Biase 1997; Manderson 2003; Stubbs 1980; Varner 1983; Wojcicki 2001.

In Murphy 2008, two trial authors received honorariums for speaking at research symposiums sponsored by Medtronic in 2004 and 2005. In Feig 2017, eight authors report grants from the Juvenile Diabetes Research Foundation during the conduct of the study. Two authors report personal fees from Novo Nordisk, Roche and Medtronic, outside the submitted work. One author reports personal fees from Abbott Diabetes Care and Medtronic (MiniMed Academia), outside the submitted work. One author sits on the Medtronic European Scientific Advisory Board. All remaining authors declare no competing interests. The authors declared that they had no competing financial interests in Petrovski 2011 and in Secher 2013, other than those reported under 'funding' interests. In Voormolen 2018, one of the trial authors received a research grant from ZonMW (the Netherlands Organization for Health Research and Development) and a second author received research grants from Abbott, Dexcom, Medtronic and Sensonics, and also received personal fees from Roche Diabetes Care and Sensonics. A third author is supported by an NHMRC Practitioner Fellowshop (GNT1082548) and reports consultancy for ObsEVa, Merck and Guerbet. All other authors declare no support from any organization or conflict of interest.

See the Characteristics of included studies table for more details.

Random sequence generation

Five studies (Feig 2017; Murphy 2008; Secher 2013; Varner 1983; Voormolen 2018) described the random sequence generation using computer‐generated random numbers or a random number sequence (low risk of bias). Six trials (di Biase 1997; Hanson 1984; Manderson 2003; Petrovski 2011; Stubbs 1980; Wojcicki 2001) did not report how the sequence was generated (unclear risk of bias). One study was quasi‐randomised, allocating women to alternating groups (Dalfrà 2009) (high risk of bias).

Allocation concealment

Adequate and secure concealment of allocation was described in four trials (low risk of bias) (Feig 2017; Manderson 2003; Murphy 2008; Secher 2013); in one trial the randomisation schedule was created remotely by a programme manager, encrypted, and maintained in a secure database, with no access from the research team (Feig 2017), sealed envelopes were used in two of the trials (Manderson 2003; Murphy 2008), while the fourth (Secher 2013) used an automated telephone allocation service (Paravox) provided by an independent organisation. There was no concealment of allocation in Wojcicki 2001 and Dalfrà 2009 (high risk of bias). The other trials only mentioned the participants were randomly allocated into intervention or control groups without describing if there was any concealment of allocation (unclear risk of bias).

Blinding of participants and personnel

As different techniques or timing of glucose monitoring were compared, blinding of neither participants nor assessors was feasible. However, since outcome measures were objective it is unlikely that lack of blinding introduced a risk of bias and so all studies were assessed as being at low risk.

Blinding of outcome assessors

As different techniques or timing of glucose monitoring were compared, blinding of neither participants nor assessors was feasible. However, since outcome measures were objective it is unlikely that lack of blinding introduced a risk of bias so all studies were assessed as being at low risk.

Primary outcomes

Continuous glucose monitoring may reduce the composite outcome of hypertensive disorders of pregnancy (risk ratio (RR) 0.58, 95% confidence interval (CI) 0.39 to 0.84; 2 studies, 384 women; low‐quality evidence,Analysis 1.1), although this did not translate into a clear reduction for pre‐eclampsia, see secondary outcomes below.

Due to moderate heterogeneity, we used random‐effects analysis for caesarean section and there was no clear reduction in rate of caesarean section (average RR 0.94, 95% CI 0.75 to 1.18; 3 studies, 427 women; I² = 41%; moderate‐quality evidence, Analysis 1.2), or large‐for‐gestational age (average RR 0.84, 95% CI 0.57 to 1.26; 3 studies, 421 women; I² = 70%; low‐quality evidence, Analysis 1.3). There was not enough evidence to assess perinatal mortality (RR 0.82, 95% CI 0.05 to 12.61, 71 infants, 1 study, Analysis 1.4, low‐quality evidence) or the composite of neonatal mortality or morbidity (RR 0.80, 95% CI 0.61 to 1.06; 1 study, 200 women) as the evidence was based on single studies of low‐quality.

Neurosensory disability
This outcome was not reported.

Secondary outcomes

There was no clear reduction in pre‐eclampsia (RR 0.65, 95% CI 0.39 to 1.08; 4 studies, 609 women; moderate‐quality evidence,Analysis 1.6) or to pregnancy‐induced hypertension (RR 0.67, 95% CI 0.38 to 1.16; 2 studies, 384 women; low‐quality evidence,Analysis 1.7) with CGM. There was little difference between groups in behaviour changes associated with the intervention as measured using the Hypoglycaemia Fear Survey (HFS II) (Lamb 2017) behaviour subscale at 34 weeks' gestation (mean difference (MD) 1.00, 95% CI ‐1.06 to 3.06; 1 study, 214 women, Analysis 1.8). The 15 items in HFS behaviour subscale measures behaviours aimed at avoiding hypoglycaemia and its possible negative consequences, with higher scores indicating higher fear of hypoglycaemia, with scores ranging from zero to 60.

There was also little difference in sense of well‐being and quality of life as measured using the Short‐Form‐12 (SF‐12) and Problem Areas in Diabetes (PAID) (Venkataraman 2015) which were measured at 34 weeks' gestation (total score) (MD ‐0.70, 95% CI ‐2.50 to 1.10; 1 study, 214 women, Analysis 1.9) (MD 0.80, 95% CI ‐3.06 to 4.66; 1 study, 214 women, Analysis 1.10). The Short‐Form‐12 (SF‐12) is a health‐related quality‐of‐life questionnaire. It consists of 12 questions that measure eight domains assessing physical and mental health. Physical health domains include General Health (GH), Physical Functioning (PF), Role Physical (RP), and Body Pain (BP). Mental health domains include Vitality (VT), Social Functioning (SF), Role Emotional (RE), and Mental Health (MH). The instrument has been validated across a number of chronic diseases and conditions. Physical and Mental Health Composite Scales combine the 12 items, with a high score of 50 equating to good mental and physical health (Huo 2018). The Problem Areas in Diabetes (PAID) instrument was developed to measure emotional distress in people with diabetes. It is a 20‐item scale consisting of emotional problems commonly reported in type 1 and type 2 diabetes mellitus, and has been found to be a valid and reliable scale in Western populations (Venkataraman 2015), with scores ranging from zero to 100, with higher scores reflecting greater emotional distress. The CGM group scored slightly higher in their Blood Glucose Monitoring System Rating Questionnaire (BGMSRQ) (Peyrot 2009) total score at 34 weeks' gestation (MD 4.30, 95% CI 0.73 to 7.87; 1 study, 214 women, Analysis 1.11). This questionnaire aims to measure different aspects about the method of blood glucose monitoring: measures relate to convenience, interference, burden, control, overall satisfaction, desire to switch monitoring system, willingness to recommend current monitoring system, and comparison of current and prior blood glucose monitoring system.

CGM may make little or no difference to maternal glycaemic control as indicated by HbA1c levels (glycated haemoglobin): the mean HbA1c level in the continuous monitoring group was 0.37% lower, 0.78% lower to 0.04% higher (MD ‐0.37 %, 95% CI ‐0.78 to 0.04; 2 studies, 258 women; I² = 81%, Analysis 1.12) and although more women in the continuous monitoring group achieved HbA1c levels less than or equal to 6.5% (48 mmol/mol) at 34 weeks (RR 1.27, 95% CI 1.00 to 1.62; 1 study, 187 women, Analysis 1.13), the results are based on a single study.

There was no clear difference between groups for the following outcomes.

1. Maternal hypoglycaemia (severe) (RR 0.92, 95% CI 0.43 to 1.95; 1 study,154 women, Analysis 1.14)

2. Miscarriage (RR 1.24, 95% CI 0.47 to 3.26; 3 studies, 439 women, Analysis 1.15)

3. Stillbirth (RR 0.34, 95% CI 0.01 to 8.17; 1 study, 211 infants, Analysis 1.16)

4. Neonatal mortality (RR 0.92, 95% CI 0.13 to 6.37; 2 studies, 256 infants, Analysis 1.17)

5. Gestational age at birth (weeks) (MD 0.10 weeks, 95% CI ‐0.57 to 0.77; 1 study, 68 women, Analysis 1.18)

6. Preterm birth < 37 weeks (RR 0.96, 95% CI 0.72 to 1.29; 3 studies, 430 women, Analysis 1.19)

7. Preterm birth < 34 weeks (RR 0.46, 95% CI 0.17 to 1.28; 1 study, 211 women, Analysis 1.20)

8. Macrosomia (average RR 0.84, 95% CI 0.61 to 1.17; 3 studies, 451 women, I² = 34%, Analysis 1.21)

9. Birthweight (kg) (MD ‐0.13 kg, 95% CI ‐0.38 to 0.12; 2 studies, 267 infants, I² = 49%, Analysis 1.22)

10. Small‐for‐gestational age (RR 2.40, 95% CI 0.55 to 10.51; 2 studies, 269 infants, Analysis 1.23)

11. Head circumference (cm) (MD ‐0.20, 95% CI ‐0.79 to 0.39; 1 study, 160 infants, Analysis 1.24)

12. Length (crown‐heel length cm) (MD ‐0.20, 95% CI ‐0.79 to 0.39; 1 study, 160 infants, Analysis 1.25)

13. Adipositiy (sum of four skin folds mm) (MD ‐0.20, 95% CI ‐1.98 to 1.58; 1 study, 160 infants, Analysis 1.26)

14. Shoulder dystocia (RR 3.00, 95% CI 0.12 to 72.77; 1 study, 200 infants, Analysis 1.27)

15. Respiratory distress syndrome (RR 1.00, 95% CI 0.41 to 2.41; 1 study, 200 infants, Analysis 1.28)

16. Neonatal hypoglycaemia (RR 0.66, 95% CI 0.48 to 0.93; 3 studies, 428 infants, Analysis 1.29)

17. Neonatal hyperbilirubinaemia (RR 0.81, 95% CI 0.52 to 1.26; 1 study, 200 infants, Analysis 1.30)

18. Relevant biomarkers associated with the intervention (cord blood c‐peptide levels > 566 pmol/L) (RR 0.95, 95% CI 0.68 to 1.33; 1 study, 200 infants, Analysis 1.31)

19. Relevant biomarkers associated with the intervention (cord blood c‐peptide levels > 2725 pmol/L) (RR 1.00, 95% CI 0.33 to 3.00; 1 study, 200 infants, Analysis 1.32)

20. Major and minor anomalies (RR 0.71, 95% CI 0.16 to 3.13; 2 studies, 285 infants, Analysis 1.33)

21. Number of hospital admissions (mother) (RR 1.25, 95% CI 0.84 to 1.85; 1 study, 207 women, Analysis 1.34)

22. Neonatal intensive care unit admissions (average RR 0.76, 95% CI 0.42 to 1.35; 2 studies, 274 infants, Analysis 1.35)

23. Birth trauma (shoulder dystocia, bone fracture, nerve palsy) (RR 5.00, 95% CI 0.24 to 102.85; 1 study, 200 infants, Analysis 1.37)

24. Diabetic ketoacidosis (RR 1.01, 95% CI 0.14 to 7.03; 1 study, 207 women, Analysis 1.38)

It may reduce neonatal hypoglycaemia (RR 0.66, 95% CI 0.48 to 0.93; 3 studies, 428 infants, Analysis 1.29) and NICU admission of more than 24 hours (RR 0.63, 95% CI 0.42 to 0.93; 1 study, 200 infants, Analysis 1.36).

None of the studies reported on our remaining secondary outcomes.

Primary outcomes

It is uncertain whether self‐monitoring reduces the risk of caesarean section (risk ratio (RR) 0.78, 95% confidence interval (CI) 0.40 to 1.49, 1 study, 28 women, Analysis 2.1, very low‐quality evidence) (Varner 1983). Varner 1983 also reported perinatal mortality and it was too small to show any differences between groups (perinatal mortality: RR 3.00, 95% CI 0.13 to 67.91, 1 study, 28 infants, very low‐quality evidence, Analysis 2.2).

Hypertensive disorders of pregnancy, large‐for‐gestational age, neonatal mortality and morbidity composite and neurosensory disability were not reported in either study.

Secondary outcomes

It is uncertain whether self‐monitoring makes any difference in maternal glycaemic control for post‐prandial blood glucose (MD ‐0.70 mmol/L, 95% CI ‐2.15 to 0.75; 1 study, 13 women, Analysis 2.3), or HbA1c (MD ‐0.10 %, 95% CI ‐1.93 to 1.73, 1 study, 28 women, Analysis 2.4). There were too few women to show any differences in miscarriage (RR 1.00, 95% CI 0.07 to 14.55, 1 study, 30 women, Analysis 2.5), neonatal mortality (RR 3.00, 95% CI 0.13 to 67.91, 1 study, 28 women, Analysis 2.6), or respiratory distress syndrome (RR 3.00, 95% CI 0.13 to 67.91, 1 study, 28 infants, Analysis 2.9). It is uncertain whether there are any differences in gestational age between self‐monitoring groups (MD 0.40 weeks, 95% CI ‐1.65 to 2.45, 1 study, 28 infants, Analysis 2.7), and or in infant birthweight (MD ‐0.18 kg, 95% CI ‐0.49 to 0.13, 2 studies, 41 infants, Analysis 2.8) due to limitations in small sample sizes.

Again it is uncertain whether there are any differences for neonatal hypoglycaemia (RR 0.57, 95% CI 0.21 to 1.52, 1 study, 28 infants, Analysis 2.10), neonatal jaundice (hyperbilirubinaemia) (RR 0.56, 95% CI 0.25 to 1.24, 1 study, 28 infants, Analysis 2.11), hypocalcaemia (RR 1.00, 95% CI 0.07 to 14.45, 1 study, 28 infants, Analysis 2.12), polycythaemia (RR 0.33, 95% CI 0.01 to 7.55, 1 study, 28 infants, Analysis 2.13) and neonatal cord vein C‐peptide (MD 0.13 ng/nl, 95% CI ‐0.50 to 0.76, 1 study, 28 infants, Analysis 2.14).

None of the studies reported on our remaining secondary outcomes.

Primary outcomes

This study of 100 women did not report on the composite outcome, hypertensive disorders of pregnancy. It reported pre‐eclampsia and hypertension in pregnancy, but as separate outcomes.

The results were uncertain for caesarean section (RR 0.96, 95% CI 0.65 to 1.44, Analysis 3.2, very low‐quality evidence), and the sample size was too small to assess perinatal mortality (RR 0.85, 95% CI 0.05 to 13.24, Analysis 3.3, very low‐quality evidence).

Large‐for‐gestational age, mortality or morbidity composite, and neurosensory disability were not reported.

Secondary outcomes

It is uncertain whether there is any difference between self‐monitoring and hospitalisation were shown in the reported secondary outcomes: placental abruption (RR 1.70, 95% CI 0.16 to 18.19, Analysis 3.6); preterm birth < 37 weeks (RR 0.85, 95% CI 0.45 to 1.60, Analysis 3.7); respiratory distress syndrome (RR 2.56, 95% CI 0.28 to 23.74, Analysis 3.8); neonatal hypoglycaemia (RR 1.01, 95% CI 0.50 to 2.03, Analysis 3.9); neonatal jaundice (hyperbilirubinaemia) (RR 2.27, 95% CI 0.64 to 8.07, Analysis 3.10); major anomalies (RR 0.27, 95% CI 0.03 to 2.54, Analysis 3.11).

As would be expected from the nature of the intervention, a lower proportion of women in the self‐monitoring group had antenatal hospital admission (RR 0.19, 95% CI 0.11 to 0.33, Analysis 3.12).

Maternal glycaemic control was reported, however only mean blood glucose was given without standard deviations, and HbA1c was only presented graphically, so we were not able to include these data in the analyses. The mean blood glucose values during the study period were 6.0 mmol/L for the hospital group and 5.9 mmol/L for the home group.

Outcomes that were not pre‐specified

There were no differences between self‐monitoring and hospitalisation in terms of feeding difficulties (RR 0.85, 95% CI 0.41 to 1.78, Analysis 3.13).

None of the studies reported on our remaining secondary outcomes.

Primary outcomes

In one study of 61 women (61 infants), it is uncertain whether there is any difference between pre‐prandial and post‐prandial glucose monitoring for caesarean section (RR 1.45, 95% CI 0.92 to 2.28, Analysis 4.1, very low‐quality evidence), large‐for‐gestational age (RR 1.16, 95% CI 0.73 to 1.85; Analysis 4.2, very low‐quality evidence) and perinatal mortality (RR 2.91, 95% CI 0.12 to 68.66, Analysis 4.3, very low‐quality evidence).

The study did not report the composite outcomes, hypertensive disorders of pregnancy (including pre‐eclampsia, pregnancy‐induced hypertension, eclampsia), mortality or morbidity composite, or neurosensory disability.

Secondary outcomes

It is uncertain whether there are any differences between pre‐prandial and post‐prandial glucose monitoring for the following outcomes: pre‐eclampsia (RR 6.43, 95% CI 0.82 to 50.11, Analysis 4.4); weight gain in pregnancy (MD ‐0.90 kg, 95% CI ‐3.86 to 2.06, Analysis 4.5); use of additional pharmacotherapy shown by insulin dose in units/day and units/kg (MD ‐17.40 units/day, 95% CI ‐43.41 to 8.61, Analysis 4.6; MD ‐0.20 units/kg, 95% CI ‐0.45 to 0.05, Analysis 4.7); glycaemic control shown by mean HbA1c (MD 0.30 %, 95% CI ‐0.08 to 0.68, Analysis 4.8); stillbirth (RR 2.91, 95% CI 0.12 to 68.66, Analysis 4.9); gestational age at birth (MD 0.20 weeks, 95% CI ‐0.84 to 1.24, Analysis 4.10); preterm birth < 37 weeks (RR 1.33, 95% CI 0.62 to 2.84, Analysis 4.11); macrosomia (RR 2.18, 95% CI 0.75 to 6.32, Analysis 4.12), birthweight (MD 0.24 kg, 95% CI ‐0.10 to 0.58, Analysis 4.13); subscapular skinfold thickness (adiposity) (MD 0.60 mm, 95% CI ‐0.18 to 1.38, Analysis 4.14); birth trauma (shoulder dystocia, bone fracture, nerve palsy) (RR 0.48, 95% CI 0.05 to 5.06, Analysis 4.16); respiratory distress syndrome (RR 0.97, 95% CI 0.06 to 14.78, Analysis 4.17); neonatal hypoglycaemia (RR 1.09, 95% CI 0.48 to 2.45, Analysis 4.18); neonatal jaundice (hyperbilirubinaemia) (RR 1.16, 95% CI 0.40 to 3.40, Analysis 4.19); cord IGF‐1 (MD 1.30 μg/L, 95% CI ‐0.70 to 3.30, Analysis 4.20); neonatal glucose at age one hour (not pre‐specified) (MD ‐0.20, 95% CI ‐0.88 to 0.48, Analysis 4.21); transient tachypnoea (not pre‐specified) (RR 2.58, 95% CI 0.76 to 8.81, Analysis 4.22); and neonatal intensive care admissions (RR 1.04, 95% CI 0.62 to 1.74, Analysis 4.23).

Infants in the pre‐prandial monitoring group had higher triceps skinfold thickness (adiposity) (MD 0.60 mm, 95% CI 0.04 to 1.16, Analysis 4.15), although the difference is small and should be considered in the context of no clear difference in large‐for‐gestational age, birthweight, macrosomia, and subscapular skinfold thickness.

None of the studies reported on our remaining secondary outcomes.

Primary outcomes

Again, it is uncertain from one study (Dalfrà 2009) whether there is any difference between automated telemedicine monitoring and conventional monitoring for caesarean section (RR 0.96, 95% CI 0.62 to 1.48, 1 study, 32 women, Analysis 5.1, very low‐quality evidence) and the composite of neonatal mortality or morbidity (RR 1.18, 95% CI 0.53 to 2.62, 1 study, 32 infants, Analysis 5.2).

di Biase 1997 and Wojcicki 2001 did not report these primary outcomes, and none of the studies contributing data to this comparison reported hypertensive disorders of pregnancy, large‐for‐gestational age, perinatal mortality (stillbirth and neonatal mortality), and neurosensory disability.

Secondary outcomes

In one study of 20 women (di Biase 1997), women in the automated telemedicine group had a higher mean insulin requirement at the end of the study (MD 18.40 units/day, 95% CI 12.88 to 23.92, Analysis 5.5). The women in the automated telemedicine group also had lower mean maternal fasting blood glucose before breakfast and before lunch at the end of the study (before breakfast: MD ‐1.00 mmol/L, 95% CI ‐1.22 to ‐0.78, Analysis 5.6; before lunch: MD ‐1.10 mmol/L, 95% CI ‐1.32 to ‐0.88, Analysis 5.7). There was high heterogeneity between studies for maternal HbA1c (random‐effects MD ‐0.17 %, 95% CI ‐0.82 to 0.48, 3 studies, 82 women, Tau² = 0.27, I² = 82%, Analysis 5.8) and maternal post‐prandial blood glucose (random‐effects MD ‐0.80 mmol/L, 95% CI ‐1.67 to 0.08, 3 studies, 50 women,Tau² = 0.35, I² = 86%, Analysis 5.9). Post hoc sensitivity analyses show that this was due to measurements from di Biase 1997. This study showed differences between groups in HbA1c and post‐prandial blood glucose, however the other two studies did not. It seems likely that the higher insulin doses given to women in the automated telemedicine group resulted in lower blood glucose measures.

It was uncertain whether there was any difference between groups for: weight gain in pregnancy (MD ‐0.70, 95% CI ‐4.95 to 3.55, 1 study, 32 women, Analysis 5.10); use of additional insulin therapy (RR 1.00, 95% CI 0.89 to 1.12, 1 study, 32 women, Analysis 5.4); gestational age (MD 0.24 weeks, 95% CI ‐0.39 to 0.88, 3 studies, 84 women,Analysis 5.3); macrosomia (RR 1.18, 95% CI 0.31 to 4.43, 1 study, 32 infants, Analysis 5.11); or birthweight (MD ‐0.16 kg, 95% CI ‐0.64 to 0.32, 1 study, 32 infants, Analysis 5.12).

The percentage of maternal hypoglycaemic episodes was reported by Wojcicki 2001, however, the total of all blood glucose data were not available, therefore the frequency was not estimable.

None of the studies reported on our remaining secondary outcomes.

Primary outcomes

It is uncertain whether constant CGM makes any difference to rates of caesarean section (RR 0.77, 95% CI 0.33 to 1.79, 1 study, 25 women, very low‐quality evidence, Analysis 6.1). Other primary outcomes were not reported (hypertensive disorders of pregnancy, large‐for‐gestational age, perinatal mortality (stillbirth and neonatal mortality), mortality or morbidity composite, and neurosensory disability).

Secondary outcomes

Constant CGM makes little or no difference to weight gain in pregnancy (MD 0.50 kg, 95% CI ‐1.82 to 2.82, 1 study, 25 women, Analysis 6.2), insulin dosage (third trimester: MD ‐0.03, 95% CI ‐1.30 to 1.24, 1 study, 25 women, Analysis 6.3); maternal blood glucose (first trimester: MD ‐0.50 mmol/L, 95% CI ‐2.70 to 1.70, 1 study, 25 women, Analysis 6.4; third trimester: MD ‐0.14 mmol/L, 95% CI ‐2.00 to 1.72, 1 study, 25 women, Analysis 6.5); maternal HbA1c (first trimester: MD ‐0.30 %, 95% CI ‐1.13 to 0.53, 1 study, 25 women, Analysis 6.6; third trimester: MD ‐0.09 %, 95% CI ‐0.69 to 0.51, 1 study, 25 women, Analysis 6.7), maternal hypoglycaemia (RR 0.54, 95% CI 0.06 to 5.24, 1 study, 25 women, Analysis 6.8), diabetic ketoacidosis (not pre‐specified) (RR 0.36, 95% CI 0.02 to 8.05, 1 study, 25 women, Analysis 6.9), preterm birth < 37 weeks (RR 1.08, 95% CI 0.08 to 15.46, 1 study, 25 infants, Analysis 6.10), and macrosomia (RR 1.08, 95% CI 0.08 to 15.46, 1 study, 25 infants, Analysis 6.11). There were no events for neonatal hypoglycaemia (1 study, 25 infants Analysis 6.12).

None of the studies reported on our remaining secondary outcomes.