eMedicine Specialties > Endocrinology > Diabetes Mellitus

Diabetes Mellitus and Pregnancy: Treatment & Medication

Author: Thomas R Moore, MD, Chairman, Professor, Department of Reproductive Medicine, University of California at San Diego School of Medicine
Contributor Information and Disclosures

Updated: May 21, 2009

Treatment

Medical Care

  • Prepregnancy management of women with preexisting diabetes
    • If a reduction in diabetes-associated neonatal morbidity is to be achieved, counsel the patient before conception and perform a medical risk assessment in all women with overt diabetes and those with a history of gestational diabetes mellitus during a previous pregnancy.  
    • Key features of an effective diabetes management program
      • Perform a thorough assessment of cardiovascular, renal, and ophthalmologic status.
      • Institute a regimen of frequent and regular monitoring of both preprandial and postprandial capillary glucose levels.
      • Controversy exists as to whether the target glucose levels to be maintained during diabetic pregnancy should be designed to limit macrosomia or to closely mimic nondiabetic pregnancy profiles. The Fifth International Workshop Conference on Gestational Diabetes35 currently recommends the following:
        • Fasting plasma glucose –90-99 mg/dL (5.0–5.5  mmol/L) and
        • One-hour postprandial plasma glucose less than 140  mg/dL (7.8 mmol/L) or
        • Two-hour postprandial plasma glucose less than 120-127 mg/dL (6.7–7.1 mmol/L) 
      • The insulin regimen should result in a smooth glucose profile throughout the day, with no hypoglycemic reactions between meals or at night. Initiate the regimen early enough before pregnancy so that the glycohemoglobin level is lowered into the reference range for at least 3 months before conception.
      • Patients should take a prenatal vitamin containing at least 1.0 mg of folic acid daily for at least 3 months prior to conception to minimize the risk of neural tube defects in the fetus.
      • The development of family, financial, and personal resources necessary to achieve successful pregnancy is important. Pay particular attention to support systems that permit extended bedrest in the third trimester if necessary. 
    • Preemptive outreach
      • In many perinatal centers, diabetes-in-pregnancy programs focus on outreach to nonpregnant reproductive-aged women with diabetes in order to minimize the morbidity attendant to poor periconceptional control.
      • Urge nonpregnant women to continue to avoid pregnancy until their HbA1C value is in within the reference range (<6.5%).  
  • Pregnancy management of women with diabetes mellitus 
    • Dietary therapy  
      • The goal of dietary therapy is to avoid single large meals and foods with a large percentage of simple carbohydrates. A total of 6 feedings per day is preferred, with 3 major meals and 3 snacks to limit the amount of energy intake presented to the bloodstream at any interval. Examples include foods with complex carbohydrates and cellulose, such as whole grain breads and legumes.
      • Carbohydrates should account for no more than 50% of the diet, with protein and fats equally accounting for the remainder.30 However, moderate restriction of carbohydrates to 35–40% has been shown to decrease maternal glucose levels and improve maternal and fetal outcomes.36
      • Nutritional therapy should be supervised by a trained professional, ideally a registered dietitian, with formal dietary assessment and counseling provided at several points. For obese women (BMI >30 kg/m2), a 30–33% calorie restriction (to 25 kcal/kg actual weight per day or less) has been shown to reduce hyperglycemia and plasma triglycerides with no increase in ketonuria. 
    • Glucose monitoring  
      • The availability of capillary glucose test strips has revolutionized the management of diabetes, and these should now be considered the standard of care for pregnancy monitoring. The discipline of measuring and recording blood glucose levels prior to and after meals clearly has a positive effect on improving glycemic control.
      • Individualize the frequency and timing of home glucose monitoring. A typical schedule involves capillary glucose checks upon awakening in the morning, 1 hour after breakfast, before and after lunch, before dinner, and at bedtime. Place emphasis on gaining and sustaining compliance with the target glucose levels mentioned above. Superb glycemic control requires attention to both preprandial and postprandial glucose levels.  
    • Insulin therapy  
      • The goal of insulin therapy during pregnancy is to achieve glucose profiles similar to those of nondiabetic pregnant women. Given that healthy pregnant women maintain their postprandial blood sugar excursions within a relatively narrow range (70-120 mg/dL), the task of reproducing this profile is requires meticulous daily attention by both the patient and clinician.
      • Insulins lispro, aspart, regular and NPH are well-studied in pregnancy and regarded as safe and efficacious.  Insulin glargine is less well-studied, and given its long pharmacologic effect, may exacerbate periods of maternal hypoglycemia.37
      • As pregnancy progresses, the increasing fetal demand for glucose fasting and the progressive lowering of fasting and between-meal blood sugar levels increases the risk of symptomatic hypoglycemia. Upward adjustment of short-acting insulins to control postprandial glucose surges within the target band only exacerbates the tendency to interprandial hypoglycemia. Thus, any insulin regimen for pregnant women requires combinations and timing of insulin injections quite different from those that are effective in the nonpregnant state. Further, the regimens must be continuously modified as the patient progresses from the first to the third trimester and insulin resistance rises. Strive to stay ahead of the rising need for insulin, and increase insulin dosages preemptively.  
    • Insulin pump  
      • In a select group of patients, use of an insulin pump may improve glycemic control while enhancing patient convenience. These devices can be programmed to infuse varying basal and bolus levels of insulin, which change smoothly even while the patient sleeps or is otherwise preoccupied.
      • The effectiveness of continuous subcutaneous insulin infusion in pregnancy is well established.38,39 Hieronimus et al compared outcomes of 33 pregnant women managed with insulin pump to 23 receiving multiple injections, reporting similar HbA1c levels, macrosomia rates, and cesarean rates.40 Lapolla et al reported a small cohort of 25 women treated with insulin pump in pregnancy compared to conventional insulin treatment (n=68) and found no41 differences in glycemic control or perinatal outcome.42  
    • Oral hypoglycemic agents - Glyburide37   
      • Interest in the second-generation oral sulfonyurea, glyburide, has been rekindled following reports of its effectiveness and safety.41   
      • Glyburide is minimally transported across the human placenta.  This is probably largely due to the high plasma protein binding coupled with a short half-life.43,41  In addition, a human placenta perfusion study demonstrated active glyburide transport from the fetus to the mother.44
      • Glyburide should not be used in the first trimester because its effects, if any, on the embryo are unknown.  Research in this area, though needed, has been difficult given the known teratogenic effects of the first generation agents, which readily crossed the placenta.
      • A randomized trial comparing glyburide to insulin was published in 2000, studying 404 pregnancies. At the conclusion of this trial, there was no difference between the groups in the mean maternal blood glucose, the percentage of infants who were large for gestational age, the birthweight, or neonatal complications. Only 4% of the glyburide study arm required addition of insulin to achieve glucose control.41
      • Since this study, several prospective and retrospective studies involving more than 775 pregnancies have concluded glyburide is equally as safe and efficacious as insulin.
      • All studies comparing glyburide to traditional insulin have demonstrated similar levels of glycemic control. Most studies show no differences in maternal or neonatal outcomes with glyburide.
      • Success rates for achieving glycemic control with glyburide vary from 79-86%. Studies evaluating predictors of failure with glyburide cite the following risk factors: advanced maternal age, earlier gestational age at diagnosis, higher gravidity and parity, and higher mean fasting glucose.45,46,47,48
      • Glyburide has been shown to be safe in breastfeeding, with no transfer into human milk. 
    • Oral hypoglycemic agents — Metformin  
      • Metformin is a biguanide, which functions mainly by decreasing hepatic glucose output.
      • Metformin crosses the placenta and cord levels have demonstrated even higher levels than maternal levels.49
      • An initial retrospective study of 50 patients on metformin was concerning for increased rates of preeclampsia and perinatal mortality when metformin was used in the third trimester.50  It should be noted that in this study the patients on metformin had a higher BMI and were also older than the patient on glyburide or insulin.
      • Since this initial study, several other prospective and retrospective studies involving over 300 patients have demonstrated similar efficacy, safety, and maternal and fetal outcomes. Subsequent studies have not confirmed the increased rates of preeclampsia or perinatal mortality.
      • There is currently an ongoing randomized controlled trial that may help answer the many questions regarding metformin use in pregnancy. 
  • Peripartal management of patients and fetuses with diabetes  
    • Prenatal obstetric management 
      • The goals of management of third-trimester pregnancies in women with diabetes are to prevent stillbirth and asphyxia, while minimizing maternal and fetal morbidity associated with delivery.
      • Monitoring fetal growth is essential to select the proper timing and route of delivery. This is accomplished by frequent testing for fetal well-being and serial ultrasonographic examinations to follow fetal size.
    • Periodic fetal biophysical testing  
      • Various fetal biophysical tests are available to the clinician to ensure that the fetus is well oxygenated, including fetal heart rate testing, fetal movement assessment, ultrasonographic biophysical scoring, and fetal umbilical Doppler studies.
      • If applied properly, most of these can be used with confidence to provide assurance of fetal well-being while awaiting fetal maturity.

Table 3. Biophysical Tests of Fetal Well-Being for Diabetic Pregnancy  

Open table in new window

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Table

Test

Frequency

Reassuring Result

Comment

Fetal movement counting

Every night from 28 wk

10 movements in <60 min

Performed in all patients

Nonstress test (NST)

Twice weekly

2 heart rate accelerations in 20 min

Begin at 28-34 wk with insulin-dependent diabetes, and begin at 36 wk in diet-controlled GDM.

Contraction stress test

Weekly

No heart rate decelerations in response to 3 contractions in 10 min

Same as for NST

Ultrasonographic biophysical profile

Weekly

Score of 8 in 30 min

3 movements = 2
1 flexion = 2
30 s breathing = 2
2 cm amniotic fluid = 2

Test

Frequency

Reassuring Result

Comment

Fetal movement counting

Every night from 28 wk

10 movements in <60 min

Performed in all patients

Nonstress test (NST)

Twice weekly

2 heart rate accelerations in 20 min

Begin at 28-34 wk with insulin-dependent diabetes, and begin at 36 wk in diet-controlled GDM.

Contraction stress test

Weekly

No heart rate decelerations in response to 3 contractions in 10 min

Same as for NST

Ultrasonographic biophysical profile

Weekly

Score of 8 in 30 min

3 movements = 2
1 flexion = 2
30 s breathing = 2
2 cm amniotic fluid = 2

      • Initiate testing early enough to avoid significant stillbirth but not so early that a high rate of false-positive test results is encountered. In patients with poor glycemic control, intrauterine growth restriction or significant hypertension begin formal biophysical testing as early as 28 weeks. In patients who are at lower risk, most centers begin formal fetal testing by 34 weeks. Fetal movement counting is performed in all pregnancies from 28 weeks onward.
      • There is no consensus regarding antenatal testing in gestational diabetes with good diet control.
    • Assessing fetal growth  
      • Monitoring fetal growth continues to be a challenging and imprecise process. Although the tools available now, serial plotting of fetal growth parameters, are superior to those used previously for clinical estimations, accuracy is still only within ±15%.
      • In the obese fetus, the inaccuracies are further magnified. In 1992, Bernstein and Catalano reported that significant correlation exists between the degree of error in the ultrasonogram-based estimation of fetal weight and the percent of body fat on the fetus (r = 0.28, P <.05).51 Perhaps this is why no single formula has proven to be adequate in identifying a macrosomic fetus with certainty.
      • Despite problems with accuracy, ultrasonogram-based estimations of fetal size have become the standard of care. Estimate fetal size once or twice at least 3 weeks apart in order to establish a trend. Time the last examination to be at 36-37 weeks' gestation or as close to the planned delivery date as possible.  
  • Timing and route of delivery  
    • Select the timing of delivery to minimize morbidity for the mother and fetus. Delaying delivery to as near as possible to the expected date of confinement helps maximize cervical maturity and improves the chances of spontaneous labor and vaginal delivery. However, the risks of advancing fetal macrosomia, birth injury, and in utero demise increase as the due date approaches.
    • Although delivery as early as 37 weeks might reduce the risk of shoulder dystocia, a concomitant increase in the incidence of failed labor inductions and poor neonatal pulmonary status would also occur. Because fetal growth from 37 weeks onward may be 100-150 g/wk, the reduction in net fetal weight and the risk of shoulder dystocia by inducing labor 2 weeks early may theoretically improve outcome.
    • In 1993, when Kjos et al compared the outcomes associated with labor induction in patients with gestational diabetes at 38 weeks versus expectant management with fetal testing, they found that expectant management increased the gestational age at delivery by 1 week, but the cesarean delivery rate was not significantly different. However, the prevalence of infants who were macrosomic in the expectantly managed group (23%) was significantly greater than those in the active induction group (10%). This suggests that routine induction of women with diabetes on or before 39 weeks' gestation does not increase the risk of cesarean delivery and may reduce the risk of macrosomia.52
    • If the fetus is not macrosomic and results from biophysical testing are reassuring, the obstetrician can await spontaneous labor. In patients with gestational diabetes mellitus and superb glycemic control, continued fetal testing and expectant management can be considered until 41 weeks' gestation. In the fetus with an abdominal circumference significantly larger than the head circumference or an estimated fetal weight above 4000 grams, consider induction. After 40 or more weeks, the benefits of continued conservative management are likely to be less than the danger of fetal compromise. Induction of labor before 41 weeks' gestation in pregnant women with diabetes, regardless of the readiness of the cervix, is prudent.
    • An optimal time for delivery of most diabetic pregnancies is typically on or after the 39th week. Deliver a patient with diabetes before 39 weeks' gestation without documented fetal lung maturity only for compelling maternal or fetal indications. For elective induction prior to 38.5 weeks, fetal lung maturity should be verified via amniocentesis.
    • Because the risk of shoulder dystocia and fetal injury in labor is increased 3-fold in diabetic pregnancy, elective cesarean section should be considered if the fetus is suspected to be significantly obese. The AmericanCollege of Obstetricians and Gynecologists recommends offering diabetic patients cesarean delivery if the fetal weight is estimated to be 4500 grams or more. 

Medication

Clinicians and gestational diabetes mellitus patients are reluctant to start insulin therapy, but it is key to achieving a good outcome. Research suggests that early intervention with insulin or glyburide is superior to diet therapy alone. Determine the choice of insulin and regimen based on the patient's individual glucose profile. Postprandial glucose levels become consistently above the target with diet therapy. When more than 20% of postprandial blood glucose levels exceed 130 mg/dL, administer lispro insulin (4-8 USC initially) before meals. If more than 10 U of regular insulin is needed before the noon meal, adding 8-12 U of NPH insulin before breakfast helps achieve control. When more than 10% of fasting glucose levels exceed 95 mg/dL, initiate 6-8 U NPH insulin hs. Titrate doses prn according to blood glucose levels.37

Insulins

Essential in regulating carbohydrate, protein, and fat metabolism. Primarily affect carbohydrate homoeostasis by binding to specific cell-surface receptors on insulin-sensitive tissues (eg, liver, muscles, adipose tissue).


Insulin (Novolin, Humulin, Humalog, Novolog, Lente, Iletin, NPH)

DOC for all types of diabetes mellitus during pregnancy. Stimulates proper use of glucose by cells and reduces blood glucose levels.

Adult

0.5-1 U/kg/d SC in divided doses; base dose on IBW; titrate dose to maintain a premeal and bedtime glucose level of 80-110 mg/dL; combine short- and longer-acting insulin to maintain blood glucose within target

Pediatric

Administer as in adults

Medications that may decrease hypoglycemic effects include acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid estrogens, ethacrynic acid, calcitonin, oral contraceptives, diazoxide, dobutamine phenothiazines, cyclophosphamide, dextrothyroxine, lithium carbonate, epinephrine, morphine sulfate, and niacin
Medications that may increase hypoglycemic effects include calcium, ACE inhibitors, alcohol, tetracyclines, beta-blockers, lithium carbonate, anabolic steroids, pyridoxine, salicylates, MAOIs, mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate, fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone

Documented hypersensitivity; hypoglycemia

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hyperthyroidism may increase renal clearance, and more may be needed to treat hyperkalemia; hypothyroidism may delay insulin turnover, requiring less insulin to treat hyperkalemia; monitor glucose carefully; dose adjustments may be necessary in patients diagnosed with renal and hepatic dysfunction

Antidiabetic agent, oral

These agents reduce glucose levels through various mechanisms.


Metformin (Glucophage)

Reduces hepatic glucose output, decreases intestinal absorption of glucose, and increases glucose uptake in the peripheral tissues (muscle and adipocytes). Major drug used in obese type-2 diabetic patients. Available as immediate-release (IR) or extended-release (ER) products. Only the IR is approved for children.

Adult

Initial IR: 500 mg PO bid
Maintenance IR dose: 850 mg PO tid

Pediatric

<10 years: Not established
>10 years: Administer as in adults

Diuretics, thyroid products, oral contraceptives, phenytoin, calcium channel blocking drugs, phenothiazines may decrease effects of metformin; cimetidine may increase metformin levels

Documented hypersensitivity; acute myocardial infarction, septicemia, renal disease

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal insufficiency; discontinue therapy before performing any surgical procedures; impaired liver function


Glyburide (Micronase, DiaBeta, Glynase, PresTab)

Appears to acutely lower blood glucose by stimulating release of insulin from pancreas, an effect dependent on functioning beta cells in pancreatic islets. Mechanism by which DiaBeta lowers blood glucose during long-term administration not clearly established.

Adult

No fixed dosage; fasting blood glucose must be measured periodically to determine minimum effective dose
2.5-5 mg/d PO, with breakfast or first may meal, is usual starting dose; not to exceed 20 mg/d PO; patients who may be more sensitive to hypoglycemic drugs should be started at 1.25 mg/d PO

Pediatric

Not established.

Clofibrate, fenfluramine, histamine H2 antagonists, androgens, azole antifungals, anticoagulants, chloramphenicol, fluconazole, gemfibrozil, magnesium salts, methyldopa, MAOIs, probenecid, salicylates, sulfinpyrazone, urinary acidifiers, NSAIDs, and sulfonamides may enhance hypoglycemic effects; closely observe patient for hypoglycemia; when such drugs are withdrawn, closely observe patient for loss of control
Possible interaction between glyburide and fluoroquinolone antibiotics has been reported, resulting in potentiation of hypoglycemic action of glyburide (mechanism not known)
Possible interactions between glyburide and coumarin derivatives have been reported that may either potentiate or weaken effects of coumarin derivatives (mechanism not known)
Nicotinic acid, oral contraceptives, isoniazid, hydantoins, estrogens, diazoxide, corticosteroids, cholestyramine, beta-blockers, calcium channel blockers, phenothiazines, rifampin, thiazide diuretics, urinary alkalinizers, and sympathomimetics may decrease hypoglycemic effects; closely monitor patient for loss of control; when withdrawn, closely observe patient for hypoglycemia
Potential interaction between PO miconazole and PO hypoglycemic agents leading to severe hypoglycemia has been reported; whether interaction also occurs with IV, topical, or vaginal preparations of miconazole is not known
May increase effects of digitalis glycosides

Documented hypersensitivity; diabetic ketoacidosis, with or without coma; type 1 diabetes mellitus

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hepatic and renal impairment; cardiovascular disorders may occur; risk factors include elderly age, malnutrition, irregular eating, impaired renal function, and possibly hepatic dysfunction (if prolonged or recurrent, hospital admission should be strongly considered); may cause rash; nausea, vomiting, leukopenia, agranulocytosis, aplastic anemia (very rare), intrahepatic cholestasis (very rare), disulfiram reaction, flushing, headache, nausea, and SIADH causing hyponatremia

More on Diabetes Mellitus and Pregnancy

Overview: Diabetes Mellitus and Pregnancy
Differential Diagnoses & Workup: Diabetes Mellitus and Pregnancy
Treatment & Medication: Diabetes Mellitus and Pregnancy
Follow-up: Diabetes Mellitus and Pregnancy
References
Further Reading
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Keywords

gestational diabetes mellitus, gestational diabetes, diabetes mellitus, diabetes, insulin, glucose, blood sugar, metformin, diabetes type 2, diabetic, diabetes 2, hyperglycemia, hypoglycemia, diabetes diet, diabetes treatment, mellitus, diabetes mellitus type 2, diabetes symptoms, diabetes diagnosis, high blood sugar, type 2 diabetes mellitus, type II diabetes mellitus, DM, DM type 2, adult-onset diabetes mellitus, infants of diabetic mothers, IDMs, infant of diabetic mother, IDM, maternal hyperglycemia, fetal hyperglycemia, diabetes inpregnancy,diabetes-associatedbirth defects, diabeticbirth defects, gestational DM, macrosomia, macrosomic infant, macrosomic fetus, diabetic pregnancy, fetal macrosomia

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Contributor Information and Disclosures

Author

Thomas R Moore, MD, Chairman, Professor, Department of Reproductive Medicine, University of California at San Diego School of Medicine
Disclosure: Nothing to disclose.

Medical Editor

Robert K Zurawin, MD, Associate Professor, Director of Baylor College of Medicine Program for Minimally Invasive Gynecology, Director of Fellowship Program, Minimally Invasive Surgery, Department of Obstetrics and Gynecology, Baylor College of Medicine
Robert K Zurawin, MD is a member of the following medical societies: American Association of Gynecologic Laparoscopists, American College of Obstetricians and Gynecologists, American Society for Reproductive Medicine, Association of Professors of Gynecology and Obstetrics, Central Association of Obstetricians and Gynecologists, Harris County Medical Society, North American Society for Pediatric and Adolescent Gynecology, and Texas Medical Association
Disclosure: Johnson and Johnson Honoraria Speaking and teaching; Conceptus Honoraria Speaking and teaching; Biosphere Medical Honoraria Speaking and teaching; Eli Lilly Honoraria Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Romesh Khardori, MD, Chief, Division of Endocrinology, Metabolism and Molecular Medicine, Professor, Department of Internal Medicine, Southern Illinois University School of Medicine
Romesh Khardori, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Medical Association, American Society of Andrology, Endocrine Society, and Illinois State Medical Society
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

Carl V Smith, MD, The Distinguished Chris J and Marie A Olson Chair of Obstetrics and Gynecology, Professor, Department of Obstetrics and Gynecology, University of Nebraska Medical Center
Carl V Smith, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Institute of Ultrasound in Medicine, American Medical Association, Arkansas Medical Society, Association of Professors of Gynecology and Obstetrics, Central Association of Obstetricians and Gynecologists, Council of University Chairs of Obstetrics and Gynecology, Nebraska Medical Association, and Society for Maternal-Fetal Medicine
Disclosure: Nothing to disclose.

 
 
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