Care of the Laboring Woman with Diabetes

Care of the Laboring Woman with Diabetes

Maribeth Inturrisi

Epidemiology of Diabetes

Diabetes is a significant public health challenge for the United States. According to the 2014 report from the Centers for Disease Control (CDC), in the United States1:

  • 29.1 million (9.3% of the US population) has diabetes

  • 21.0 million are diagnosed

  • 8.1 million (28% of people) with diabetes are undiagnosed

  • 86 million (37% of US adults aged 20 years and older) have prediabetes

  • 13.4 million adult women have diabetes

Like diabetes, obesity is a national epidemic with an increase in both prevalence and incidence. Rates of obesity and diabetes parallel each other. In states where obesity is >29%, diabetes is >9%. In 2013, these rates existed in 45 states.2 Obesity is one of the highest risk factors for the development of T2DM.3 Age, gender, and race also affect the prevalence of diabetes. Diabetes is increased in pregnant women >25 years of age and in non-Hispanic Blacks, Hispanic/Latino Americans, American Indians, East Indians, Alaska Natives, Asian Americans, and Native Hawaiian and Pacific Islanders (Table 13.1).1,4


BMI ≥25 kg/m2 or ≥23 kg/m2 in Asian Americans and have additional risk factors
Previous history of: GDM, macrosomia, unexplained stillbirth, malformed infant
Family history of overt diabetes among first-degree relatives
High-risk ethnic groups: African American, American Indian, Hispanic/Latina, Asian/Pacific Islander, South-East Asian, East Indian
Chronic use of medications which adversely affect normoglycemia (steroids, betamimetics, atypical antipsychotics)
History of prediabetes, polycystic ovarian syndrome, coronary vascular disease, hypertension, hyperlipidemia, acanthosis nigricans
Family history of overt diabetes among first-degree relatives
Physical inactivity
From American Diabetes Association. (2015). Management of diabetes in pregnancy. Sec. 12. In Standards of medical care in diabetes—2015. Diabetes Care, 38(s1), S77–S79.

During pregnancy, 90% of all cases of diabetes are women with gestational diabetes mellitus (GDM). Approximately 9.2% of pregnant women in the United States are diagnosed with GDM.5 Depending on race and ethnicity of the population, and upon method of diagnosis, the prevalence may range from 2% to 18%.1,5 Within the postpartum period 5% to 10% of women with GDM are found to have diabetes, usually type 2.6

Women with a history of GDM have a 35% to 60% chance of developing T2DM within the 10 to 20 years of the index pregnancy. GDM represents one of the highest risk factors for developing T2DM.3

Classification of Diabetes

In 1997, the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus eliminated the old categories of insulin-dependent diabetes mellitus (IDDM) and non–insulin-dependent diabetes mellitus (NIDDM) and established new terminology based on pathophysiology and not on use of insulin (Table 13.2).


HbA1C ≥6.5%. The test should be performed in a laboratory using a method that is NGSP-certified and standardized to the DCCT assay.a
FPG ≥126 mg/dL. Fasting is defined as no caloric intake for at least 8 hrs.a
2-hr plasma glucose ≥200 mg/dL during an OGTT. The test should be performed as described by the WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.a
In a woman with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL.
a In the absence of unequivocal hyperglycemia, result should be confirmed by repeat testing.
From American Diabetes Association. (2015). Management of diabetes in pregnancy. Sec. 12. In Standards of medical care in diabetes—2015. Diabetes Care, 38(s1), S77–S79.

NOTE: Our current terminology uses the Arabic 1 and 2 (type 1 and type 2) instead of the Roman numerals I and II.

In 2003, the committee recognized two categories in which glucose metabolism is defective—impaired fasting glucose (IFG) and impaired glucose tolerance (IGT). IFG and IGT are risk factors for future diabetes and cardiovascular disease. Blood glucose values indicative of prediabetes are values above the normal range but not in the range of overt diabetes. This category is important because these BG values are associated with other metabolic disorders such as obesity, hyperlipidemia, cardiovascular disease, and polycystic ovarian syndrome. Prediabetes (preDM) is similar to gestational diabetes. They both share the pathophysiology of T2DM and they are both primarily treated with lifestyle interventions: healthy eating and being active. Each condition has a conversion rate to T2DM of about 50% over the subsequent 10 years after diagnosis. In the Diabetes Prevention Program, people with prediabetes who are treated with diet, exercise and/or, metformin delayed T2DM beyond 5 years.7,8,9 (See Table 13.3 for the categories associated with an increased risk for diabetes.)


Impaired fasting glucose (IFG) FPG 100 to 125 mg/dL
Impaired glucose tolerance (IGT) 2-hr plasma glucose after a 75-g glucose load (OGTT): 140 to 199 mg/dL
From American Diabetes Association. (2015). Management of diabetes in pregnancy. Sec. 12. In Standards of medical care in diabetes—2015. Diabetes Care, 38(s1), S77–S79.

The primary categories of diabetes include T1DM and T2DM with GDM and prediabetes as high-risk conditions leading to T2DM. While there are other less common categories of diabetes, the following table will summarize the characteristics of T1DM, T2DM, PreDM, and GDM. See Table 13.4: characteristics of diabetes, prediabetes, and gestational diabetes. Understanding the differences and similarities between these categories is essential to the optimum care of women with diabetes during pregnancy. The common denominator among all categories of diabetes is hyperglycemia and its adverse effects.


Incidence 5–10% 90–95% 30% 2–18%

  • Autoimmune destruction of pancreas
  • Reduces the facilitation of glucose into cells
  • Over time, very little to no insulin is produced
  • Results in hyperglycemia
  • High levels of glucose destroy blood vessels resulting in end-organ disease

  • Abnormal insulin secretion and/or liver, muscle, and fat cell resistance to insulin
  • Increases the demand on the pancreas to produce more insulin
  • Beta cell exhaustion occurs
  • Results in hyperglycemia/end-organ disease

  • Mild–moderate insulin resistance and decreased insulin effectiveness
  • BG higher than normal, not in range of overt diabetes
  • Due to risk factors 50% develop T2DM in 10 y

  • Mild–moderate insulin resistance and decreased insulin effectiveness
  • BG higher than normal, not in range of overt diabetes
  • Due to severe placenta-mediated insulin resistance

  • Genetic susceptibility and a triggering environmental insult
  • A virus or “toxin” activates gene expression, turning antibodies on to the insulin-secreting cells of the pancreas

  • Genetic or environmental (obesity/lifestyle)
  • One third of individuals with T2DM are under or at normal BMI
Same as T2DM Same as T2DM

  • Weight loss
  • Hyperphagia
  • Polyuria
  • Polydipsia
  • Hyperglycemia
  • Dehydration
  • Ketoacidosis
  • Coma

  • Chronic fatigue
  • Frequent infections such as UTIs, vaginal yeast, slow healing sores
  • May present with vascular complications (HTN, MI, stroke, microalbuminuria, visual changes)
  • Ketoacidosis is relatively rare

  • May be asymptomatic or similar to T2DM
  • Ketoacidosis is absent

  • May be asymptomatic or similar to T2DM
  • Ketoacidosis is absent

  • C-peptide low or absent
  • Glutamic decarboxylase 65(GAD-65)
  • Other anti-insulin antibodies
  • Sensitive to exogenous insulin

  • C peptide initially high or normal
  • Autoantibodies usually absent
  • Acanthosis nigricans
  • Relatively resistant to insulin

  • C-peptide normal or elevated
  • Autoantibodies usually absent
  • Acanthosis nigricans
  • Relatively resistant to insulin

  • C-peptide normal or elevated
  • Autoantibodies usually absent
  • Acanthosis nigricans
  • Relatively resistant to insulin

  • Most diagnosed in childhood
  • Almost half of T1DM is diagnosed after age 20 as latent autoimmune diabetes of the adult (LADA)

  • Most diagnosed in adulthood
  • When combined with obesity, may be seen in children and teens

  • May be diagnosed at puberty in high-risk children
  • Only one third are diagnosed, most remain undiagnosed

  • Diagnosed during pregnancy
  • Incidence related to population and method of diagnosis
Ethnicity Highest in non-Hispanic whites Highest in non-White ethnic groups Highest in non-White ethnic groups Highest in non-White ethnic groups
Insulin use

  • MUST have exogenous insulin
  • “Sensitive” to insulin requiring relatively low doses except during pregnancy when insulin resistance mediated by the placenta
  • Multiple daily injections (MDI) or continuous subcutaneous infusion of insulin (CSII)

  • Can be controlled with healthy lifestyle habits, with weight loss or weight-loss surgery
  • May use oral agents alone or in combination with insulin or (MDI or CSII)

  • No insulin but may benefit from Metformin

  • Most achieve normoglycemia with diet and exercise alone (GDMA1)
  • About 30–40% require medication either oral or insulin (GDMA2)
Predisposing risk factors

  • First-degree relative with DM
  • Non-Hispanic white ancestry
  • Age <20 yrs but increasing adult onset
  • Baby >4 Kg
  • Presence of other autoimmune diseases such as thyroiditis, celiac, cystic fibrosis, rheumatoid arthritis, lupus

  • First-degree relative with DM
  • Non-White ethnicity ancestry
  • Age >45 yrs but increasing in teens and young adults
  • BMI >25
  • Previous history of abnormal glucose tolerance, i.e., GDM
  • Acanthosis nigricans
  • Baby >9 lb
  • Sedentary lifestyle
  • Hypertension ≥140/90 mm Hg.
  • Chronic use glycogenic medications, i.e., Steroids, atypical anti psychotics

  • Same as type 2

  • Same as type 2
From Centers for Disease Control and Prevention. (2014). National diabetes report. . Accessed May 1, 2015; Centers for Disease Control and Prevention. (2011). National diabetes fact sheet. Atlanta, GA: United States Department of Health and Human Services; American Diabetes Association. (2015). Management of diabetes in pregnancy. Sec. 12. In Standards of medical care in diabetes—2015. Diabetes Care, 38(s1), S77–S79; Committee on Practice Bulletins—Obstetrics. (2013). Practice Bulletin No.137: Gestational diabetes mellitus. Obstetrics & Gynecology, 122, 406–416; Daley, J. (2014). Diabetes in pregnancy. In Simpson, K., & Creehan, P. (Eds.), Perinatal nursing (4th ed., pp. 203–223); Barbour, L. A., McCurdy, C. E., Hernandez, T. L., et al. (2007). Cellular mechanisms for insulin resistance in normal pregnancy and gestational diabetes. Diabetes Care, 30 (suppl 2), S112–S119.

Adverse Perinatal Outcomes of Hyperglycemia During Pregnancy

Effects of diabetes on women are unique because hyperglycemia can affect not only the woman’s health but also that of her unborn child and that child’s lifelong health. During pregnancy, women with pre-existing diabetes, type 1 (T1DM) and type 2 (T2DM), have the most risk for perinatal morbidity and mortality. Risks to the fetus depend on the level and severity of maternal hyperglycemia prior to pregnancy, during the time of conception, and throughout gestation.12,13 If glycemic control is poor (HbA1C >7%) during conception and in the first trimester during organogenesis (first 8 weeks’ gestation, when major organs are developing), congenital anomalies or miscarriage can occur. Miscarriage rates for women with pre-existing diabetes are as high as 30%. Cardiac and neural tube defects are the most common malformations.14

Hyperglycemia during the second and third trimesters of pregnancy can result in excessively large babies posing short- and long-term risks to both mother and child. These risks affect women with T1DM, T2DM, and GDM.15,16,17

This is the result of elevated maternal blood glucose freely crossing the placenta while insulin cannot. The fetus then produces its own insulin resulting in hyperinsulinemia. High levels of insulin combined with high levels of glucose in the fetus result in storage of excess fat in the abdomen of the fetus leading to macrosomia.18,19 The third trimester is the time of rapid weight gain, development of muscle mass and fat stores for the newborn.

Congenital malformations are not common in GDM. Maternal hyperglycemia generally develops at the end of the second trimester when placental hormones increase maternal insulin resistance. Maternal insulin secretion must double to maintain normoglycemia.11 Insulin resistance will continue to rise through the third trimester, often tripling the requirement for insulin secretion from the pancreas. Women with normal carbohydrate metabolism are able to produce enough endogenous insulin to maintain normoglycemia. Women with defective carbohydrate metabolism have mild–severe hyperglycemia depending on the severity of their defect. For this reason, screening for GDM is recommended at 24 to 28 weeks’ gestation for all pregnant women who have not
already been diagnosed with diabetes or hyperglycemia.20,21 See Table 13.5 that outlines adverse effects of hyperglycemia on pregnancy outcomes during the second half of pregnancy.



  • Palsies (birth injuries)
  • Polycythemia–jaundice
  • Poor feeding
  • Pulmonary immaturity
  • Prolonged nursery stay
  • Rarely—stillborn

  • Polyhydramnios
  • Preeclampsia
  • Preterm birth
  • Pyelonephritis
  • Dystocia (abnormal labor)
  • Cesarean birth
Insulin resistance
Metabolic Syndrome
Type 1 and 2: worsening of retinopathy
Type 1 and 2: Worsening of nephropathy
GDM: metabolic syndrome
GDM: type 2 diabetes

Diagnosing Gestational Diabetes

For over 50 years in the United States, the diagnosis of diagnosing gestational diabetes (GDM) has been based on criteria that predict the future risk of the mother for developing T2DM. O’Sullivan and Mahan focused on subsequent maternal disease in 1,700 women using a 100-g OGTT at 28 weeks’ gestation.24 Diagnosing GDM has been based on identifying women at risk for type 2 diabetes in their future and not on perinatal outcomes. Blood glucose cutoffs for the 3-hour, 100-g OGTT were based on a statistical calculation and not on levels of glycemia with increasing risks for adverse outcomes. The 3-hour OGTT cutoffs have been adjusted as blood glucose laboratory determination has changed. The last adjustment was made by Carpenter and Coustan in 1982 and was adopted by ACOG and ADA.

Countries in most of the world have used a 2-hour, 75-g OGTT using various blood glucose cut points derived in various ways. Inconsistent diagnosing criteria across the world preclude any accurate study of GDM; therefore we cannot apply study findings universally limiting the development of best practices.

Overt diabetes, characterized by moderate to severe hyperglycemia, clearly increases the risk of adverse pregnancy outcome. In order to know who and when to treat mild hyperglycemia (AKA GDM), one must know what level of glucose intolerance during pregnancy, short of diabetes, is associated with the risk of adverse perinatal outcomes. This information could help to develop a global, evidence-based method of diagnosing GDM. The Hyperglycemia and Adverse Pregnancy Outcomes (HAPO) study published in 2008 focused on fetal effects of maternal hyperglycemia in 25,505 pregnant women at 15 centers in 9 countries using a 2-hour, 75-g OGTT at 24 to 28 weeks’ gestation. The HAPO epidemiologic study was the first to conclusively establish a relationship between maternal glucose concentrations and undesirable perinatal outcomes (macrosomia, neonatal hyperinsulinemia, neonatal hypoglycemia, and preeclampsia) in women not previously diagnosed with diabetes. There was a continuous, positive, independent relationship between maternal BG and percent newborn body fat and between cord C-peptide concentrations and percent newborn fat. This suggests that the relationship between maternal glycemia and fetal fat deposition is mediated by fetal insulin production.25

The International Association of Diabetes in Pregnancy Study Group (IADPSG) convened a group of experts to translate the findings of the HAPO study to a method of diagnosing GDM that could be used globally. In 2010, the recommendations suggested BG cut points which represented an odds ratio of 1.75 of risk to experience the adverse outcomes. A one-step, 2-hour Oral Glucose Tolerance Test (using 75 g of Glucola) was recommended to be administered to all pregnant women, not previously diagnosed with diabetes at 24 to 28 weeks’ gestation. Blood glucose cut points were as follows: fasting ≥92 mg/dL, 1 hour, ≥180 mg/dL, and 2 hour ≥153 mg/dL. GDM
is diagnosed if 1 value is abnormal. The ADA adopted the one-step method in 2011 but ACOG chose to stay with the two-step method (Table 13.6).


Research basis Predicts future risk of maternal T2DM Predicts adverse perinatal outcomes for mother and newborn
Administered at 24–28 weeks’ gestation Uses 2 steps: Nonfasting
1-hr 50-g Glucola GLT; if >129 or 139 mg/dL, then administer fasting 3-hr 100-g
Glucola OGTT
Uses one step: Eliminates 1-hr GLT. All women are tested with fasting 2-hr 75-g Glucola OGTT
Cut points for abnormal values Fasting 95;
   1 hr 180;
   2 hr 155;
   3 hr 140
Fasting 92;
   1 hr 180;
   2 hr 153
Diagnosis requirements 2 abnormal values 1 abnormal value
Prevalence of GDM in USA 2–14% ∼18%
From American Diabetes Association. (2015). Management of diabetesin pregnancy. Sec. 12. In Standards of medical care in diabetes—2015. Diabetes Care, 38(s1), S77–S79; Committee on Practice Bulletins—Obstetrics. (2013). Practice Bulletin No.137: Gestational diabetes mellitus. Obstetrics & Gynecology, 122, 406–416; International Association of Diabetes and Pregnancy Study Groups Consensus Panel, Metzger, B. E., Gabbe, S. G., Persson, B., et al. (2010). International association of diabetes and pregnancy study groups recommendations on the diagnosis and classification of hyperglycemia in pregnancy. Diabetes Care, 33(3), 672–682; World Health Organization. (2013). Diagnostic criteria and classification of hyperglycemia first detected in pregnancy. Geneva: World Health Org., (WHO/NMH/MND/13.2).

The IADPSG criteria will identify approximately 18% of all pregnant women in the United States as having GDM.26 This was thought to place an undue demand on the provider, healthcare system, and the woman’s pregnancy. The controversy continues until more data can be supplied which supports the identification and treatment of this high-risk group of woman and their offspring. Currently, the World Health Organization, American Diabetes Association, ACE, and many countries in Europe and Asia have adopted the IADPSG guidelines.

The ADA and ACOG agree that women with high risk factors for T2DM should be tested for undiagnosed type 2 diabetes at the first prenatal visit using one of the methods of diagnosing diabetes in the nonpregnant population (see Table 13.2 for diagnosing diabetes in the nonpregnant population). This recommendation makes it possible to diagnose T2DM (and rarely T1DM) in pregnancy so that aggressive treatment can begin early and women with undiagnosed overt diabetes can be identified and appropriately followed up postpartum.26

Normal Glucose Metabolism

The nutritive substance used in the greatest quantities by humans is carbohydrate. Carbohydrates (CHO) are ingested with the food we eat or produced by our liver. After being converted into glucose, CHO is utilized by all our cells, especially by our muscles, which should constitute nearly half our body mass.

Production and consumption of CHO is so well regulated that a constant BG level is maintained between approximately 70 and 110 mg/dL. The constancy of the BG level is controlled by a complex physiological homeostatic mechanism because BG level is such an important factor in many chemical and physiological processes.

Normal glucose metabolism involves the following pathways

  • While eating, carbohydrates are broken down by the stomach into glucose.

  • Glucose is absorbed into the blood via the intestine.

  • Glucose in the blood stimulates the pancreas to release insulin.

  • Insulin is released in two phases from the pancreatic β cells in the islets of Langerhans:

    • First phase of insulin response refers to the change in insulin concentration relative to the elevation in glucose concentration within the first 5 minutes after glucose is sensed.

    • Second phase of insulin response refers to the rate of insulin release relative to the glucose concentration 5 to 60 minutes after glucose is sensed. This gradual release of insulin is under the feedback control of the blood glucose. Hyperglycemia increases the secretion of insulin and hypoglycemia diminishes or completely inhibits it.

  • Insulin causes the following actions:

    • Stimulates entry of glucose into cells for utilization as energy

    • Promotes the storage of glucose as glycogen in muscles and liver cells

    • Inhibits release of glucose from the liver or from muscle glycogen

    • Stimulates entry of amino acids into cells

    • Enhances fat storage and prevents the mobilization of fat for energy

    • Inhibits the formation of glucose from noncarbohydrates (e.g., amino acids)

  • Glucagon is secreted from the alpha cells of the pancreas:

    • Stops the production of insulin when BG drops below 70 mg/dL

    • Causes the release of glucose from glycogen (liver)

    • Releases fatty acids from stored triglycerides (fat)

The balance between these two hormones (insulin and glucagon) holds metabolism “on the line,” promoting a stable homeostasis of glucose in the blood.

Many metabolic changes occur during pregnancy to optimize the growth of the fetus. Because the fetus depends entirely on the mother for its supply of energy, maternal adaptations must occur to increase glucose supply to the fetus. Initially human chorionic gonadotropin (HCG) stimulates the corpus luteum (the part of the follicle left behind in the ovary during ovulation) to produce estrogen and progesterone in the first 10 weeks after conception, until the placental cells can do so by themselves. By approximately 8 to 15 weeks’ gestation glucose homeostasis is altered by the increases in estrogen and progesterone that cause pancreatic β-cell hyperplasia (multiplication of cells), with subsequent increased insulin secretion. Since insulin resistance has not yet developed, women with pre-existing diabetes often experience hypoglycemia as a result of the following factors:

  • Increased glucose utilization (developing fetus) causes approximately a 10% reduction in maternal BG

  • Increased insulin secretion (pancreatic hyperplasia) results in increased glycogen stores and decreased hepatic glucose production causing the fasting BG to lower (Fig. 13.1)

FIGURE 13.1 Insulin requirements in pregnancy. (From California Department of Public Health. California Diabetes and Pregnancy Program. Retrieved from:

In the second and third trimesters, levels of human placental lactogen (HPL), human placental growth hormone (hPGH), progesterone, estrogen, tumor necrosis factor alpha (TNF-α), leptin, and cortisol increase progressively and cause increasing tissue resistance to insulin action.11

Maternal cells are “blinded” by placental hormones inhibiting recognition of insulin. As hormone levels rise, insulin resistance increases and the maternal pancreas secretes more insulin. Maternal hyperinsulinemia provides the fetus with adequate substrate to grow (Glucose). Normal pregnancy can be viewed as a progressive condition of insulin resistance, hyperinsulinemia,
and mild postprandial hyperglycemia. The mild postprandial hyperglycemia serves to increase the amount of time that maternal glucose levels are elevated above the basal after a meal, thereby increasing the flux of ingested nutrients from mother to the fetus and enhancing fetal growth.

Maternal hyperglycemia (diabetes during pregnancy) results when the mother’s cells already have trouble recognizing insulin (insulin resistance) as in T2DM, prediabetes, polycystic ovarian syndrome, metabolic syndrome, obesity, or a pre-existing inherited tissue defect. Insufficient insulin secretion may also be a factor in maternal hyperglycemia when the woman’s pancreas cannot produce the extra insulin needed to meet increasing pregnancy demands.

Accelerated Starvation of Pregnancy

Throughout pregnancy, there is an increased risk for fasting ketosis due to the following metabolic factors during pregnancy that allow energy to come from sources other than carbohydrates such as fats and protein (protects fetus from lack of carbohydrate):

  • Increased levels of fatty acids

  • Increased triglycerides

  • Increased ketones (pregnant women form ketones within a few hours of not eating—for this reason small frequent meals every 2 to 3 hours are recommended during pregnancy)

These metabolic factors cause increased fat breakdown, and decreased maternal glucose production in the fasting state. This allows for increased utilization of fat stores for maternal energy, therefore protecting muscle mass from breakdown.

Antepartum Management for Women with Hyperglycemia during Pregnancy

Healthy Eating

By far the most important way to control BG is to eat a healthy diet. The three cornerstones in the treatment of all types of diabetes during pregnancy include the following:

  • Balanced meal plan

  • Carbohydrate control

  • Weight management

NOTE: A registered dietitian (RD) who is knowledgeable concerning pregnancy and diabetes should be consulted to create an individualized, culturally appropriate meal plan.

Being Active

Just as healthy eating is essential to the management of hyperglycemia for all types of diabetes, exercise must also be incorporated into the plan of care. Being active for 30 to 60 minutes per day is encouraged because muscle activity does the following:

  • Increases insulin sensitivity lowering blood glucose levels3

  • Increases utilization of glucose, especially after a meal3

  • Improves blood glucose control and may eliminate the need for insulin therapy28

  • Reduces risk of excessive weight gain29,30

  • Decreases risk of preeclampsia31

  • Reduced the weight of the newborn by approximately 150 g.32 A woman with T1DM should check her BG before, during, and after exercise. If the BG is <100 mg/dL, she should consume 15 to 30 g CHO to prevent hypoglycemia. She should always carry her meter and glucose tabs or a snack. If the BG >200 mg/dL, she should not exercise until BG is less than 180 mg/dL. If there are urine ketones present she should give an insulin correction and drink several glasses of water and wait to exercise until the ketones have cleared. Physical activity does not always improve BG control especially in an insulin deficient state. BG will continue to rise. For women with T1DM exercise can only lower BG if adequate insulin is available.33

Self-Monitoring of Blood Glucose

The goal of antepartum management is to achieve BG values as close to normal as is safe to reduce the risk of adverse perinatal outcomes. The BG values, which have the most significant effect on fetal macrosomia and cesarean birth are the fasting and the peak BG after a meal.34,35

The HAPO study found that 11.9% of pregnant women had a fasting BG greater than 90 mg/dL in the beginning of the third trimester. This cutoff detected 22.1% of LGA neonates and 15.1% of primary cesarean deliveries.19 Nondiabetic, pregnant women wearing a continuous glucose monitoring system (CGMS) were shown to have a peak postprandial time (min) 70 ± 13.36 In diabetic and nondiabetic pregnancies, maximal postprandial glucose excursions occur between 60 and 90 minutes after meal ingestion and correlate more closely with 1- than 2-hour postprandial measurements.36 Some authors suggest that 60 minutes is a reasonable time to identify the peak postprandial since it is easier for women to remember and is closest to the average time from first bite of carbohydrate to peak BG.35,37 Therefore, checking the 1-hour BG after the first bite of carbohydrate has been selected to represent the peak for most diabetes in pregnancy programs.

In an earlier study Langer found that when the mean daily BG value was 87 to 100 mg/dL, the rate of large for gestational age (LGA) and macrosomia was comparable to that in the general population, which is approximately 10%. Of importance to note is that fasting hyperglycemia greater than 105 mg/dL is associated with an increased risk of intrauterine fetal death (IUFD) in the last 4 to 8 weeks’ gestation.38 When the mean BG was greater than 105 mg/dL the incidence of LGA increased more than twofold. The HbA1c had no relationship in the third trimester to these outcomes and could not be used to evaluate thresholds for improving outcomes in terms of macrosomia.39

Establishing target BG has been challenging. While the fasting BG target of less than 90 mg/dL is somewhat evidenced based26 there are no studies that show how close to “normal” the peak postprandial should be to show a significant improvement in outcomes (see Table 13.7).


Mean 83.7 ± 8
Fasting 75 ± 12
Preprandial 78 ± 11
Peak postprandial 110 ± 16
Peak postprandial time (min) 70 ± 13
1-hr postprandial 105 ± 13
2-hr postprandial 97 ± 11
Mean blood glucose at nighttime (mg/dL) 68 ± 10
From Hod, M., & Yogev, Y. (2007). Goals of metabolic management of gestational diabetes. Diabetes Care, 30(suppl 2), S180–S187.

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Jul 10, 2020 | Posted by in NURSING | Comments Off on Care of the Laboring Woman with Diabetes

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