Your activity: 10158 p.v.
your limit has been reached. plz Donate us to allow your ip full access, Email: [email protected]

Gestational diabetes mellitus: Obstetric issues and management

Gestational diabetes mellitus: Obstetric issues and management
Author:
Aaron B Caughey, MD, PhD
Section Editor:
Erika F Werner, MD, MS
Deputy Editor:
Vanessa A Barss, MD, FACOG
Literature review current through: Feb 2022. | This topic last updated: Feb 18, 2022.

INTRODUCTION — Guidelines consistently recommend screening pregnant patients for gestational diabetes at 24 to 28 weeks of gestation. An increasing number of these patients are being diagnosed with gestational diabetes mellitus (GDM), concomitant with the obesity epidemic. (See "Gestational diabetes mellitus: Screening, diagnosis, and prevention".)

The clinician caring for pregnant patients with GDM should be knowledgeable about the maternal and fetal consequences of the disorder (eg, increased risk of preeclampsia and macrosomia), management of hyperglycemia, pregnancy monitoring, management of pregnancy complications, postpartum care, and long-term follow-up. This topic will discuss most of these issues, but glycemic control is reviewed in detail separately:

(See "Gestational diabetes mellitus: Glycemic control and maternal prognosis".)

(See "Pregestational (preexisting) and gestational diabetes: Intrapartum and postpartum glycemic control".)

CONSEQUENCES OF GDM — In addition to routine pregnancy issues, the prenatal care of patients with GDM focuses on identifying and managing conditions that are increased among patients with glucose impairment. In contrast to patients with pregestational diabetes, patients with true GDM are not at increased risk of having an infant with congenital malformations because the onset of the disorder is after organogenesis, and they do not experience diabetes-related vasculopathy because of the short duration of the disorder. However, it is important to note that some patients diagnosed with GDM actually have unrecognized preexisting diabetes if they were not screened prior to or early in pregnancy.

Short-term consequences — Complications of pregnancy more common in GDM include:

Large for gestational age (LGA) infant and macrosomia – LGA (commonly defined as fetal or neonatal weight at or above the 90th centile for gestational age) and macrosomia (usually defined as birth weight ≥4500 grams) are the most common adverse neonatal outcomes associated with GDM.

Both GDM and obesity are associated with an increased risk of LGA. In one report, the prevalence of LGA among patients with GDM who were normal weight versus obese was 13.6 and 22.3 percent, respectively; these figures are almost twofold higher than those for patients without GDM who were normal weight versus obese: 7.7 and 12.7 percent, respectively [1]. Although illustrative, factors other than maternal weight affect the infant's birth weight. Randomized trials have consistently demonstrated that maternal hyperglycemia significantly increases the chances of having an LGA or macrosomic infant [2-5] and excessive maternal gestational weight gain (>40 pounds [18 kg]) doubles the risk [6]. Maternal hyperglycemia increases the risk for LGA and macrosomia because it leads to increased transplacental transfer of glucose and other nutrients, which induce fetal hyperinsulinism and, in turn, accelerated fetal growth that is asymmetric (normal head size but broader shoulders and increased thoracic and abdominal diameters compared with infants of mothers without diabetes). A prospective cohort study observed that accelerated fetal growth may begin as early as 20 to 28 weeks of gestation [7].

Macrosomia and fetal truncal asymmetry are associated with an increased risk of operative birth (cesarean or instrumental vaginal) and adverse neonatal outcomes, such as shoulder dystocia and its associated complications: brachial plexus injury, fracture, and neonatal depression [8-15]. (See "Fetal macrosomia" and "Shoulder dystocia: Risk factors and planning delivery of high-risk pregnancies" and "Large for gestational age newborn".)

Preeclampsia and gestational hypertension – Patients with GDM are at higher risk of developing preeclampsia and gestational hypertension than patients without GDM. Insulin resistance is the cause of GDM and also appears to be associated with development of preeclampsia and gestational hypertension, which may account for this association [16-25]. (See "Preeclampsia: Clinical features and diagnosis" and "Gestational hypertension".)

Polyhydramnios – Polyhydramnios is more common in patients with GDM. The etiology in GDM is unclear, although a contribution from fetal polyuria secondary to fetal hyperglycemia has been suggested. Its impact in GDM versus non-GDM pregnancies is also uncertain. Two studies reported GDM-related polyhydramnios did not significantly increase perinatal morbidity or mortality [26,27], while a third study reported a markedly increased risk of stillbirth in all nonanomalous pregnancies with polyhydramnios, whether or not these were also complicated by GDM [28]. (See "Polyhydramnios: Etiology, diagnosis, and management".)

Stillbirth – Patients with GDM and suboptimal glucose control appear to have an increased risk of stillbirth compared with the general obstetric population [29-31]. The risk of stillbirth does not appear to be increased in patients with good glycemic control, though ascertainment of good control can be challenging [32].

Neonatal morbidity – Neonates of pregnancies complicated by GDM have been reported to be at increased risk of multiple, often transient, morbidities, including hypoglycemia, hyperbilirubinemia, hypocalcemia, hypomagnesemia, polycythemia, respiratory distress, and/or cardiomyopathy [33,34]. These risks are related, in large part, to maternal hyperglycemia.

In contrast to historical studies, a secondary analysis of data from the Antenatal Late Preterm Steroids (ALPS) trial found that GDM was not associated with a clinically significant difference in neonatal respiratory outcomes; however, information about each participant's glucose control and diabetes treatment was not available [35]. Good glycemic control may have reduced the risk of respiratory problems in the infants of patients with GDM. Baseline differences between patients with GDM versus those without GDM in this study may also account for the findings. (See "Infants of women with diabetes".)

Long-term consequences — Risks associated with GDM extend beyond the pregnancy and neonatal period.

GDM is a strong marker for maternal development of type 2 diabetes, including diabetes-related vascular disease. (See "Gestational diabetes mellitus: Glycemic control and maternal prognosis", section on 'Long-term risk'.)

GDM increases the offspring's risk for developing obesity, impaired glucose tolerance, and diabetes. Poorly controlled maternal diabetes during pregnancy may impact neurodevelopmental outcome; however, evidence is circumstantial and of poor quality. (See "Infants of women with diabetes", section on 'Long-term outcome'.)

PREGNANCY MANAGEMENT — Maintaining good glycemic control is the key intervention for reducing the frequency and/or severity of complications related to GDM. The author's general approach to pregnancy management in GDM is shown in the algorithm (algorithm 1).

Glucose monitoring and control — Glycemic control is the cornerstone of management of any diabetic pregnancy. Glucose monitoring, medical nutritional therapy, exercise, and the use of insulin and antihyperglycemic agents are discussed in detail separately. Briefly, antepartum glycemic targets are:

Fasting blood glucose concentration: <95 mg/dL (5.3 mmol/L)

One-hour postprandial blood glucose concentration: <140 mg/dL (7.8 mmol/L)

Two-hour postprandial glucose concentration: <120 mg/dL (6.7 mmol/L)

There are no standard criteria for describing suboptimal versus poor glucose control. We consider glucose values 20 to 30 percent above the target range suboptimal. (See "Gestational diabetes mellitus: Glycemic control and maternal prognosis".)

Fetal surveillance

A1 GDM with good glucose control — Patients who are euglycemic with nutritional therapy alone (ie, class A1 GDM) and who have no other pregnancy complications (eg, no macrosomia, preeclampsia, growth restriction, polyhydramnios, or oligohydramnios) do not appear to be at increased risk of stillbirth [36]; therefore, omitting antenatal fetal surveillance (nonstress test [NST] and amniotic fluid index, biophysical profile [BPP]) is a reasonable approach for these patients, but practice patterns vary given the range of existing data on this issue.

The American College of Obstetricians and Gynecologists (ACOG) has suggested antenatal fetal assessment beginning at 32 weeks of gestation for patients with GDM and suboptimal glycemic control on nutritional therapy [37]. No specific recommendations were made for fetal assessment in patients with well-controlled glucose levels on nutritional therapy, except for assessment of amniotic fluid volume; this decision was left to local practice patterns.

If the practitioner chooses to order NSTs or BPPs, the tests can be begun closer to term than 32 weeks (eg, 36 weeks) since no increased risk of stillbirth has been demonstrated in this population.

A2 GDM or A1 GDM with suboptimal glucose control — We obtain twice weekly NSTs plus an amniotic fluid index beginning at 32 weeks of gestation in patients who need insulin or an oral antihyperglycemic agent to achieve good glycemic control and in all patients with suboptimal glycemic control (algorithm 1). Ideally, patients with suboptimal glucose control will be brought under better control with diet and/or medication. (See "Overview of antepartum fetal assessment".)

The evidence supporting antenatal fetal testing in pregnancies complicated by GDM consists primarily of data from observational series that report no or rare fetal losses among a group of pregnancies monitored by various antenatal testing regimens [38,39]. There are no randomized trials evaluating antenatal obstetric management of patients with GDM specifically, and findings from the small number of cohort and case-control studies are inconclusive.

The practice pattern that has evolved over decades is to base use of fetal testing on (1) the severity of GDM (ie, whether euglycemia is achieved and whether it is achieved by nutritional therapy or by pharmacologic therapy) and (2) the presence of other risk factors for adverse pregnancy outcome (eg, advanced maternal age, past history of stillbirth, presence of comorbidities such as chronic hypertension).

The timing for initiating testing in the third trimester, the frequency of testing, and the tests utilized (eg, NST, BPP) vary by institution and practice setting.

As some studies have reported that patients with GDM are at increased risk of stillbirth [40,41], we agree with expert opinion, which generally recommends that patients who require insulin or an oral antihyperglycemic agent (ie, class A2 GDM (table 1)) to maintain euglycemia or who have suboptimally controlled blood glucose levels should be managed the same way as patients with pregestational diabetes or other conditions placing the pregnancy at increased risk of adverse outcome. These patients typically undergo periodic antenatal testing, usually initiated at approximately 32 weeks of gestation. Although we perform NSTs with an amniotic fluid index twice per week, there is no strong evidence favoring twice weekly testing over weekly testing or initiating testing at 32 weeks versus later in gestation. For example, some medical centers begin NST weekly at 32 weeks and increase to twice weekly at 36 weeks.

As discussed above, ACOG has suggested antenatal fetal assessment beginning at 32 weeks of gestation for patients treated with insulin or oral agents, even when good glycemic control is achieved with drug therapy, and for patients with suboptimal glucose control on medical nutritional therapy [37].

Monitoring fetal growth — We perform a single third-trimester ultrasound examination at 36 to 39 weeks to estimate fetal weight in all patients with GDM, regardless of degree of metabolic control or requirement for insulin or oral antihyperglycemic agents. Identification of accelerated fetal growth before birth may be useful to identify maternal-fetal pairs who may benefit from scheduled cesarean birth to avoid trauma from shoulder dystocia [42].

In view of the limitations of the available data discussed below, a broad spectrum of practice patterns has evolved. Some clinicians also obtain an ultrasound examination early in the third trimester to identify fetal growth acceleration as this appears to be a sign of suboptimal glycemic control [43]. Others use the information to identify maternal-fetal pairs that may benefit from induction of labor before the fetus grows too large. Still others obtain serial ultrasound examinations every four weeks from diagnosis until birth to identify accelerated fetal growth; tighter glycemic control in these pregnancies may reduce the risk of macrosomia [44,45].

Similar to the situation with antenatal testing, some providers do not monitor fetal growth sonographically in euglycemic patients with A1 GDM (medical nutritional therapy alone) because of concerns that false-positive findings will lead to iatrogenic complications. As an example, one study reported an increase in cesarean birth among patients who had a third-trimester ultrasound examination, even after controlling for birth weight [46].

Estimation of fetal weight is challenging because no method of fetal growth assessment performs well; all current methods are neither particularly sensitive nor specific, especially for identifying the large for gestational age (LGA) fetus [47-49]. One review of pregnant patients with diabetes treated with insulin found that the sonographically estimated fetal weight had to be ≥4800 grams for there to be at least a 50 percent chance that the infant's birth weight would be ≥4500 grams [50]. Studies in nondiabetic pregnancies report similar results [51]. Investigators have tried to find a more sensitive modality to estimate fetal weight, but there is little evidence that these experimental modalities can improve on existing two-dimensional ultrasound technology [52-55]. The diagnosis of LGA/macrosomia is discussed in detail separately. (See "Fetal macrosomia", section on 'Diagnosis' and "Fetal macrosomia", section on 'Patients with diabetes'.)

Management of selected antenatal complications — As discussed above (see 'Consequences of GDM' above), the following antenatal complications are more prevalent in patients with GDM.

Preeclampsia and gestational hypertension – Management of preeclampsia and gestational hypertension is similar to that in patients without GDM. Labetalol can be used for management of severe hypertension; hypoglycemic symptoms are unlikely to be masked in patients with GDM. (See "Preeclampsia: Management and prognosis" and "Gestational hypertension" and "Hypoglycemia in adults with diabetes mellitus".)

However, administration of antenatal corticosteroids (ACS), if indicated, has hyperglycemic effects, beginning approximately 12 hours after the first steroid dose and lasting for approximately five days [56,57]. We monitor capillary blood glucose concentrations regularly (eg, at least every four times daily, but more frequently depending on glucose levels and difficulty in obtaining control) beginning 12 hours after the first dose of betamethasone and continuing for 24 hours after the second dose. We then reduce the frequency to four times per day if glucose levels are reasonably well controlled. If a fasting level exceeds 100 mg/dL (5.5 mmol/L) or a postprandial level exceeds 140 mg/mL (7.8 mmol/L), we would treat with subcutaneous insulin.

ACS are generally not recommended at ≥34 weeks of gestation in patients with diabetes. While the Antenatal Late Preterm Steroids (ALPS) trial found a modest benefit in late preterm gestations, this trial specifically excluded patients with diabetes because of concerns for impact on glycemic control. (See "Antenatal corticosteroid therapy for reduction of neonatal respiratory morbidity and mortality from preterm delivery".)

Preterm labor – Management of preterm labor is the same as that in patients without GDM. Indomethacin and nifedipine are first-line agents for tocolysis, with the choice dependent on gestational age. If these agents are contraindicated, terbutaline can be used, but maternal glucose levels need to be monitored since beta agonists can increase glucose levels. For fasting levels >100 mg/dL (5.5 mmol/L) or postprandial levels >140 mg/mL (7.8 mmol/L), we treat with subcutaneous insulin. (See "Inhibition of acute preterm labor".)

Coadministration of ACS accentuates the increase in glucose levels. Gestational ages for use (ie, <34 weeks), monitoring, and treatment are as described above for patients with preeclampsia or gestational hypertension.

Macrosomia and prediction/prevention of shoulder dystocia – Macrosomia is diagnosed by ultrasound and often accompanied by polyhydramnios. A major concern in the birth of the macrosomic fetus is the occurrence of shoulder dystocia. Issues regarding induction of fetuses <4500 grams versus expectant management are reviewed separately. (See "Shoulder dystocia: Risk factors and planning delivery of high-risk pregnancies", section on 'Women with diabetes'.)

Scheduled cesarean birth is typically offered to patients with GDM and estimated fetal weight ≥4500 grams to prevent shoulder dystocia. (See 'Scheduled cesarean birth for fetal weight ≥4500 grams' below.)

Timing of birth — One of the key issues of the management of patients with GDM is whether to induce labor and, if so, when. The major potential benefits of induction are avoidance of late stillbirth and avoidance of birth-related complications of continued fetal growth, such as shoulder dystocia or cesarean birth for failure to progress. The potential disadvantages are the risks of induction (eg, longer labor, increased tendency for intervention) and increased neonatal morbidity if the induction is before 39 weeks. Increasing evidence suggests that induction of labor in patients with GDM does not result in higher cesarean birth rates than expectant management [58-60].

The optimal timing of birth in GDM has not been evaluated in well-designed trials. The available data [58,61-66] are inadequate to allow a strong evidence-based recommendation; thus, common practice varies somewhat worldwide [45,67].

A1 GDM with good glucose control — Our approach, and the practice pattern that has evolved in many institutions, is to manage pregnancies of patients who remain euglycemic with nutritional therapy and exercise alone (A1 GDM) by beginning a discussion about the possibility of induction of labor and the tradeoffs of induction versus expectant management when the pregnancy reaches 39+0 weeks of gestation, and scheduling an induction between 39+0 to 41+0 weeks of gestation; induction reduces the risks associated with late-term (41+0 to 41+6) and postterm (≥42+0) pregnancy. (See "Postterm pregnancy".)

This relatively noninterventional approach is based on the favorable outcomes reported in a classic uncontrolled case series of 196 patients with class A diabetes managed this way [36]. Although clinical practice varies from institution to institution, there is generally consensus that these patients should not be electively delivered before 39+0 weeks of gestation [68]. Timing of induction between 39+0 and 41+0 weeks is more controversial.

While a study using decision analysis found that fetal and neonatal mortality may be minimized by birth at 38 weeks of gestation, this mathematical model alone is insufficient for changing our clinical practice [69]. ACOG has opined that birth should not be planned before 39+0 weeks of gestation unless otherwise indicated and that expectant management up to 40+6 weeks is generally appropriate with antepartum testing [37].

A2 GDM and A1 GDM with suboptimal glucose control — For patients with GDM whose glucose levels are medically managed with insulin or oral agents (A2 GDM) and patients with A1 GDM with suboptimal glucose control, we suggest induction of labor at 39+0 weeks of gestation based on data from a retrospective cohort study of patients with GDM suggesting that the infant mortality rate at 39+0 weeks (8.7 out of 10,000) was statistically lower than the risk of stillbirth plus infant mortality with expectant management over an additional week (15.2 out of 10,000) [40]. In addition, induction may reduce the risk of shoulder dystocia compared with later birth since birth weight should be less in the absence of ongoing growth in utero [61,62].

Early term birth (37+0 to 38+6 weeks) is not indicated in uncomplicated A2 GDM with well-controlled glucose levels as the risk of stillbirth is low while neonatal morbidity rates are increased at this gestational age [70]; however, if a concomitant medical condition (eg, hypertension) is present or glycemic control is suboptimal on pharmacologic therapy, birth should be undertaken as clinically indicated prior to 39+0 weeks of gestation [61,62]. Fetal weight also needs to be considered. (See 'Scheduled cesarean birth for fetal weight ≥4500 grams' below.)

ACOG suggests birth at 39+0 to 39+6 weeks of gestation for patients with A2 GDM that is well controlled with medication [70]. However, guidance for patients with suboptimal glycemic control on pharmacologic therapy is less precise. They suggest birth at 37+0 to 38+6 weeks of gestation may be reasonable, but that birth prior to 37+0 weeks should only be done when more aggressive efforts to control blood sugars, such as hospitalization, have failed [37].

Scheduled cesarean birth for fetal weight ≥4500 grams — Scheduled cesarean birth to avoid birth trauma is typically offered to patients at 39+0 weeks with GDM and estimated fetal weight ≥4500 grams. The fetal weight threshold at which scheduled cesarean birth should be performed to reduce the risk of birth trauma from shoulder dystocia is controversial. It has been estimated that in diabetic pregnancies with an estimated fetal weight of ≥4500 grams, 443 cesareans would need to be performed to prevent one permanent brachial plexus injury [42]. Whether this tradeoff justifies the increased risks of cesarean birth is unclear. The ACOG practice bulletin on GDM recommends discussing the risks and benefits of scheduled cesarean birth with patients with GDM and estimated fetal weight ≥4500 grams [37].

Glycemic monitoring during labor and birth — Insulin requirements usually decrease during labor as oral caloric intake is typically reduced and the work of labor, particularly uterine contractions, requires extra energy. Patients with GDM who were euglycemic without use of insulin or oral antihyperglycemic drugs during pregnancy do not normally develop hyperglycemia during labor and birth and thus do not need their blood glucose levels checked. However, because of concerns about the validity of baseline glycemic assessments in the outpatient environment, some practitioners and centers choose to assess blood glucose levels in labor.

Patients with GDM who used insulin or oral antihyperglycemic drugs to maintain antepartum euglycemia may need insulin during labor and birth to maintain euglycemia. Periodic assessment of maternal glucose levels during labor and treatment of hyperglycemia are prudent, although intrapartum maternal hyperglycemia leading to an adverse neonatal outcome is infrequent [71].

The goal of treatment is to reduce the risk of neonatal hypoglycemia. Although prolonged neonatal hypoglycemia is primarily due to fetal exposure to chronic hyperglycemia during pregnancy and resultant fetal pancreatic hyperplasia, transient hypoglycemia can be caused by intrapartum maternal hyperglycemia, which induces an acute rise in fetal insulin [72-76].

Intrapartum glucose monitoring and management of insulin and oral antihyperglycemic medications during spontaneous labor, before induction, and before scheduled cesarean birth are discussed in detail separately. (See "Pregestational (preexisting) and gestational diabetes: Intrapartum and postpartum glycemic control".)

Management of labor for fetal weight ≥4500 grams — If a patient with estimated fetal weight ≥4500 grams decides to undergo a trial of labor, we follow labor progress closely and perform an operative vaginal birth only if second stage descent has been normal because forceps- or vacuum-assisted birth is associated with a higher risk of shoulder dystocia and brachial plexus injury, with the risk even higher with the use of vacuum as compared with forceps [77,78]. (See "Shoulder dystocia: Risk factors and planning delivery of high-risk pregnancies", section on 'Planning delivery in high-risk pregnancies'.)

POSTPARTUM MANAGEMENT AND FOLLOW-UP — Patients with GDM should be able to resume a normal diet postpartum. After birth, the hyperglycemic effects of placental hormones dissipate rapidly. Thus, most patients revert back to their prepregnancy glycemic status shortly after birth, ranging from almost immediately to a week postpartum. Postpartum glucose monitoring and therapy, if indicated, are reviewed separately. (See "Pregestational (preexisting) and gestational diabetes: Intrapartum and postpartum glycemic control", section on 'Women with gestational diabetes'.)

Breastfeeding — Breastfeeding should be encouraged since it benefits both mother and child. (See "Maternal and economic benefits of breastfeeding" and "Infant benefits of breastfeeding".)

Breastfeeding improves maternal glucose metabolism and thus may reduce the glucose levels obtained during a postpartum glucose tolerance test (GTT) [79-81], especially if the patient breastfeeds during the test [82]. Theoretically, this could lead to a spurious result.

Several prospective studies have reported that breastfeeding decreased the long-term incidence of type 2 diabetes after a diagnosis of GDM compared with not breastfeeding [83-86]. Higher lactation intensity and longer duration were inversely associated with the risk, independent of weight loss and after adjusting for risk factors for type 2 diabetes (sociodemographic characteristics, prenatal metabolic status and course, perinatal outcome, lifestyle behaviors).

Contraception — While any type of contraception is acceptable as long as the usual medical contraindications to use are absent, we recommend long-acting reversible contraception (eg, intrauterine device [IUD], contraceptive implant) because of the minimal risk of unplanned pregnancy with these methods [87]. There is no convincing evidence that hormonal contraceptives (estrogen-progestin or progestin-only) increase the user's risk of developing diabetes [88]. Choosing contraceptives with lower systemic hormone levels should, in theory, minimize any changes in metabolic parameters. If a patient is concerned about hormonal issues, a copper-releasing IUD is a good alternative.

Screening for overt diabetes — Since some patients with GDM may have previously unrecognized type 2 diabetes mellitus, we agree with the Endocrine Society recommendations to check glucose concentrations for 24 to 72 hours after birth to exclude ongoing hyperglycemia [89]. If fasting glucose concentrations suggest overt diabetes (fasting glucose ≥126 mg/dL [7 mmol/L] or a postprandial glucose is ≥200 mg/dL [11.1 mmol/L]), treatment of hyperglycemia is warranted; the type of treatment (diet, exercise, weight reduction, medication) should be decided on a case-by-case basis, often with consultation from a diabetologist.

Patients who have fasting glucose levels below 126 mg/dL (7 mmol/L) after birth should have a two-hour 75 gram oral GTT 4 to 12 weeks postpartum to test for diabetes or prediabetes. (See "Gestational diabetes mellitus: Glycemic control and maternal prognosis", section on 'Follow-up'.)

Patients with diabetes are managed as medically appropriate. (See "Initial management of hyperglycemia in adults with type 2 diabetes mellitus".)

Patients with a normal GTT are counseled about their future risk of developing type 2 diabetes and cardiovascular disease, encouraged to adopt lifestyle changes for risk reduction (eg, healthy diet, weight loss, exercise), and informed about the importance of close follow-up with their primary care provider and rescreening at appropriate intervals. These issues are discussed in detail separately. (See "Gestational diabetes mellitus: Glycemic control and maternal prognosis", section on 'Follow-up' and "Screening for type 2 diabetes mellitus".)

Screening for depression — Although screening for depression is indicated in all postpartum patients, clinicians should be aware that postpartum depression is more common among patients with diabetes (pregestational or gestational) than in nondiabetic patients [90]. (See "Postpartum unipolar major depression: Epidemiology, clinical features, assessment, and diagnosis", section on 'Screening'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Diabetes mellitus in pregnancy".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Gestational diabetes (diabetes that starts during pregnancy) (The Basics)")

Beyond the Basics topics (see "Patient education: Gestational diabetes (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Screening for and birth of the macrosomic fetus

Ultrasound – We perform a single third-trimester ultrasound at 36 to 39 weeks to screen for macrosomia in all patients with gestational diabetes mellitus (GDM). (See 'Monitoring fetal growth' above.)

Scheduled cesarean birth – Scheduled cesarean birth to avoid birth trauma is typically offered at 39+0 weeks to patients with GDM (any class) and an estimated fetal weight ≥4500 grams. These patients should be counseled about the poor predictive ability of ultrasound estimates of fetal weight and the risks and benefits of cesarean birth in the current and future pregnancies. (See 'Scheduled cesarean birth for fetal weight ≥4500 grams' above.)

Fetal surveillance and timing of birth in patients with A1 GDM well controlled with nutritional medical therapy alone – These patients are not at increased risk for stillbirth.

Antenatal fetal surveillance – We do not order antenatal fetal testing (nonstress test, biophysical profile) in these patients unless they have a standard obstetric indication for fetal surveillance (eg, growth restriction). (See 'Fetal surveillance' above.)

Timing of induction – For candidates for vaginal birth, we offer induction of labor at 39+0 weeks of gestation and suggest performing induction by 41+0 weeks of gestation (Grade 2C), as with other late term pregnancies. (See 'Timing of birth' above and "Postterm pregnancy".)

Fetal surveillance and timing of birth in patients with A2 GDM (ie, on pharmacologic therapy) or A1 GDM with suboptimal glucose control – These patients may be at increased risk for stillbirth.

Antenatal fetal surveillance – We suggest a standard form of antenatal fetal testing. The optimal testing regimen has not been established from rigorous studies. We order twice weekly antenatal testing, using a nonstress test with an amniotic fluid index, starting at 32 weeks of gestation. Ideally, patients with suboptimal glucose control will be brought under better control with diet and/or medication. (See 'Fetal surveillance' above.)

Timing of induction – For candidates for vaginal birth, we suggest induction of labor at 39+0 weeks of gestation (Grade 2C). Potential benefits include lower rates of: macrosomia and large for gestational age infants, shoulder dystocia, cesarean birth, and stillbirth. If a concomitant medical condition (eg, hypertension) is present or glycemic control is suboptimal on pharmacologic therapy, birth should be undertaken as clinically indicated prior to 39+0 weeks of gestation. (See 'Timing of birth' above.)

The American College of Obstetricians and Gynecologists suggests birth at 39+0 to 39+6 weeks of gestation for patients with A2 GDM that is well controlled with medication. For patients with suboptimal glycemic control on pharmacologic therapy, birth at 37+0 to 38+6 weeks may be reasonable, but that birth prior to 37+0 weeks should only be done when more aggressive efforts to control blood sugars, such as hospitalization, have failed.

Postpartum care

Breastfeeding – All patients should be encouraged to breastfeed. A potential benefit of breastfeeding is that it improves glucose metabolism in the short term. (See 'Breastfeeding' above.)

Contraception – While any type of contraception is acceptable as long as the usual medical contraindications to use are absent, we suggest long-acting reversible contraception to minimize the risk of unplanned pregnancy. (See 'Contraception' above.)

Postpartum testing for diabetes – All patients with GDM should have a two-hour 75 gram oral glucose tolerance test between 4 and 12 weeks postpartum (see 'Postpartum management and follow-up' above):

-Those with a normal test should be informed of their future increased risk for diabetes and cardiovascular disease, counseled about preventive measures that they can adopt, and informed of the need for rescreening at periodic intervals.

-Those with diabetes are managed as medically appropriate.

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Michael F Greene, MD, who contributed to an earlier version of this topic review.

REFERENCES

  1. Black MH, Sacks DA, Xiang AH, Lawrence JM. The relative contribution of prepregnancy overweight and obesity, gestational weight gain, and IADPSG-defined gestational diabetes mellitus to fetal overgrowth. Diabetes Care 2013; 36:56.
  2. HAPO Study Cooperative Research Group, Metzger BE, Lowe LP, et al. Hyperglycemia and adverse pregnancy outcomes. N Engl J Med 2008; 358:1991.
  3. Crowther CA, Hiller JE, Moss JR, et al. Effect of treatment of gestational diabetes mellitus on pregnancy outcomes. N Engl J Med 2005; 352:2477.
  4. Kwik M, Seeho SK, Smith C, et al. Outcomes of pregnancies affected by impaired glucose tolerance. Diabetes Res Clin Pract 2007; 77:263.
  5. Garner P, Okun N, Keely E, et al. A randomized controlled trial of strict glycemic control and tertiary level obstetric care versus routine obstetric care in the management of gestational diabetes: a pilot study. Am J Obstet Gynecol 1997; 177:190.
  6. Hillier TA, Pedula KL, Vesco KK, et al. Excess gestational weight gain: modifying fetal macrosomia risk associated with maternal glucose. Obstet Gynecol 2008; 112:1007.
  7. Sovio U, Murphy HR, Smith GC. Accelerated Fetal Growth Prior to Diagnosis of Gestational Diabetes Mellitus: A Prospective Cohort Study of Nulliparous Women. Diabetes Care 2016; 39:982.
  8. Dooley SL, Metzger BE, Cho NH. Gestational diabetes mellitus. Influence of race on disease prevalence and perinatal outcome in a U.S. population. Diabetes 1991; 40 Suppl 2:25.
  9. Lipscomb KR, Gregory K, Shaw K. The outcome of macrosomic infants weighing at least 4500 grams: Los Angeles County + University of Southern California experience. Obstet Gynecol 1995; 85:558.
  10. Lazer S, Biale Y, Mazor M, et al. Complications associated with the macrosomic fetus. J Reprod Med 1986; 31:501.
  11. Rouse DJ, Owen J. Prophylactic cesarean delivery for fetal macrosomia diagnosed by means of ultrasonography--A Faustian bargain? Am J Obstet Gynecol 1999; 181:332.
  12. Bérard J, Dufour P, Vinatier D, et al. Fetal macrosomia: risk factors and outcome. A study of the outcome concerning 100 cases >4500 g. Eur J Obstet Gynecol Reprod Biol 1998; 77:51.
  13. Stotland NE, Caughey AB, Breed EM, Escobar GJ. Risk factors and obstetric complications associated with macrosomia. Int J Gynaecol Obstet 2004; 87:220.
  14. Cohen BF, Penning S, Ansley D, et al. The incidence and severity of shoulder dystocia correlates with a sonographic measurement of asymmetry in patients with diabetes. Am J Perinatol 1999; 16:197.
  15. Nesbitt TS, Gilbert WM, Herrchen B. Shoulder dystocia and associated risk factors with macrosomic infants born in California. Am J Obstet Gynecol 1998; 179:476.
  16. Casey BM, Lucas MJ, Mcintire DD, Leveno KJ. Pregnancy outcomes in women with gestational diabetes compared with the general obstetric population. Obstet Gynecol 1997; 90:869.
  17. Yogev Y, Xenakis EM, Langer O. The association between preeclampsia and the severity of gestational diabetes: the impact of glycemic control. Am J Obstet Gynecol 2004; 191:1655.
  18. Innes KE, Wimsatt JH, McDuffie R. Relative glucose tolerance and subsequent development of hypertension in pregnancy. Obstet Gynecol 2001; 97:905.
  19. Joffe GM, Esterlitz JR, Levine RJ, et al. The relationship between abnormal glucose tolerance and hypertensive disorders of pregnancy in healthy nulliparous women. Calcium for Preeclampsia Prevention (CPEP) Study Group. Am J Obstet Gynecol 1998; 179:1032.
  20. Carpenter MW. Gestational diabetes, pregnancy hypertension, and late vascular disease. Diabetes Care 2007; 30 Suppl 2:S246.
  21. Yogev, Chen, Hod, et al. Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study: preeclampsia. Am J Obstet Gynecol 2010; 202:255.e1.
  22. Parretti E, Lapolla A, Dalfrà M, et al. Preeclampsia in lean normotensive normotolerant pregnant women can be predicted by simple insulin sensitivity indexes. Hypertension 2006; 47:449.
  23. Sierra-Laguado J, García RG, Celedón J, et al. Determination of insulin resistance using the homeostatic model assessment (HOMA) and its relation with the risk of developing pregnancy-induced hypertension. Am J Hypertens 2007; 20:437.
  24. Hauth JC, Clifton RG, Roberts JM, et al. Maternal insulin resistance and preeclampsia. Am J Obstet Gynecol 2011; 204:327.e1.
  25. Bryson CL, Ioannou GN, Rulyak SJ, Critchlow C. Association between gestational diabetes and pregnancy-induced hypertension. Am J Epidemiol 2003; 158:1148.
  26. Shoham I, Wiznitzer A, Silberstein T, et al. Gestational diabetes complicated by hydramnios was not associated with increased risk of perinatal morbidity and mortality. Eur J Obstet Gynecol Reprod Biol 2001; 100:46.
  27. Biggio JR Jr, Wenstrom KD, Dubard MB, Cliver SP. Hydramnios prediction of adverse perinatal outcome. Obstet Gynecol 1999; 94:773.
  28. Pilliod RA, Page JM, Burwick RM, et al. The risk of fetal death in nonanomalous pregnancies affected by polyhydramnios. Am J Obstet Gynecol 2015; 213:410.e1.
  29. Girz BA, Divon MY, Merkatz IR. Sudden fetal death in women with well-controlled, intensively monitored gestational diabetes. J Perinatol 1992; 12:229.
  30. Aberg A, Rydhström H, Källén B, Källén K. Impaired glucose tolerance during pregnancy is associated with increased fetal mortality in preceding sibs. Acta Obstet Gynecol Scand 1997; 76:212.
  31. Dudley DJ. Diabetic-associated stillbirth: incidence, pathophysiology, and prevention. Obstet Gynecol Clin North Am 2007; 34:293.
  32. Langer O, Rodriguez DA, Xenakis EM, et al. Intensified versus conventional management of gestational diabetes. Am J Obstet Gynecol 1994; 170:1036.
  33. Blank A, Grave GD, Metzger BE. Effects of gestational diabetes on perinatal morbidity reassessed. Report of the International Workshop on Adverse Perinatal Outcomes of Gestational Diabetes Mellitus, December 3-4, 1992. Diabetes Care 1995; 18:127.
  34. Hod M, Merlob P, Friedman S, et al. Gestational diabetes mellitus. A survey of perinatal complications in the 1980s. Diabetes 1991; 40 Suppl 2:74.
  35. Werner EF, Romano ME, Rouse DJ, et al. Association of Gestational Diabetes Mellitus With Neonatal Respiratory Morbidity. Obstet Gynecol 2019; 133:349.
  36. Gabbe SG, Mestman JG, Freeman RK, et al. Management and outcome of class A diabetes mellitus. Am J Obstet Gynecol 1977; 127:465.
  37. ACOG Practice Bulletin No. 190: Gestational Diabetes Mellitus. Obstet Gynecol 2018; 131:e49.
  38. Kjos SL, Leung A, Henry OA, et al. Antepartum surveillance in diabetic pregnancies: predictors of fetal distress in labor. Am J Obstet Gynecol 1995; 173:1532.
  39. Landon MB, Gabbe SG. Antepartum fetal surveillance in gestational diabetes mellitus. Diabetes 1985; 34 Suppl 2:50.
  40. Rosenstein MG, Cheng YW, Snowden JM, et al. The risk of stillbirth and infant death stratified by gestational age in women with gestational diabetes. Am J Obstet Gynecol 2012; 206:309.e1.
  41. Cheng YW, Chung JH, Block-Kurbisch I, et al. Treatment of gestational diabetes mellitus: glyburide compared to subcutaneous insulin therapy and associated perinatal outcomes. J Matern Fetal Neonatal Med 2012; 25:379.
  42. Rouse DJ, Owen J, Goldenberg RL, Cliver SP. The effectiveness and costs of elective cesarean delivery for fetal macrosomia diagnosed by ultrasound. JAMA 1996; 276:1480.
  43. Kjos SL, Schaefer-Graf UM. Modified therapy for gestational diabetes using high-risk and low-risk fetal abdominal circumference growth to select strict versus relaxed maternal glycemic targets. Diabetes Care 2007; 30 Suppl 2:S200.
  44. Ben-Haroush A, Chen R, Hadar E, et al. Accuracy of a single fetal weight estimation at 29-34 weeks in diabetic pregnancies: can it predict large-for-gestational-age infants at term? Am J Obstet Gynecol 2007; 197:497.e1.
  45. Hod M, Kapur A, Sacks DA, et al. The International Federation of Gynecology and Obstetrics (FIGO) Initiative on gestational diabetes mellitus: A pragmatic guide for diagnosis, management, and care. Int J Gynaecol Obstet 2015; 131 Suppl 3:S173.
  46. Little SE, Edlow AG, Thomas AM, Smith NA. Estimated fetal weight by ultrasound: a modifiable risk factor for cesarean delivery? Am J Obstet Gynecol 2012; 207:309.e1.
  47. Engstrom JL, Work BA Jr. Prenatal prediction of small- and large-for-gestational age neonates. J Obstet Gynecol Neonatal Nurs 1992; 21:486.
  48. Humphries J, Reynolds D, Bell-Scarbrough L, et al. Sonographic estimate of birth weight: relative accuracy of sonographers versus maternal-fetal medicine specialists. J Matern Fetal Neonatal Med 2002; 11:108.
  49. Johnstone FD, Prescott RJ, Steel JM, et al. Clinical and ultrasound prediction of macrosomia in diabetic pregnancy. Br J Obstet Gynaecol 1996; 103:747.
  50. McLaren RA, Puckett JL, Chauhan SP. Estimators of birth weight in pregnant women requiring insulin: a comparison of seven sonographic models. Obstet Gynecol 1995; 85:565.
  51. Smith GC, Smith MF, McNay MB, Fleming JE. The relation between fetal abdominal circumference and birthweight: findings in 3512 pregnancies. Br J Obstet Gynaecol 1997; 104:186.
  52. Hackmon R, Bornstein E, Ferber A, et al. Combined analysis with amniotic fluid index and estimated fetal weight for prediction of severe macrosomia at birth. Am J Obstet Gynecol 2007; 196:333.e1.
  53. Scioscia M, Scioscia F, Vimercati A, et al. Estimation of fetal weight by measurement of fetal thigh soft-tissue thickness in the late third trimester. Ultrasound Obstet Gynecol 2008; 31:314.
  54. Cromi A, Ghezzi F, Di Naro E, et al. Large cross-sectional area of the umbilical cord as a predictor of fetal macrosomia. Ultrasound Obstet Gynecol 2007; 30:861.
  55. Higgins MF, Russell NM, Mulcahy CH, et al. Fetal anterior abdominal wall thickness in diabetic pregnancy. Eur J Obstet Gynecol Reprod Biol 2008; 140:43.
  56. Mathiesen ER, Christensen AB, Hellmuth E, et al. Insulin dose during glucocorticoid treatment for fetal lung maturation in diabetic pregnancy: test of an algorithm [correction of analgoritm]. Acta Obstet Gynecol Scand 2002; 81:835.
  57. Refuerzo JS, Garg A, Rech B, et al. Continuous glucose monitoring in diabetic women following antenatal corticosteroid therapy: a pilot study. Am J Perinatol 2012; 29:335.
  58. Feghali MN, Caritis SN, Catov JM, Scifres CM. Timing of delivery and pregnancy outcomes in women with gestational diabetes. Am J Obstet Gynecol 2016; 215:243.e1.
  59. Alberico S, Businelli C, Wiesenfeld U, et al. Gestational diabetes and fetal growth acceleration: induction of labour versus expectant management. Minerva Ginecol 2010; 62:533.
  60. Sutton AL, Mele L, Landon MB, et al. Delivery timing and cesarean delivery risk in women with mild gestational diabetes mellitus. Am J Obstet Gynecol 2014; 211:244.e1.
  61. Kjos SL, Henry OA, Montoro M, et al. Insulin-requiring diabetes in pregnancy: a randomized trial of active induction of labor and expectant management. Am J Obstet Gynecol 1993; 169:611.
  62. Lurie S, Insler V, Hagay ZJ. Induction of labor at 38 to 39 weeks of gestation reduces the incidence of shoulder dystocia in gestational diabetic patients class A2. Am J Perinatol 1996; 13:293.
  63. Conway DL, Langer O. Elective delivery of infants with macrosomia in diabetic women: reduced shoulder dystocia versus increased cesarean deliveries. Am J Obstet Gynecol 1998; 178:922.
  64. Lurie S, Matzkel A, Weissman A, et al. Outcome of pregnancy in class A1 and A2 gestational diabetic patients delivered beyond 40 weeks' gestation. Am J Perinatol 1992; 9:484.
  65. Peled Y, Perri T, Chen R, et al. Gestational diabetes mellitus--implications of different treatment protocols. J Pediatr Endocrinol Metab 2004; 17:847.
  66. Alberico S, Erenbourg A, Hod M, et al. Immediate delivery or expectant management in gestational diabetes at term: the GINEXMAL randomised controlled trial. BJOG 2017; 124:669.
  67. Biesty LM, Egan AM, Dunne F, et al. Planned birth at or near term for improving health outcomes for pregnant women with gestational diabetes and their infants. Cochrane Database Syst Rev 2018; 1:CD012910.
  68. Spong CY, Mercer BM, D'alton M, et al. Timing of indicated late-preterm and early-term birth. Obstet Gynecol 2011; 118:323.
  69. Niu B, Lee VR, Cheng YW, et al. What is the optimal gestational age for women with gestational diabetes type A1 to deliver? Am J Obstet Gynecol 2014; 211:418.e1.
  70. American College of Obstetricians and Gynecologists’ Committee on Obstetric Practice, Society for Maternal-Fetal Medicine. Medically Indicated Late-Preterm and Early-Term Deliveries: ACOG Committee Opinion, Number 831. Obstet Gynecol 2021; 138:e35.
  71. Ryan EA, Al-Agha R. Glucose control during labor and delivery. Curr Diab Rep 2014; 14:450.
  72. Flores-le Roux JA, Sagarra E, Benaiges D, et al. A prospective evaluation of neonatal hypoglycaemia in infants of women with gestational diabetes mellitus. Diabetes Res Clin Pract 2012; 97:217.
  73. Barrett HL, Morris J, McElduff A. Watchful waiting: a management protocol for maternal glycaemia in the peripartum period. Aust N Z J Obstet Gynaecol 2009; 49:162.
  74. Andersen O, Hertel J, Schmølker L, Kühl C. Influence of the maternal plasma glucose concentration at delivery on the risk of hypoglycaemia in infants of insulin-dependent diabetic mothers. Acta Paediatr Scand 1985; 74:268.
  75. Kenepp NB, Kumar S, Shelley WC, et al. Fetal and neonatal hazards of maternal hydration with 5% dextrose before caesarean section. Lancet 1982; 1:1150.
  76. Jovanovic L. Glucose and insulin requirements during labor and delivery: the case for normoglycemia in pregnancies complicated by diabetes. Endocr Pract 2004; 10 Suppl 2:40.
  77. Caughey AB, Sandberg PL, Zlatnik MG, et al. Forceps compared with vacuum: rates of neonatal and maternal morbidity. Obstet Gynecol 2005; 106:908.
  78. Demissie K, Rhoads GG, Smulian JC, et al. Operative vaginal delivery and neonatal and infant adverse outcomes: population based retrospective analysis. BMJ 2004; 329:24.
  79. Tigas S, Sunehag A, Haymond MW. Metabolic adaptation to feeding and fasting during lactation in humans. J Clin Endocrinol Metab 2002; 87:302.
  80. Lenz S, Kühl C, Hornnes PJ, Hagen C. Influence of lactation on oral glucose tolerance in the puerperium. Acta Endocrinol (Copenh) 1981; 98:428.
  81. Kjos SL, Henry O, Lee RM, et al. The effect of lactation on glucose and lipid metabolism in women with recent gestational diabetes. Obstet Gynecol 1993; 82:451.
  82. Gunderson EP, Crites Y, Chiang V, et al. Influence of breastfeeding during the postpartum oral glucose tolerance test on plasma glucose and insulin. Obstet Gynecol 2012; 120:136.
  83. Gunderson EP, Hurston SR, Ning X, et al. Lactation and Progression to Type 2 Diabetes Mellitus After Gestational Diabetes Mellitus: A Prospective Cohort Study. Ann Intern Med 2015; 163:889.
  84. Ziegler AG, Wallner M, Kaiser I, et al. Long-term protective effect of lactation on the development of type 2 diabetes in women with recent gestational diabetes mellitus. Diabetes 2012; 61:3167.
  85. Ley SH, Chavarro JE, Li M, et al. Lactation Duration and Long-term Risk for Incident Type 2 Diabetes in Women With a History of Gestational Diabetes Mellitus. Diabetes Care 2020; 43:793.
  86. Gunderson EP, Lewis CE, Lin Y, et al. Lactation Duration and Progression to Diabetes in Women Across the Childbearing Years: The 30-Year CARDIA Study. JAMA Intern Med 2018; 178:328.
  87. Curtis KM, Tepper NK, Jatlaoui TC, et al. U.S. Medical Eligibility Criteria for Contraceptive Use, 2016. MMWR Recomm Rep 2016; 65:1.
  88. Lopez LM, Grimes DA, Schulz KF. Steroidal contraceptives: effect on carbohydrate metabolism in women without diabetes mellitus. Cochrane Database Syst Rev 2014; :CD006133.
  89. Blumer I, Hadar E, Hadden DR, et al. Diabetes and pregnancy: an endocrine society clinical practice guideline. J Clin Endocrinol Metab 2013; 98:4227.
  90. Kozhimannil KB, Pereira MA, Harlow BL. Association between diabetes and perinatal depression among low-income mothers. JAMA 2009; 301:842.
Topic 4800 Version 58.0

References

1 : The relative contribution of prepregnancy overweight and obesity, gestational weight gain, and IADPSG-defined gestational diabetes mellitus to fetal overgrowth.

2 : Hyperglycemia and adverse pregnancy outcomes.

3 : Effect of treatment of gestational diabetes mellitus on pregnancy outcomes.

4 : Outcomes of pregnancies affected by impaired glucose tolerance.

5 : A randomized controlled trial of strict glycemic control and tertiary level obstetric care versus routine obstetric care in the management of gestational diabetes: a pilot study.

6 : Excess gestational weight gain: modifying fetal macrosomia risk associated with maternal glucose.

7 : Accelerated Fetal Growth Prior to Diagnosis of Gestational Diabetes Mellitus: A Prospective Cohort Study of Nulliparous Women.

8 : Gestational diabetes mellitus. Influence of race on disease prevalence and perinatal outcome in a U.S. population.

9 : The outcome of macrosomic infants weighing at least 4500 grams: Los Angeles County + University of Southern California experience.

10 : Complications associated with the macrosomic fetus.

11 : Prophylactic cesarean delivery for fetal macrosomia diagnosed by means of ultrasonography--A Faustian bargain?

12 : Fetal macrosomia: risk factors and outcome. A study of the outcome concerning 100 cases>4500 g.

13 : Risk factors and obstetric complications associated with macrosomia.

14 : The incidence and severity of shoulder dystocia correlates with a sonographic measurement of asymmetry in patients with diabetes.

15 : Shoulder dystocia and associated risk factors with macrosomic infants born in California.

16 : Pregnancy outcomes in women with gestational diabetes compared with the general obstetric population.

17 : The association between preeclampsia and the severity of gestational diabetes: the impact of glycemic control.

18 : Relative glucose tolerance and subsequent development of hypertension in pregnancy.

19 : The relationship between abnormal glucose tolerance and hypertensive disorders of pregnancy in healthy nulliparous women. Calcium for Preeclampsia Prevention (CPEP) Study Group.

20 : Gestational diabetes, pregnancy hypertension, and late vascular disease.

21 : Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study: preeclampsia.

22 : Preeclampsia in lean normotensive normotolerant pregnant women can be predicted by simple insulin sensitivity indexes.

23 : Determination of insulin resistance using the homeostatic model assessment (HOMA) and its relation with the risk of developing pregnancy-induced hypertension.

24 : Maternal insulin resistance and preeclampsia.

25 : Association between gestational diabetes and pregnancy-induced hypertension.

26 : Gestational diabetes complicated by hydramnios was not associated with increased risk of perinatal morbidity and mortality.

27 : Hydramnios prediction of adverse perinatal outcome.

28 : The risk of fetal death in nonanomalous pregnancies affected by polyhydramnios.

29 : Sudden fetal death in women with well-controlled, intensively monitored gestational diabetes.

30 : Impaired glucose tolerance during pregnancy is associated with increased fetal mortality in preceding sibs.

31 : Diabetic-associated stillbirth: incidence, pathophysiology, and prevention.

32 : Intensified versus conventional management of gestational diabetes.

33 : Effects of gestational diabetes on perinatal morbidity reassessed. Report of the International Workshop on Adverse Perinatal Outcomes of Gestational Diabetes Mellitus, December 3-4, 1992.

34 : Gestational diabetes mellitus. A survey of perinatal complications in the 1980s.

35 : Association of Gestational Diabetes Mellitus With Neonatal Respiratory Morbidity.

36 : Management and outcome of class A diabetes mellitus.

37 : ACOG Practice Bulletin No. 190: Gestational Diabetes Mellitus.

38 : Antepartum surveillance in diabetic pregnancies: predictors of fetal distress in labor.

39 : Antepartum fetal surveillance in gestational diabetes mellitus.

40 : The risk of stillbirth and infant death stratified by gestational age in women with gestational diabetes.

41 : Treatment of gestational diabetes mellitus: glyburide compared to subcutaneous insulin therapy and associated perinatal outcomes.

42 : The effectiveness and costs of elective cesarean delivery for fetal macrosomia diagnosed by ultrasound.

43 : Modified therapy for gestational diabetes using high-risk and low-risk fetal abdominal circumference growth to select strict versus relaxed maternal glycemic targets.

44 : Accuracy of a single fetal weight estimation at 29-34 weeks in diabetic pregnancies: can it predict large-for-gestational-age infants at term?

45 : The International Federation of Gynecology and Obstetrics (FIGO) Initiative on gestational diabetes mellitus: A pragmatic guide for diagnosis, management, and care.

46 : Estimated fetal weight by ultrasound: a modifiable risk factor for cesarean delivery?

47 : Prenatal prediction of small- and large-for-gestational age neonates.

48 : Sonographic estimate of birth weight: relative accuracy of sonographers versus maternal-fetal medicine specialists.

49 : Clinical and ultrasound prediction of macrosomia in diabetic pregnancy.

50 : Estimators of birth weight in pregnant women requiring insulin: a comparison of seven sonographic models.

51 : The relation between fetal abdominal circumference and birthweight: findings in 3512 pregnancies.

52 : Combined analysis with amniotic fluid index and estimated fetal weight for prediction of severe macrosomia at birth.

53 : Estimation of fetal weight by measurement of fetal thigh soft-tissue thickness in the late third trimester.

54 : Large cross-sectional area of the umbilical cord as a predictor of fetal macrosomia.

55 : Fetal anterior abdominal wall thickness in diabetic pregnancy.

56 : Insulin dose during glucocorticoid treatment for fetal lung maturation in diabetic pregnancy: test of an algorithm [correction of analgoritm].

57 : Continuous glucose monitoring in diabetic women following antenatal corticosteroid therapy: a pilot study.

58 : Timing of delivery and pregnancy outcomes in women with gestational diabetes.

59 : Gestational diabetes and fetal growth acceleration: induction of labour versus expectant management.

60 : Delivery timing and cesarean delivery risk in women with mild gestational diabetes mellitus.

61 : Insulin-requiring diabetes in pregnancy: a randomized trial of active induction of labor and expectant management.

62 : Induction of labor at 38 to 39 weeks of gestation reduces the incidence of shoulder dystocia in gestational diabetic patients class A2.

63 : Elective delivery of infants with macrosomia in diabetic women: reduced shoulder dystocia versus increased cesarean deliveries.

64 : Outcome of pregnancy in class A1 and A2 gestational diabetic patients delivered beyond 40 weeks' gestation.

65 : Gestational diabetes mellitus--implications of different treatment protocols.

66 : Immediate delivery or expectant management in gestational diabetes at term: the GINEXMAL randomised controlled trial.

67 : Planned birth at or near term for improving health outcomes for pregnant women with gestational diabetes and their infants.

68 : Timing of indicated late-preterm and early-term birth.

69 : What is the optimal gestational age for women with gestational diabetes type A1 to deliver?

70 : Medically Indicated Late-Preterm and Early-Term Deliveries: ACOG Committee Opinion, Number 831.

71 : Glucose control during labor and delivery.

72 : A prospective evaluation of neonatal hypoglycaemia in infants of women with gestational diabetes mellitus.

73 : Watchful waiting: a management protocol for maternal glycaemia in the peripartum period.

74 : Influence of the maternal plasma glucose concentration at delivery on the risk of hypoglycaemia in infants of insulin-dependent diabetic mothers.

75 : Fetal and neonatal hazards of maternal hydration with 5% dextrose before caesarean section.

76 : Glucose and insulin requirements during labor and delivery: the case for normoglycemia in pregnancies complicated by diabetes.

77 : Forceps compared with vacuum: rates of neonatal and maternal morbidity.

78 : Operative vaginal delivery and neonatal and infant adverse outcomes: population based retrospective analysis.

79 : Metabolic adaptation to feeding and fasting during lactation in humans.

80 : Influence of lactation on oral glucose tolerance in the puerperium.

81 : The effect of lactation on glucose and lipid metabolism in women with recent gestational diabetes.

82 : Influence of breastfeeding during the postpartum oral glucose tolerance test on plasma glucose and insulin.

83 : Lactation and Progression to Type 2 Diabetes Mellitus After Gestational Diabetes Mellitus: A Prospective Cohort Study.

84 : Long-term protective effect of lactation on the development of type 2 diabetes in women with recent gestational diabetes mellitus.

85 : Lactation Duration and Long-term Risk for Incident Type 2 Diabetes in Women With a History of Gestational Diabetes Mellitus.

86 : Lactation Duration and Progression to Diabetes in Women Across the Childbearing Years: The 30-Year CARDIA Study.

87 : U.S. Medical Eligibility Criteria for Contraceptive Use, 2016.

88 : Steroidal contraceptives: effect on carbohydrate metabolism in women without diabetes mellitus.

89 : Diabetes and pregnancy: an endocrine society clinical practice guideline.

90 : Association between diabetes and perinatal depression among low-income mothers.