Gestational diabetes mellitus: Glucose

management and maternal prognosis

Author:
Celeste Durnwald, MD
Section Editors:
David M Nathan, MD
Erika F Werner, MD, MS
Deputy Editor:
Vanessa A Barss, MD, FACOG
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Aug 2022. | This topic last updated: Mar 18, 2022.

INTRODUCTION Treatment of gestational diabetes mellitus (GDM) can

improve pregnancy outcome. Many patients can achieve glucose target levels with
nutritional therapy alone, but up to 30 percent will require pharmacotherapy [1].
Even patients with mildly elevated glucose levels who do not meet standard
criteria for GDM may have more favorable pregnancy outcomes if treated since the
relationship between glucose levels and adverse pregnancy outcomes such as
macrosomia exists continuously across the spectrum of increasing glucose levels
[2-9].
Glucose management in patients with GDM is reviewed here. Screening, diagnosis,
and obstetric management are discussed separately. (See "Gestational diabetes
mellitus: Screening, diagnosis, and prevention" and "Gestational diabetes mellitus:
Obstetric issues and management".)

RATIONALE FOR TREATMENT Treatment of GDM is important to

minimize maternal and neonatal morbidity. In a U S Preventive Services Task Force

meta-analysis of randomized trials, compared with no treatment, appropriate
management of GDM (nutritional therapy, self-blood glucose monitoring,
administration of insulin when target blood glucose concentrations are not met
with diet alone) resulted in reductions in [10]:
●Preeclampsia (7.2 versus 11.7 percent; relative risk [RR] 0.62, 95% CI 0.43-
0.89; three trials, moderate quality)
●Birth weight >4000 g (8.4 versus 17.4 percent; RR 0.50, 95% CI 0.35-0.71; five
trials, moderate quality)
 ●Shoulder dystocia (1.5 versus 3.5 percent; RR 0.42, 95% CI 0.23-0.77; three
trials, moderate quality)

The only identified potential harm from treatment of GDM was an increased
number of prenatal visits; however, the frequency and consequences of maternal
hypoglycemia in patients treated with insulin were not reported. No statistically
significant differences in rates of cesarean birth, induction of labor, small for
gestational age newborns, neonatal hypoglycemia, neonatal hyperbilirubinemia,
neonatal respiratory complications, birth trauma, or neonatal intensive care unit
admission were demonstrated compared with no treatment, although the quality
of evidence was low.

Some authors have suggested that avoiding maternal obesity and excessive
gestational weight gain may be more important than detecting and treating GDM
because maternal weight may be more closely related to adverse outcomes,
particularly fetal overgrowth, than glucose intolerance [11]. However, data from
the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study refute this
hypothesis. In HAPO, both obesity and GDM (International Association of Diabetes
and Pregnancy Study Groups criteria) were independently predictive of
macrosomia, preeclampsia, primary cesarean birth, and neonatal adiposity [2].
Few trials have evaluated long-term effects of maternal treatment of GDM on
offspring. In a study of 500 offspring of treated versus untreated mothers with
mild GDM, treatment during pregnancy did not reduce late adverse metabolic
outcomes (eg, obesity, glucose intolerance) in offspring age 5 to 10 years [12]. This
finding may reflect lack of a true treatment effect, inadequate treatment of
hyperglycemia during pregnancy, the mildness of the glucose intolerance, or
inadequate power to show modest differences in outcome because of the low
prevalence of these disorders prior to puberty, and the small numbers of study
participants. (Mild GDM was defined as fasting plasma glucose <95 mg/dL and two
of three timed measurements that exceeded established thresholds [one hour,
180 mg/dL; two hours, 155 mg/dL; three hours, 140 mg/dL]).

MEDICAL NUTRITIONAL THERAPY Medical nutritional therapy is the

process by which the dietary plan is tailored for patients with diabetes, based on
medical, lifestyle, and personal factors. Patients with GDM should receive medical
nutritional counseling by a registered dietitian (when possible) upon diagnosis and
be placed on an appropriate diet. The goals are to [13]:
●Achieve normoglycemia
 ●Prevent ketosis
●Provide adequate nutrition
●Provide adequate gestational weight gain based on maternal body mass
index (BMI)
●Contribute to fetal well-being
Most patients (up to 85 percent) with GDM based on Carpenter and Coustan
criteria can achieve target glucose levels with lifestyle modification alone [3,14]. A
detailed review of medical nutritional therapy for individuals with diabetes can be
found separately. (See "Nutritional considerations in type 1 diabetes mellitus".)
The specific diet that achieves optimum maternal and newborn outcomes in GDM
is unclear [15-17]. A key simple, achievable intervention is to emphasize the
benefits of elimination, or at least reduction, of consumption of sugar-sweetened
beverages (eg, soft drinks, fruit drinks) and encourage drinking water instead.
Noncaloric sweeteners may be used in moderation. Traditionally, restricting
carbohydrate intake (particularly simple carbohydrates) has been favored because
it appears to reduce postprandial hyperglycemia [18] and fetal overgrowth
[19,20].
In a systematic review of randomized trials comparing a variety of dietary
interventions (eg, low glycemic index, DASH, low carbohydrate, energy restriction,
soy protein, fat modification, ethnic, high fiber) with conventional dietary
recommendations for patients with GDM (18 trials, 1151 participants), dietary
intervention overall reduced fasting and postprandial glucose levels (fasting: -4.07
mg/dL, 95% CI -7.58 to -0.57; postprandial -7.78 mg/dL, 95% CI -12.27 to -3.29),
need for medication (relative risk [RR] 0.65, 95% CI 0.47-0.88), birth weight (-170.62
g, 95% CI -333.64 to -7.60), and macrosomia (RR 0.49, 95% CI 0.27-0.88) [16]. When
analyzed by diet subtype, low glycemic index, DASH, low carbohydrate, and
ethnicity-based diets had beneficial effects on maternal glucose levels. A limitation
of the analysis was that all of the trials had small sample sizes.
Probiotics and high fiber diets do not appear to improve glycemic control [21,22].
Meal plan — A typical meal plan for patients with GDM includes three small- to
moderate-sized meals and two to four snacks. Ongoing adjustment of the meal
plan is based upon results of self-glucose monitoring, appetite, and weight-gain
patterns, as well as consideration for maternal dietary preferences and work,
leisure, and exercise schedules.

Close follow-up is important to ensure nutritional adequacy. Individual assessment

and self-blood glucose monitoring are used to determine and modify specific
nutrition/food recommendations. If insulin therapy is added to nutritional therapy,
a primary goal is to maintain carbohydrate consistency at meals and snacks to
facilitate insulin adjustments.

Calories — The caloric requirements of patients with GDM are the same as those
for pregnant patients without GDM [23]. For individuals with a prepregnancy BMI
in the healthy range, caloric requirements in the first trimester are the same as
before pregnancy and generally increase by 340 calories per day in the second
trimester and 452 calories per day in the third trimester [24]. Individuals who are
underweight, overweight, or obese should work with a registered dietician to
determine their specific caloric requirements. (See "Gestational weight gain".)
Carbohydrate intake — Once the caloric needs are calculated, carbohydrate
intake is determined as it is the primary nutrient affecting postprandial glucose
levels. The total amount of carbohydrate consumed, the distribution of
carbohydrate intake over meals and snacks, and the type of carbohydrate
consumed can be manipulated to blunt postprandial hyperglycemia.
Dietary Reference Intakes (DRI) for all pregnant people is a minimum of 175 g of
carbohydrate per day and 28 g of fiber [23]. There is sparse evidence from
randomized trials as to the ideal carbohydrate intake for individuals with GDM. We
limit carbohydrate intake to 40 percent of total calories while ensuring that
ketonuria does not ensue [25,26]. Adequately powered studies are needed to
evaluate the effect of various dietary interventions on perinatal outcomes in GDM.
Many patients will need individual adjustment of the amount of carbohydrate by
15 to 30 g at each meal, depending on their postprandial glucose levels, which are
directly dependent upon the carbohydrate content of the meal or snack [27]. The
postprandial glucose rise can be blunted if the diet is carbohydrate restricted.
However, reducing carbohydrates to decrease postprandial glucose levels may
lead to higher consumption of fat, which may have adverse effects on maternal
insulin resistance and fetal body composition.
In a meta-analysis of randomized trials of dietary intervention in patients with
GDM, low carbohydrate diets had a favorable effect on postprandial blood glucose
concentrations and significantly lowered the need for insulin therapy but did not
affect other maternal or newborn outcomes (eg, macrosomia, cesarean birth,
gestational weight gain), although the data were insufficient to detect small or
moderate statistical differences in obstetric outcomes between the patient groups
[28]. (See "Dietary carbohydrates", section on 'Glycemic index' and "Nutritional
considerations in type 2 diabetes mellitus", section on 'Glycemic index and
glycemic load'.)
Protein and fat intake — The remaining calories come from protein (20 percent
of total calories or approximately 71 g per day [23]) and fats (40 percent of total
calories; saturated fat intake should be <7 percent of total calories). Protein intake
should be distributed throughout the day and included in all meals and snacks to
promote satiety, slow the absorption of carbohydrates into the bloodstream, and
provide adequate calories.

A bedtime high-protein snack is recommended to prevent accelerated (ie,

starvation) ketosis overnight and maintain fasting glucose levels within the target
range.

Gestational weight gain/loss — After prescribing the diet, it is important to pay

attention to subsequent changes in weight. In a retrospective cohort study
including over 31,000 patients with GDM, those with appropriate gestational
weight gain (table 1) had optimal outcomes, while excessive gestational weight
gain was associated with a significantly increased risk of having a large for
gestational age newborn, preterm birth, and cesarean birth [29]. Although
suboptimal weight gain increased the likelihood of avoiding pharmacotherapy of
GDM and decreased the likelihood of having a large for gestational age newborn,
there were also more small for gestational age newborns in this group (7.3 versus
5.6 percent). The data in this study were not corrected for potential confounders,
such as smoking. (See "Obesity in pregnancy: Complications and maternal
management" and "Gestational weight gain", section on 'Recommendations for
gestational weight gain'.)
Some patients experience minimal weight loss (one to five pounds) or weight
stabilization for the first few weeks after beginning nutritional therapy, which
should be evaluated in the overall context of gestational weight gain and ongoing
surveillance of weight gain in the weeks thereafter. Weight loss is generally not
recommended during pregnancy, although controversy exists regarding this
recommendation for patients with obesity, especially class II or III. For pregnant
people with obesity, a modest energy restriction of 30 percent below the DRI for
pregnant people (175 g carbohydrate, 71 g protein, 28 g fiber [23]) can often be
achieved while meeting gestational weight gain recommendations and without
causing ketosis [30]. (See "Gestational weight gain", section on 'Recommendations
for gestational weight gain'.)

EXERCISE Adults with diabetes are encouraged to perform 30 to 60

minutes of moderate-intensity aerobic activity (40 to 60 percent maximal oxygen

uptake [VO2max]) on most days of the week (at least 150 minutes of moderate-
intensity aerobic exercise per week). A program of moderate exercise is
recommended as part of the treatment plan for patients with diabetes as long as
they have no medical or obstetric contraindications to this level of physical activity.
Exercise that increases muscle mass, including circuit training, appears to improve
glucose management, primarily from increased tissue sensitivity to insulin. As a
result, exercise can reduce both fasting and postprandial blood glucose
concentrations and, in some patients with GDM, the need for insulin may be
obviated [31]. (See "Exercise during pregnancy and the postpartum
period" and "Effects of exercise in adults with diabetes mellitus".)

GLUCOSE MONITORING Patients should self-monitor their glucose

concentrations. Glucose meters measure capillary blood glucose, almost all

available glucose meters provide plasma equivalent values rather than whole-
blood glucose values. Thus, results from most available glucose meters and
venous plasma glucose measured in a laboratory should be comparable.
(See "Glucose monitoring in the management of nonpregnant adults with
diabetes mellitus".)
Intermittent self-monitoring of blood glucose — We suggest that patients self-
monitor blood glucose levels [32-35]:
●Before breakfast (ie, fasting glucose level) and
●At one or at two hours after the beginning of each meal

Results should be recorded in a glucose log, along with dietary information. This
facilitates recognition of glycemic patterns and helps to interpret results stored in
the memory of glucose meters.

We prefer the one-hour postprandial measurement as it corresponds more closely

to the maximum insulin peak in patients using rapid-acting insulin analogs. The
value of fasting plus postprandial versus preprandial measurement was suggested
by a trial that randomly assigned 66 insulin-treated patients with GDM to
management according to results of fasting plus postprandial monitoring (one
hour after meals) or according to preprandial-only blood glucose concentrations
[36]. Postprandial monitoring had several benefits as compared with preprandial
monitoring: better glycemic management (glycated hemoglobin [A1C] value 6.5
versus 8.1 percent), a lower incidence of large for gestational age newborns (12
versus 42 percent), and a lower rate of cesarean birth for cephalopelvic
disproportion (12 versus 36 percent).
Can the frequency of self-monitoring be reduced? — When initially diagnosed
with GDM, we ask patients to measure their blood glucose concentration at least
four times daily, as described above (see 'Intermittent self-monitoring of blood
glucose' above). Multiple daily measurements allow recognition of patients who
should begin pharmacologic therapy.
There is no strong evidence regarding the frequency of glucose testing,
particularly in patients on nutritional therapy who consistently have glucose levels
in the target range (see 'Glucose target' below) [37,38], but decreasing the
frequency of testing to every other day in specific patients with mild GDM (defined
as no more than intermittent glucose elevations that are 5 to 10 mg/dL above
targets), no signs of fetal overgrowth (defined as abdominal circumference (AC)
>75th percentile or estimated fetal weight (EFW) ≥90th percentile), and normal
amniotic fluid volume (ie, no polyhydramnios), likely improves the patient's quality
of life.
In a randomized trial of patients with GDM on nutritional therapy who
demonstrated glucose levels in the target range after one week of four times daily
glucose testing, those assigned to every other day testing had similar birth
weights and frequency of macrosomia as those who continued to test four times
daily [39].
Continuous glucose monitoring — Continuous glucose monitoring (CGM) allows
determination of peak postprandial glucose levels, mean glucose level, episodes of
nocturnal hyperglycemia, and percent time in range for a 24-hour period. We do
not routinely use CGM in patients with GDM because of cost and it has not been
proven to improve maternal or fetal outcome, but few trials have been performed.
When CGM was compared with frequent self-monitoring of blood glucose in a
meta-analysis of two small randomized trials, outcomes were similar for both
approaches: cesarean birth (risk ratio [RR] 0.91, 95% CI 0.68-1.20), large for
gestational age newborn (RR 0.67, 95% CI 0.43-1.05), neonatal hypoglycemia (RR
0.79, 95% CI 0.35-1.78) [40]. There were no perinatal deaths. Larger trials may
clarify whether the favorable trends that were observed are real.

Although use of CGM has no clear advantages for most patients, it may be
considered in patients who cannot consistently check fingerstick glucose levels and
are willing to wear a device. Cost may be a barrier to use.

Glucose target — The American Diabetes Association (ADA) and the American
College of Obstetricians and Gynecologists (ACOG) recommend the following
upper limits for glucose levels, with insulin therapy initiated if they are exceeded,
but acknowledge that these thresholds have been extrapolated from
recommendations proposed for pregnant patients with preexisting diabetes
[23,41]:
 ●Fasting and preprandial 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)
These targets are well above the mean glucose values in pregnant people without
diabetes described in a literature review of studies of the normal 24-hour glycemic
profile of pregnant people [42]. In this review, which had a total of 255 pregnant
people without diabetes who were mostly in the late third trimester and without
obesity, the pooled weighted mean glucose values (±1 SD) were fasting 71±8
mg/dL (3.9±0.4 mmol/L), one-hour postprandial 109±13 mg/dL (6.0±0.7 mmol/L),
two-hour postprandial 99±10 mg/dL (5.5±0.6 mmol/L), and 24-hour glucose 88±10
mg/dL (4.9±0.6 mmol/L). These levels were derived from measurements on whole
blood, plasma, self-monitored capillary glucose measurements, or tissue fluid
(CGM). Although glucose levels in whole blood, plasma, and interstitial fluid differ,
there was some consistency in the results. If two standard deviations are added to
the means outlined in the systematic review, the upper limit of normal fasting
glucose would be 87 mg/dL (4.8 mmol/L), the corresponding one-hour
postprandial value would be 135 mg/dL (7.5 mmol/L), and the upper limit of
normal two-hour value would be 119 mg/dL (6.6 mmol/L); while the fasting value is
somewhat lower than the target 95 mg/dL (5.3 mmol/L), the postprandial values
are not dissimilar to the targets described above.
Glycated hemoglobin — A1C may be a helpful ancillary test in assessing glycemic
management during pregnancy [43,44]. It is not clear whether or how often it
should be monitored in patients with GDM with glucose levels are in the target
range. If measured and there is a discrepancy between the A1C and glucose
values, then potential causes should be investigated. (See "Measurements of
glycemic control in diabetes mellitus", section on 'Racial/ethnic
differences' and "Measurements of glycemic control in diabetes mellitus", section
on 'Unexpected or discordant values'.)
High-quality normative data for A1C in each trimester are not available. A1C values
tend to be lower in pregnant compared with nonpregnant people [45] because the
average blood glucose concentration is approximately 20 percent lower in
pregnant people, and in the first half of pregnancy, there is a rise in red cell mass
and a slight increase in red blood cell turnover [46,47]. Other factors that have
been reported to affect A1C values include race (although it is not clear whether
the higher A1C levels observed in Black persons compared with White persons are
due to differences in glucose levels or racial differences in the glycation of
hemoglobin [48]) and iron status (chronic iron deficiency anemia increases A1C,
treatment of iron deficiency anemia with iron lowers A1C). Sources of variation in
A1C levels are discussed in detail separately. (See "Measurements of glycemic
control in diabetes mellitus", section on 'Glycated hemoglobin (A1C)'.)

MONITORING FOR KETONURIA We do not routinely monitor urinary

ketones in pregnant people with GDM, as diabetic ketoacidosis is extremely rare in

patients first diagnosed with diabetes during pregnancy [49,50]. Episodes of
physiological ketonemia and ketonuria are not uncommon in pregnancy and can
occur with hypocaloric diets [51]. Studies have reported inconsistent findings
regarding a potential association between ketonuria and impaired cognitive
outcome in offspring [52-56].

PHARMACOTHERAPY

Goal — The goal of pharmacotherapy is to manage glucose levels so that the

majority are no higher than the upper limit of the target range, without inducing
any episodes of hypoglycemia. Overly tight metabolic control (average blood
glucose levels ≤86 mg/dL [4.8 mmol/L]) has no additional benefits and increases
the risk for iatrogenic growth restriction [57,58].
Indications for pharmacotherapy
●Glucose levels above the target range – If glucose targets cannot be
maintained by medical nutritional therapy, then pharmacotherapy should be
initiated, but the degree of hyperglycemia at which the disadvantages of
initiating insulin therapy are clearly outweighed by the benefits has not been
definitively determined and varies among providers [59].
We initiate pharmacotherapy when over 30 percent of the blood glucose
values in a week are above target glucose thresholds (see 'Glucose
target' above). Our general approach is described in the algorithm (algorithm
1).
In a retrospective cohort study of patients with GDM, initiating
pharmacotherapy when 20 to 39 percent of glucose levels were above goal
compared with ≥40 percent above goal was associated with a reductions in
preterm birth (7.4 versus 15.7 percent), neonatal intensive care unit
admission (4.0 versus 11.7 percent), and large for gestational age newborn
(9.1 versus 21.2 percent) [60].
●Fetal overgrowth – Data from some randomized trials suggest that
pharmacotherapy, specifically insulin, in the subgroup of patients with
 indirect evidence of fetal hyperinsulinemia (eg, abdominal circumference [AC]
>75th percentile or estimated fetal weight [EFW] ≥90th percentile on the early
third-trimester sonogram) can reduce the occurrence of macrosomia and
large for gestational age in newborns, even in patients with GDM who are not
hyperglycemic at the time pharmacotherapy is initiated.
In a meta-analysis including only two trials, compared with conventional
hyperglycemia-based management in patients with a broad GDM severity
spectrum, initiation of pharmacotherapy based on ultrasound findings of a
large AC increased the percent of patients requiring insulin treatment (34
versus 23 percent, relative risk [RR] 1.58, 95% CI 1.14-2.20) and reduced the
occurrence of large for gestational age newborns (RR 0.58, 95% CI 0.34-0.99)
and macrosomia (RR 0.32, 95% CI 0.11-0.95) without increasing the risk for
small for gestational age newborns [61]. Rates of pregnancy-associated
hypertension and cesarean birth were similar in both groups; data on
frequency of maternal hypoglycemia were not provided.
Based on these and other findings, it is reasonable for patients with
sonographic signs of fetal overgrowth to receive insulin to decrease the risk
of large for gestational age and macrosomia despite having less than 30
percent of glucose values above target threshold.
Choice of pharmacotherapy — The pharmacotherapy options in pregnant
patients who require pharmacotherapy are insulin (and some insulin analogs) or
selected oral antihyperglycemic agents (metformin or glyburide).
We favor insulin because it is effective, easily adjusted based on glucose levels, and
safe for the fetus, whereas data are lacking regarding long-term outcomes of
offspring exposed to oral antihyperglycemic drugs in utero. We believe that oral
antihyperglycemic agents are a reasonable alternative to insulin for patients in
whom pharmacotherapy is indicated but who decline to take, or are unable to
comply with, insulin therapy. Our approach is generally consistent with national
and international guidance [1,23,41,62,63]. Some guidelines consider oral
antihyperglycemic drugs an acceptable first-line approach in selected patients,
such as those with normal fasting blood glucose levels and modest postprandial
hyperglycemia [62-64]. (See 'Society guideline links' below.)
Meta-analyses comparing use of oral antihyperglycemic agents with insulin
therapy have generally found that both approaches can improve some pregnancy
outcomes in patients with GDM or type 2 diabetes [59,65-70]. There is a trend
toward more frequent maternal hypoglycemia with use of insulin [68], and some
patients on oral agents need supplemental insulin to achieve and maintain glucose
levels in the target range [71]. However, it is difficult to draw firm conclusions
about the optimal approach because of inconsistencies in criteria for GDM, glucose
targets, patient adherence to treatment, clinical outcome measures across studies,
and lack of long-term safety data [68].
In randomized trials, compared with insulin, metformin:
●Reduced gestational weight gain (mean difference -1.31 kg, 95% CI -2.34 to -
0.27) [69]
●Reduced birth weight (mean difference -74 g, 95% CI -115 to -33) [69]
●Reduced risk for macrosomia (odds ratio [OR] 0.60, 95% CI 0.45-0.79) [69]
●Reduced risk for neonatal hypoglycemia (risk ratio [RR] 0.63, 95% CI 0.45-
0.87) [70]
●Reduced risk for pregnancy-induced hypertension (RR 0.56, 95% CI 0.37-
0.85) [70]
●Increased offspring body mass index (BMI, by 0.8 kg/m2) and adiposity by
mid-childhood [72]
●Differences in other outcomes were not statistically significant: large for
gestational age newborn (OR 0.87, 95% CI 0.66-1.14) [69], preterm birth (RR
1.18, 95% CI 0.67-2.07), small for gestational age newborn (RR 1.20, 95% CI
0.67-2.14), perinatal mortality (RR 0.82, 95% CI 0.17-3.92), cesarean birth (RR
0.97, 95% CI 0.80-1.19) [70].
In randomized trials, compared with insulin, glyburide:
●Increased mean birth weight (mean difference 290 g, 95% CI 68-511) [69]
●Increased risk for macrosomia (OR 1.38, 95% CI 1.01-1.89) [69]
●Increased the frequency of neonatal hypoglycemia (12.2 versus 7.2 percent;
difference 5.0, 95% CI 0.5-9.5) [73]
●Showed trends toward an increased risk for a large for gestational age
newborn (OR 2.49, 95% CI 0.79-7.81) and less maternal gestational weight
gain (mean difference -0.68 kg, 95% CI -1.69 to 0.34 kg) [69].
Insulin
Dose — The insulin dose required to achieve target glucose levels varies among
individuals, but the majority of studies have reported a total dose ranging from 0.7
to 2 units per kg (current pregnant weight). Dose titration to blood glucose levels is
based upon frequent self-monitoring. At least four daily glucose measurements
are required (fasting and one or two hours postprandial with the addition of pre-
lunch and pre-dinner measurements as needed) to optimize therapy and ensure
timely dose increases as insulin requirements increase with pregnancy
progression. The insulin requirement in twin gestations complicated by GDM may
double with pregnancy progression.

We do not use insulin pumps in patients with GDM because there are no data to
suggest that they are necessary or more effective than conventional therapy, and
the cost of an insulin pump is not justified over the relatively short duration of a
pregnancy. However, case reports have described successful use in some pregnant
people.

Pragmatic approach to management of hyperglycemia — Hospitalization is not

necessary to initiate insulin therapy; however, if teaching some patients the
procedures they need to know is not possible in the outpatient setting, then an
inpatient stay to utilize the expertise of the hospital's nursing staff may justify the
cost of hospitalization.

One principle we have found useful is to start with the simplest regimen and
increase the complexity as needed to address the particular situation. Typically,
regardless of body weight, insulin dosing is based on the glucose levels recorded
in the patient's blood glucose log.

The following is our general approach to management of patients diagnosed with

GDM after screening at 24 to 28 weeks who have mostly postprandial
hyperglycemia, fetal AC>75th percentile, or EFW ≥90thpercentile. Because any insulin
regimen requires serial dosing adjustments in response to specific fasting or
postprandial glucose levels, the starting dose should be considered just that, a
starting point. Weekly glucose log review is recommended so that insulin doses
can be adjusted as needed to meet target glucose levels as the pregnancy
advances. Some patients may be diagnosed with diabetes and therapy initiated
early in pregnancy (prior to 24 to 28 weeks screening); these patients are managed
differently and generally require slightly lower insulin doses since insulin
resistance is lower early in pregnancy.
●We begin with a single injection of 10 to 20 units of intermediate-acting
basal insulin (neutral protamine Hagedorn [NPH]) and 6 to 10 units of rapid-
acting insulin (lispro or aspart) in the morning immediately before breakfast;
the dose within this range is based on the degree of elevation above target
levels.
●If postprandial glucose levels throughout the day remain high, adjustments
in the rapid-acting insulin dose are typically in the range of 10 to 20 percent.
The upper end of this range is not likely to lead to hypoglycemia in patients
with both obesity and GDM unless a meal is omitted after insulin is given.
●If only the post-dinner glucose level remains elevated, then we add an
injection of 6 to 10 units of rapid-acting insulin immediately before dinner.
●If only the post-lunch glucose level remains elevated, we add an injection of
6 to 10 units of rapid-acting insulin immediately before lunch.
 ●If the fasting glucose level is elevated after postprandial levels in the target
range, we add an intermediate-acting basal insulin, preferably at bedtime but
with dinner is another option on an individualized basis. The initial dose is 0.2
units/kg body weight.
Dosing based on glucose levels and weight — An alternative approach to insulin
therapy, somewhat more complex and likely most appropriate for individuals
whose glucose levels are not well managed with simpler paradigms, is described
below:
●If only the fasting blood glucose concentration is high, an intermediate-
acting basal insulin (NPH) is given before bedtime but before dinner is
another option on an individualized basis; an initial dose of 0.2 unit/kg body
weight is utilized. A long-acting insulin analog (insulin glargine or detemir)
may be used instead if NPH insulin is not available.
●If only postprandial blood glucose concentrations are high, 6 to 10 units of
rapid-acting insulin analogs (aspart or lispro) are given immediately before
meals. (See "General principles of insulin therapy in diabetes mellitus".)
●If both preprandial and postprandial blood glucose concentrations are high
or if the patient's postprandial glucose levels can only be blunted when
starvation ketosis occurs, then a four-injection-per-day regimen is utilized,
which improved glycemic control and perinatal outcome compared with a
twice-daily regimen in one randomized trial [74], although macrosomia rates
were not impacted.
The starting dose is calculated by trimester of pregnancy and body weight:
0.9 units/kg in the second trimester and 1.0 units/kg in the third trimester,
split into basal and bolus dosing. In patients with class II or III obesity, the
initial doses of insulin may need to be increased to 1.5 to 2 units/kg to
overcome the combined insulin resistance of pregnancy and obesity.
Two-thirds of the total daily dose is administered in the morning, with two-
thirds of the morning dose given as basal insulin and one-third given as
rapid-acting insulin up to 15 minutes before breakfast. One-third of the total
daily dose is administered in the evening, with half of this dose given as
rapid-acting insulin up to 15 minutes before dinner and the other half given
as basal insulin as a nighttime dose (usually at bedtime but before dinner is
another option on an individualized basis). A lunchtime dose of rapid-acting
insulin may be added if there is continued postprandial lunch hyperglycemia.
Management of hypoglycemia — Hypoglycemia in pregnancy is defined as a
blood glucose <60 mg/dL (3.3 mmol/L). Hypoglycemia remote from meal or snack
time is rare in patients with GDM treated with pharmacotherapy, and it is treated
by administering 10 to 20 g of a fast-acting carbohydrate snack immediately. The
American Diabetes Association (ADA) suggests the following options: 4 ounces (1/2
cup) of juice or regular soda, 8 ounces (1 cup) of skim milk, or 5 to 6 hard candies
(eg, Life-Savers); glucose tablets can also be used (check package for grams per
tablet as content varies). Since the sugars in milk release more slowly into the
bloodstream than pure sugar options, the glucose pattern seen with pure sugars
(ie, rapid elevation of glucose followed by a rapid decline) may be dampened.
(See "Hypoglycemia in adults with diabetes mellitus", section on 'Reversing
hypoglycemia'.)

Patients who are feeling better may recheck their blood glucose 15 to 30 minutes
after treatment. If the glucose remains <60 mg/dL (3.3 mmol/L), repeat treatment
may be necessary. On the other hand, they may need to give themselves extra
insulin to compensate for overtreatment of the symptoms.

If low glucose values are encountered more than once at the same time of day,
insulin doses are adjusted downward accordingly.

Type of insulin — Use of insulin preparations of low antigenicity may minimize

transplacental transfer of insulin antibodies. Human insulin is the least
immunogenic of the commercially available preparations. The three rapid-acting
insulin analogs (lispro, aspart, glulisine) are comparable in immunogenicity to
human regular insulin, but only lispro and aspart have been investigated in
pregnancy and shown to have acceptable safety profiles, minimal transfer across
the placenta, and no evidence of teratogenesis. Neonatal outcomes are similar to
those of patients treated with regular insulin [59]. These two insulin analogs both
improve postprandial excursions compared with human regular insulin and are
associated with lower risk of delayed postprandial hypoglycemia.
Long-acting insulin analogs (insulin glargine, insulin detemir) have not been
studied as extensively in pregnancy, but data from patients with preexisting
(pregestational) diabetes and studies of placental transfer suggest that both
detemir and glargine are safe and effective for use in pregnancy [75-81].
(See "Pregestational (preexisting) diabetes mellitus: Antenatal glycemic control",
section on 'Type of insulin'.).
Based on available data, we prefer using human NPH insulin as part of a multiple
injection regimen in pregnant people with GDM, especially given the peak at four
to six hours after the morning dose, which can help decrease lunch postprandial
blood glucose levels without an additional dose of rapid-acting insulin [82]. The
body of data support the safety and effectiveness of NPH in pregnancy, and doses
can be adjusted frequently and quickly in response to changing requirements in
pregnant patients.
If a longer-acting insulin analog is used, we prefer detemir insulin because it can
be dosed twice a day, similar to NPH, with the advantage over NPH of more
consistent absorption and less variability in absorption among patients. Insulin
detemir is preferred over insulin glargine because it has been studied more
extensively in pregnancy and can be dosed twice per day more predictably than
glargine, as previously mentioned. (See "General principles of insulin therapy in
diabetes mellitus", section on 'Safety'.)
Oral hypoglycemic agents — Metformin and glyburide are the only noninsulin
antihyperglycemic drugs used in pregnancy. Both oral hypoglycemic agents offer
the advantage of significantly decreased cost compared with insulin.
Choosing metformin versus glyburide — Clinically important pregnancy
outcomes are generally similar for metformin and glyburide, with only limited
evidence of benefit of one oral agent over the other.
●Pregnant outcome – When compared with glyburide in meta-analyses of
randomized trials, metformin resulted in:
•Similar rates of perinatal mortality, neonatal hypoglycemia [71], and
hypertensive disorders of pregnancy [83].
•Lower mean birth weight (mean difference -191 g, 95% CI -288 to -95 g;
mean birth weight 3103 to 3360 g versus 3329 to 3463 g with glyburide)
[69].
•Less macrosomia (OR 0.32, 95% CI 0.08-1.19) and large for gestational
age infants (OR 0.38, 95% CI 0.18-0.78) [69].
•Less gestational weight gain (mean difference -2.22 kg, 95% CI -3.88 to -
0.56 kg) [69].
●Need for supplemental insulin – The frequency of treatment failure
(inability to maintain glucose levels in the target range) is similar
for glyburide and metformin and ranges from approximately 15 to 30
percent in most trials directly comparing the two drugs [71,84].
●Placental transfer – Both drugs cross the placenta (in contrast to insulin).
Fetal metformin levels are 200 percent of the maternal level
and glyburide levels are 70 percent of the maternal level, which has unknown
long-term consequences [85-87]. Although metformin and glyburide have not
been associated with an increased risk of congenital anatomic anomalies,
when either drug is prescribed, patients should be made aware that
information regarding the long-term effects of transplacental passage,
including possible fetal programming effects, are largely unknown, so
caution is warranted until more data are available [88-93].
Metformin — A typical dosing regimen is to start metformin extended release (XR)
500 mg orally once daily (with dinner) and, if tolerated, increase by 500 mg (eg,
1000 mg with dinner or 500 mg with dinner plus 500 mg with breakfast) based on
the degree of glucose elevations. The dose can then be increased by 500 to 1000
mg orally per week until reaching the usual effective dose of 1500 to 2000 mg
orally per day divided into two doses (maximum daily dose is 2500 mg) [94]. An
immediate release preparation is also available, but we prefer the XR as it may
cause fewer gastrointestinal side effects and fewer daily doses may be needed.
The most common side effects of metformin are gastrointestinal, including a
metallic taste in the mouth, mild anorexia, nausea, abdominal discomfort, and soft
bowel movements or diarrhea. These symptoms are usually mild, transient, and
reversible after dose reduction or discontinuation of the drug. Symptoms can be
mitigated by starting at a low dose with slow-dose escalation as needed. In a
clinical trial, only 2 percent of study subjects discontinued metformin because of
gastrointestinal side effects [94].
The ADA recommends avoiding metformin in patients with hypertension,
preeclampsia, or at risk for intrauterine growth restriction because metformin
suppresses mitochondrial respiration, which may adversely affect function,
growth, or differentiation of fetal or placental tissues [23,88]; however, any clinical
impact of this effect has not been observed in human pregnancies. The American
College of Obstetricians and Gynecologists (ACOG) and the Society for Maternal-
Fetal Medicine do not include this caveat in their recommendations.
Glyburide — Starting doses of 2.5 to 5 mg once daily are commonly used,
increased as needed to a maximum of 20 mg per day. Twice-daily dosing is often
necessary to maintain glucose levels in the target range. One group that
investigated glyburide pharmacokinetics in pregnancy suggested pregnant
patients take the drug 30 to 60 minutes before a meal, rather than with the meal,
to improve efficacy [95]. In this study, plasma glyburide concentrations in pregnant
patients with GDM did not increase until one hour after drug ingestion, peaked at
two to three hours, and returned to baseline by 8 to 10 hours. Thus, the drug took
longer to reach peak concentration and was metabolized more rapidly than in
nonpregnant females.
Maternal hypoglycemia is the most common side effect, and the risk was higher
than that in patients with GDM using insulin in a large trial (28.8 versus 3.5
percent; difference 25.3 percent, 95% CI 16.6-34.0) [73].
Patients who fail to achieve glycemic control with oral pharmacotherapy — If
oral pharmacotherapy alone does not adequately manage glucose levels,
supplemental insulin can be prescribed and may be easier for the patient than
switching to a multidose insulin only regimen. In contrast to nonpregnant patients,
dual use of oral agents (eg, metformin plus glyburide) is not recommended in
pregnancy because of minimal safety and efficacy data [84] and concerns about
adverse fetal effects since both drugs cross the placenta.

OBSTETRIC MANAGEMENT Obstetric management of the pregnancy is

discussed separately. (See "Gestational diabetes mellitus: Obstetric issues and

management".)

INTRAPARTUM MANAGEMENT Intrapartum glucose and insulin

management are discussed in detail separately. (See "Pregestational (preexisting)

and gestational diabetes: Intrapartum and postpartum glucose management".)

MATERNAL PROGNOSIS Most patients with GDM are normoglycemic

after giving birth. However, they are at high risk for recurrent GDM and developing
prediabetes (impaired glucose tolerance or impaired fasting glucose) or overt
diabetes over the subsequent five years. Optimum interpregnancy care to
minimize these risks has not been well-studied in randomized trials [96]. Feasibility
trials of a web-based lifestyle intervention and a telephone-based intervention
reported less postpartum weight retention in patients with GDM assigned to the
intervention, suggesting this type of behavioral intervention may have a favorable
impact [97,98].
Recurrence — GDM in one pregnancy is a strong predictor of recurrence in a
subsequent pregnancy [99]. In a study including over 65,000 pregnancies, the
frequency of GDM in the second pregnancy among patients with and without
previous GDM was 41 and 4 percent, respectively [100]. Risk factors for recurrence
include high birth weight in the index pregnancy, older maternal age, high parity,
high prepregnancy weight, and high weight between pregnancies [101,102].
Long-term risk — A history of GDM is predictive of an increased risk of developing
type 2 diabetes, metabolic syndrome, cardiovascular disease (CVD), and even type
1 diabetes. These risks appear to be particularly high in patients with both GDM
and a hypertensive disorder of pregnancy [103]. GDM has been called a "marker,"
"stress test," or "window" for future diabetes and CVD; it is not considered causal.
●Impaired glucose tolerance – As many as 30 percent of patients with GDM
have impaired glucose tolerance during the early postpartum period [104-
106].
●Type 2 diabetes – In a meta-analysis, patients with GDM were at an almost
10-fold higher risk of developing subsequent type 2 diabetes than patients
with normoglycemic pregnancies (relative risk [RR] 9.51, 95% CI 7.14-12.67;
20 studies including nearly 68,000 patients with GDM and over 1.2 million
patients without GDM) [107]. The RR was 17 within the first five years after
delivery and approximately 10 after that. Absolute risks for type 2 diabetes at
1 to 5 years, >5 to 10 years, and >10 years postdelivery follow-up were 9, 12,
and 16 percent, respectively, compared with 1 to 2 percent in the control
groups. The lifetime maternal risk for diabetes has been estimated to be as
high as 50 to 60 percent [107,108].
Waist circumference and body mass index (BMI) are the strongest
anthropometric measures associated with development of type 2 diabetes in
patients with GDM [59,109], as they are in those without GDM. Type 2
diabetes develops in 50 to 75 percent of patients with obesity (BMI ≥30 kg/m2)
and a history of GDM versus fewer than 25 percent of those with GDM who
achieve normal BMI after delivery [110-112].
Other major risk factors are gestational requirement for insulin and early
gestational age at the time of diagnosis (ie, less than 24 weeks of gestation)
[109]. Additional risk factors for impaired glucose tolerance and overt
diabetes later in life include autoantibodies (eg, glutamic acid decarboxylase,
insulinoma antigen-2), high-fasting blood glucose concentrations during
pregnancy and early postpartum, higher-fasting plasma glucose at diagnosis
of GDM and high glucose levels in the GTT, the number of abnormal values
on the glucose tolerance test, neonatal hypoglycemia, and GDM in more than
one pregnancy [59,104,105,110,113-117]. In one study, an additional
pregnancy increased the rate ratio of type 2 diabetes threefold compared
with individuals without an additional pregnancy (RR 3.34, 95% CI 1.80-6.19)
[118]. The authors hypothesized that episodes of insulin resistance contribute
to the decline in beta-cell function that leads to type 2 diabetes in many high-
risk individuals.
Parity, large birth weight, and diabetes in a first-degree relative are less
correlated with later diabetes.
●Type 1 diabetes – GDM also appears to be a risk factor for the development
of type 1 diabetes, particularly in populations with a high prevalence of this
disorder. Specific human leukocyte antigen (HLA) alleles (DR3 or DR4) may
predispose to the development of type 1 diabetes postpartum, as does the
presence of islet-cell autoantibodies [119-121] or antibodies against glutamic
acid decarboxylase or insulinoma antigen 2. GDM in lean pregnant people,
need for insulin treatment of GDM, diabetic ketoacidosis during pregnancy,
 and postpartum hyperglycemia also suggest preexisting unrecognized type 1
diabetes or high risk of developing type 1 diabetes [121]. Although testing for
antibodies is not routinely recommended, it is important for clinicians to be
aware of this association.
Distinguishing type 1 from type 2 diabetes, and monogenic forms of diabetes
(eg, maturity-onset diabetes of the young [MODY]) from type 1 and type 2
diabetes, is reviewed in detail elsewhere. (See "Clinical presentation,
diagnosis, and initial evaluation of diabetes mellitus in adults", section on
'Differentiating the cause' and "Classification of diabetes mellitus and genetic
diabetic syndromes".)
●Metabolic syndrome – At ≥three months postpartum, patients with GDM
are more likely to have metabolic syndrome, an atherogenic lipid profile, and
early vascular dysfunction than those without previous GDM [122-125]. In
one study of patients with mild GDM (ie, normal fasting glucose level on
glucose tolerance test [GTT]), approximately one-third developed metabolic
syndrome within 5 to 10 years after giving birth [125].
●Cardiovascular disease – Patients with GDM are at higher risk of
developing CVD and developing it at a younger age than those with no
history of GDM [126-129]. Even mild glucose impairment (defined as an
abnormal 50 g one-hour GTT followed by a normal 100 g three-hour GTT)
appears to identify individuals at increased risk of future development of
CVD, usually myocardial infarction or stroke [130]. Much but not all of this
excess risk is related to development of type 2 diabetes later in life.
In a pooled analysis of nine studies including over 5 million females and
>101,000 cardiovascular events, those with GDM had a twofold higher risk of
future CVD compared with those with no history of GDM (RR 1.98, 95% CI
1.57-2.50) [131]. Meta-regression analysis showed that the rates of incident
type 2 diabetes across the studies did not affect this risk and when
individuals with type 2 diabetes were excluded, GDM was still associated with
an increased risk of future CVD (RR 1.56, 95% CI 1.04, 2.32).
Follow-up
Testing — Long-term follow-up for development of type 2 diabetes is routinely
recommended for individuals with GDM [23,41].
GTT — A common approach is to perform a GTT 4 to 12 weeks after giving birth,
using the 75 g GTT, as recommended by the American Diabetes Association (ADA)
[23]. Criteria for diagnosis of diabetes and prediabetes are shown in the tables
(table 2A-B).
Since many obstetrical providers see their patients at four to six weeks
postpartum, it makes sense to order the test prior to this visit so the results are
available for counseling or to provide an opportunity for scheduling/rescheduling
if the test was not performed. Compliance with the 4- to 12-week GTT is poor;
however, there is increasing evidence that ordering the test when patients are still
hospitalized after birth increases compliance to nearly 100 percent and provides
reliable results [106,132]. In an analysis of over 200 patients with GDM who
completed a postpartum day two 75 g GTT, returned for a GTT at postpartum week
4 to 12, and had a A1C checked approximately one year after delivery, there were
no significant differences between the day two and the 4- to 12-week postpartum
GTTs in predicting impaired glucose metabolism (A1C ≥5.7 and <6.5 percent) or
diabetes (A1C ≥6.5 percent) at one year [132]. At one year postpartum, the A1C was
consistent with impaired glucose metabolism in 35 percent and diabetes in 4
percent of individuals tested.
●Effect of breastfeeding on the GTT – Breastfeeding during a two-hour 75
gram oral GTT appears to have a modest lowering effect on the two-hour
glucose level (5 percent lower on average) [133], which could affect
interpretation of a borderline test. Patients should be informed in advance
that they might need to repeat the test if this happens so they can make an
informed decision about breastfeeding during the test versus planning the
test at a time/later date when breastfeeding can be avoided. Clinicians should
consider retesting those patients whose results fall within 6 mg/dL of the
diagnostic cut points.
Fasting glucose — A fasting plasma glucose level is a reasonable alternative to
the GTT but does not allow for diagnosis of impaired glucose tolerance. A glycated
hemoglobin (A1C) can be performed in patients in whom obtaining a fasting
specimen is especially inconvenient but performs less well for diagnosis of
diabetes or prediabetes in postpartum patients because of increased peripartum
red cell turnover [134]. (See "Clinical presentation, diagnosis, and initial evaluation
of diabetes mellitus in adults", section on 'Diagnostic tests'.)
Counseling
●Patients with prediabetes – Patients who meet criteria for prediabetes are
counseled about their subsequent risk for developing overt diabetes and
referred for discussion of management options (eg, lifestyle modification
such as medical nutritional therapy, use of metformin). They should try to
achieve a BMI in the normal range through diet and exercise, and if possible,
they should avoid drugs that may adversely affect glucose tolerance (eg,
glucocorticoids). They should have yearly assessment of glycemic status.
(See "Clinical presentation, diagnosis, and initial evaluation of diabetes
mellitus in adults", section on 'Prediabetes' and "Prevention of type 2
diabetes mellitus".)
Breastfeeding may decrease the long-term risk of developing type 2 diabetes.
(See "Gestational diabetes mellitus: Obstetric issues and management",
section on 'Breastfeeding'.)
●Patients with diabetes – Patients with overt diabetes mellitus should
receive appropriate education and treatment. They should also be given
advice regarding contraception and the planning of future pregnancies,
especially the importance of good glycemic management prior to conception.
(See "Overview of general medical care in nonpregnant adults with diabetes
mellitus"and "Pregestational (preexisting) diabetes: Preconception
counseling, evaluation, and management".)
●Patients with normal test results
•Risk for future diabetes – Patients with a normal GTT should be
counseled regarding their risk of developing GDM in subsequent
pregnancies and their future risk of developing type 2 diabetes.
(See 'Recurrence' above and 'Long-term risk' above.)
•Prevention of future diabetes – Patients should be informed that
breastfeeding may decrease their long-term risk of developing type 2
diabetes. (See "Gestational diabetes mellitus: Obstetric issues and
management", section on 'Breastfeeding'.)
Lifestyle interventions (diet and exercise) are beneficial for reducing the
incidence of type 2 diabetes in persons with prediabetes [135] and these
interventions also appear to be beneficial in patients with a history of
GDM, whether or not they meet criteria for prediabetes. The annual
incidence of diabetes may be reduced by 30 to 50 percent compared with
no intervention [136,137].
Drug therapy (eg, metformin, pioglitazone) may also have a role in
preventing future type 2 diabetes. In a multicenter randomized trial, both
intensive lifestyle and metformin therapy reduced the incidence of future
diabetes by approximately 50 percent compared with placebo in patients
with a history of GDM; metformin was much more effective than lifestyle
intervention in parous patients with previous GDM [136]. This topic is
discussed in detail separately. (See "Prevention of type 2 diabetes
mellitus".)
•Follow-up laboratory testing – Long-term follow-up is essential.
Reassessment of glycemic status should be undertaken at a minimum of
every three years [23]. More frequent assessment may be important in
patients who may become pregnant again, since early detection of
diabetes is important to preconception and early prenatal care. More
frequent screening (every one or two years) may also be indicated in
 patients with other risk factors for diabetes, such as family history of
diabetes, obesity, and need for pharmacotherapy during pregnancy.
The best means of follow-up testing has not been defined. The two-hour
75 g oral GTT is the more sensitive test for diagnosis of diabetes and
impaired glucose tolerance in most populations, but the fasting plasma
glucose is more convenient, specific, and reproducible, and less
expensive. A1C is convenient and the preferred test for patients who have
not fasted overnight. (See "Screening for type 2 diabetes mellitus",
section on 'Screening tests'.)
•Prevention of future cardiovascular disease – Given increasing
evidence of an association between GDM and future CVD [138], even in
the absence of progression to type 2 diabetes, it is reasonable to discuss
healthy lifestyle behaviors (eg, heart-healthy diet, maintenance of a
healthy weight, tobacco avoidance, and physical activity) with all patients
who have had GDM [139]. (See "Overview of primary prevention of
cardiovascular disease".)
Follow-up of patients not screened for GDM — For patients who did not undergo
screening for GDM, but diabetes is suspected postpartum because of newborn
outcome (eg, hypoglycemia, macrosomia, congenital anomalies), a postpartum
GTT may be considered. A normal postpartum GTT excludes the presence of type 1
or type 2 diabetes or prediabetes; it does not exclude the possibility of GDM during
pregnancy and the future risks associated with this diagnosis. Indications for
screening and tests used for screening are discussed separately. (See "Screening
for type 2 diabetes mellitus".)

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

●Glucose monitoring – Glucose levels are monitored several times daily in

patients with gestational diabetes mellitus (GDM). We suggest glucose self-
monitoring before breakfast and at one or at two hours after the beginning
of each meal. (See 'Glucose monitoring' above.)
The frequency of testing may be decreased to every other day in specific
patients with mild GDM (defined as no more than intermittent glucose
elevations within 5 to 10 points above targets), no signs of fetal overgrowth
(defined as abdominal circumference (AC) >75th percentile or estimated fetal
weight (EFW) ≥90th percentile), and normal amniotic fluid volume (ie, no
polyhydramnios). (See 'Can the frequency of self-monitoring be
reduced?' above.)
●Glucose targets (see 'Glucose target' above)
•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)
●Treatment
•Benefits – A program of medical nutritional therapy, self-monitoring of
blood glucose levels, and pharmacotherapy, when needed, improves
some perinatal outcomes (reduction in preeclampsia, macrosomia, and
shoulder dystocia). Moderate exercise also improves glycemic control and
should be part of the treatment plan for patients with no medical or
 obstetric contraindications to this level of physical activity. (See 'Rationale
for treatment' above and 'Exercise' above.)
•Medical nutritional therapy – Medical nutritional therapy is the initial
approach. Calories are generally divided over three meals and two to four
snacks per day and are composed of approximately 40 percent
carbohydrate, 20 percent protein, and 40 percent fat. Gestational weight
gain recommendations are shown in the table (table 1). (See 'Medical
nutritional therapy' above.)
•Pharmacotherapy – Pharmacotherapy is prescribed for patients who do
not achieve adequate glycemic control with nutritional therapy and
exercise alone (ie, at least 30 percent of glucose levels meet or exceed
target thresholds within any one week) (algorithm 1). We also suggest
pharmacotherapy for patients with indirect evidence of fetal
hyperinsulinemia (eg, AC >75thpercentile or EFW ≥90th percentile on an
early third-trimester sonogram) regardless of maternal glucose levels
(Grade 2C). Pharmacotherapy can reduce the occurrence of macrosomia
and large for gestational age in newborns. (See 'Indications for
pharmacotherapy' above.)
-Insulin – We suggest prescribing insulin rather than noninsulin
antihyperglycemic drugs during pregnancy (Grade 2C). We start with
the simplest insulin regimen likely to be effective based on the
glucose levels recorded in the patient's blood glucose log and
increase the complexity as needed. An alternative approach based on
both patient weight and glucose levels is somewhat more complex
and likely most appropriate for individuals whose glucose levels are
not well managed with simpler paradigms. (See 'Insulin' above.)
-Oral antihyperglycemic drugs – Metformin and glyburide are the
only oral antihyperglycemic drugs used in pregnancy and either is a
reasonable alternative for patients who decline to take, or are unable
to comply with, insulin therapy. The long-term effects of
transplacental passage of noninsulin antihyperglycemic agents are
not known. (See 'Oral hypoglycemic agents' above.)
●Prognosis – Most patients with gestational diabetes mellitus are
normoglycemic after giving birth but are at high risk for developing recurrent
gestational diabetes mellitus, prediabetes (impaired glucose tolerance or
impaired fasting glucose), and overt diabetes. (See 'Recurrence' above
and 'Long-term risk' above.)
●Postpartum testing – Patients with GDM should be tested for type 2
diabetes mellitus after pregnancy (table 2A-B). Testing is performed 4 to 12
 weeks postpartum and, if results are normal, at least every three years
thereafter. Lifestyle interventions (eg, achieving a healthy weight,
appropriate level of physical activity/exercise) are beneficial for reducing the
incidence of type 2 diabetes and related comorbidities such as cardiovascular
disease (CVD). (See 'Maternal prognosis'above.)

ACKNOWLEDGMENTS The UpToDate editorial staff acknowledges Lois

Jovanovic, MD, Donald R Coustan, MD, and Michael Greene, MD, who contributed
to earlier versions of this topic review.
Use of UpToDate is subject to the Terms of Use.

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